As far too many Americans and Texans know, chronic pain remains a huge public health problem and one of the most prevalent reasons why people seek medical care. Chronic pain negatively impacts many aspects of a person�s life as well as the lives of their families, friends, and caregivers. It is essential that patients understand all treatment options for various types of pain.
Chiropractors are highly skilled professionals who are dedicated to providing safe and effective physician-level health care to patients suffering from back pain. Chiropractic care focuses on disorders of the musculoskeletal system and the nervous system as well as promotes a hands-on, non-drug approach to pain management and healthy lifestyles. Their expertise in the prevention, care, and rehabilitation of back, neck, joint, and head pain is critical for treating patients with various pains and disorders and can save the public from the physical and financial tolls of other treatment options. As a first line of defense against pain, chiropractors� services can help individuals heal naturally without the need for drugs or surgery.
At this time, I encourage all Texans to learn more about the vital role that chiropractors play in the health care field and how chiropractic services can benefit their lives. I commend Texas chiropractors for their commitment and efforts to improve the quality of life for all Texans by promoting effective pain management and healthy lifestyles.
Therefore, I, Greg Abbott, Governor of Texas, do hereby proclaim October 2019, to be
Chiropractic Health Month
in Texas, and urge the appropriate recognition whereof.
In official recognition whereof, I hereby affix my signature this the 18th day of September 2019.
� Governor of Texas
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Do you have back, shoulder, neck, leg pain, headaches, or stress? Pain medications work for only so long and don�t fix the problem. A chiropractor can help your symptoms. A chiropractic adjustment means that a chiropractor physically/manually adjusts the vertebrae in the spine. This procedure creates positive effects without the stress or invasiveness of surgery. A chiropractic adjustment�can be a great way to improve multiple areas of the body, along with improving overall health with non-invasive treatment.
Previous research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity on neurons. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain (0.96-1.62 ?mol/gram wet weight), their extracellular concentrations in the cortex as measured by microdialysis (1.62 ?M for L-aspartate and 9.06 ?M for L-glutamate) and their supply according to immunohistochemistry suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. EAATs which play a fundamental role in the uptake of all vesicular released L-glutamate in the central nervous system (CNS) also requires the utilization of L-aspartate. L-aspartate is perhaps as less essential as L-glutamate connected to the total excitatory activity associated with iGluRs. Along with its role as a neurotransmitter, as previously mentioned, L-aspartate is also necessary as a substrate for aspartate amino-transferase which turns into 2-oxoglutarate and L-glutamate to transport to the cortical vesicles of glutamatergic neurons which may also consequently and indirectly increase L-glutamate release. �
Other Molecules in Glutamate Signaling
One characteristic which distinguishes NMDA receptors from different iGluRs is that the activation of NMDA receptors needs the connection of a co-agonist to the glycine binding region of the receptor. By way of instance, in the retina and in the spinal cord, the origin of glycine may spillover out of glycinergic inhibitory synapses. But, in different regions of the brain with increased NMDA receptor expression, such as the hippocampal formation, reactions associated with strychnine-sensitive glycine receptors are missing, at least in adult neurons, demonstrating the absence of glycinergic inhibitory neurotransmissions. But, glycine is found in the extracellular fluid of the hippocampus at baseline amounts of roughly 1.5 ?M, which is similar to the saturation of the glycine binding region of the NMDA receptor, although these may be up- and down-regulated. The origin of extracellular glycine in the hippocampus can be neurons which release glycine through the alanine-serine-cysteine amino acid transporter 1 (asc-1). But, glycine release by astrocytes that is stimulated by depolarization and kainate, has also been demonstrated. Further research studies are required to ultimately show these outcome measures. �
Even in previous research studies of the NMDA receptor and its co-activation by glycine revealed that D-amino acids, particularly D-serine, are nearly as powerful as glycine. Only several years after, it became obvious that D-serine is found in rat and human brains at roughly one-third of their concentration of L-serine having an absolute concentration of more than 0.2 ?mol/g brain tissue. Utilizing an antiserum for D-serine, research studies demonstrated that D-serine from the brain is only found in astrocytes and its supply fits the expression of NMDA receptors. In addition, the same researchers demonstrated that D-serine is released from cultured astrocytes when exposed to L-glutamate or kainate. The abundance of D-serine is found by the degrading enzyme D-amino acid oxidase (DAO) which reveals increased expression in the hindbrain where D-serine levels are reduced as well as the synthetic enzyme serine racemase which creates D-serine from L-serine. D-Serine appears to be stored in cytoplasmic vesicles in astrocytes and it can be released by exocytosis. Long-term potentiation is dependent upon D-serine release from astrocytes in hippocampal slices, suggesting that this amino acid definitely plays a fundamental role in glutamatergic neurotransmission through NMDA receptors. Additionally in hippocampal slices, research studies found, utilizing D-serine and glycine degrading enzymes, which D-serine functions as a co-transmitter for synaptic NMDA receptors on CA1 neurons likewise which glycine functions as the endogenous co-agonist for extrasynaptic NMDA receptors. Synaptic NMDA receptors of dentate gyrus neurons utilize glycine rather than D-serine as the co-agonist. �
Taken collectively, multilayered outcome measures show that L-aspartate doesn’t simply function as an agonist on NMDA receptors but also glycine and D-serine play fundamental roles in glutamatergic neurotransmission in the human brain. But, other molecules also have been demonstrated to be relevant modulators of glutamatergic neurotransmission. �
Glutamate Activated by Other Molecules
L-homocysteate (L-HCA) has structural similarities with L-glutamate. The non-protein amino acid is an oxidation product of homocysteine that is biosynthesized from methionine in the elimination of its own terminal methyl group and it is also an intermediate of the transsulfuration pathway by which methionine may be converted to cysteine through cystathionine. Early research studies demonstrated that this amino acid can cause calcium influx in cultured neurons as safely and effectively as L-glutamate. Moreover, L-HCA revealed an increased affinity for NMDA receptors when compared to other iGluRs in binding assays associated with its capacity to cause NMDA receptor antagonist-inhibitable excitotoxicity and sodium influx. Additionally, L-HCA can trigger mGluR5 as efficiently as L-glutamate. L-HCA is found in the brain, however, the concentrations were demonstrated to be approximately 500-fold lesser than those of L-glutamate and even 100-fold lesser when compared to those of L-aspartate in different regions of the rat brain. Throughout potassium-induced stimulation, L-HCA discharge is triggered from brain slice preparations as demonstrated for L-aspartate and L-glutamate although the absolute release of HCA is approximately 50-fold lesser. Surprisingly, HCA is a very efficient competitive inhibitor of cystine and L-glutamate uptake through the cystine/glutamate antiporter system x?c, the activity that regulates and manages the extracellular extrasynaptic L-glutamate concentrations in the brain. Therefore, the impact of L-HCA on the activation of NMDA and other L-glutamate receptors may also rely on the L-HCA-induced trigger of L-glutamate through system x?c. L-HCA may play an important role in the overall stimulation of L-glutamate receptors. Nevertheless, this can change tremendously under certain conditions, e.g., in patients with high-dose methotrexate therapy, an anticancer drug which, by restricting dihydrofolate reductase, limits the tetrahydrofolate-catalyzed recycling of methionine from homocysteine. Here, L-HCA concentrations of more than 100 ?M have been demonstrated from the cerebrospinal fluid whereas L-HCA was undetectable in control subjects. Further research studies are still required to determine these outcome measures. �
Further endogenous small molecules which are believed to affect L-glutamate signaling include several intermediates of tryptophan metabolism, as shown in Figure 2. Through the activity of indoleamine 2,3-dioxygenase (IDO) or tryptophan 2,3-dioxygenase (TDO), tryptophan is turned into N-formyl-L-kynurenine which is later turned into kynurenine (KYN) by formamidase. Three pathways, two of which connect at a subsequent step, result in further metabolism. First, through the activity of kynurenine aminotransferase (KAT), KYN is converted into kynurenic acid (KYNA). KYN can also be converted to 3-hydroxykynurenine (3HK) by kynurenine monooxygenase (KMO), which can subsequently be utilized as a substrate by kynureninase for the synthesis of 3-hydroxyanthranilic acid (3HANA). Additionally, utilizing KYN as a substrate, kynureninase develops anthranilic acid (ANA), which by non-specific hydroxylation may also be converted to 3HANA. According to research studies, 3HANA finally functions as a substrate for the generation of quinolinic acid (QUIN). �
The tryptophan concentration in the rat brain is roughly 25 nmol/g wet weight and approximately 400-fold less than L-glutamate and 100-fold less than L-aspartate. The demonstrated brain levels of kynurenines are even lower with 0.4-1.6 nmol/g for QUIN, 0.01-0.07 nmol/ml for KYNA, and 0.016 nmol/g for 3HANA. Approximately 40 percent of brain KYN is locally synthesized. The metabolites of tryptophan demonstrate differential binding to plasma proteins and their transport through the barrier which is quite different. KYN and 3HK are carried through the large neutral amino acid carrier system L. Kynurenines seem to penetrate the human brain by passive diffusion. Additionally, KYNA, 3HANA, and especially ANA bind to serum proteins which then ultimately restrict and limit their diffusibility across the blood-brain barrier. �
Research studies demonstrated that QUIN, when ionophoretically utilized in rat cells, caused neuronal firing which has been prevented by an NMDA receptor antagonist, suggesting that QUIN may function as an NMDA receptor agonist. However, the EC50 for QUIN to trigger NMDA receptor currents has been shown to be roughly 1000-fold higher than the EC50 of L-glutamate. Intracerebral injection of QUIN was proven to cause ultrastructural, neurochemical, and behavioral changes similar to those caused by NMDA receptor agonists. The fact that QUIN concentrations are about 5000- to 15,000-fold lower than cerebral L-glutamate concentrations makes it unlikely that modulation of NMDA receptor signaling by QUIN plays an essential role. KYNA was demonstrated to function as an NMDA receptor antagonist. But, although infusion with the KMO inhibitor Ro 61-8048 improved cerebral extracellular KYNA concentrations 10-fold, this didn’t result in an inhibition of NMDA-mediated neuronal depolarization, a finding which challenges the belief that KYNA at near-physiological amounts directly modulates NMDA receptors. In comparison, increased KYNA in the brain induced from the KMO inhibitor JM6 decreased the extracellular cerebral L-glutamate concentration. Additionally, KYNA levels from the extracellular cerebral fluid have been associated with L-glutamate levels suggesting that even at physiological or near physiological levels, KYNA modulates L-glutamate metabolism. Both the activation of the G-protein-coupled receptor GPR35 and the inhibition of presynaptic ?7 nicotinic acetylcholine receptors are suggested in the KYNA-induced reduction in L-glutamate release. To summarize, although QUIN and L-HCA are present in the human brain, their concentrations discuss against them with roles in regulating and maintaining neurotransmission. In contrast, even though the pathways have to be defined in greater detail, evidence supports levels and the opinion that discharge can be modulated by KYNA and neurotransmission. �
Glutamate, together with aspartate and other molecules, are several of the main excitatory neurotransmitters in the human brain. Although these play a fundamental role in the overall structure and function of the central nervous system, including the brain and the spinal cord, excessive amounts of other molecules can ultimately trigger glutamate receptors. Excess glutamate can cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurological diseases. The following article describes how other molecules can activate glutamate receptors. – Dr. Alex Jimenez D.C., C.C.S.T. Insight – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Research studies suggest that L-aspartate, like L-glutamate, triggers excitatory activity. L-aspartate functions with L-glutamate in the synaptic vesicles of asymmetric excitatory synapses. But, the total concentration of these in the human brain suggest that L-aspartate is significantly less abundant than L-glutamate. Moreover, L-aspartate is a powerful agonist for NMDA receptors but not for other iGluRs with an EC50 just eight-fold higher than that of L-glutamate. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
The term excitotoxicity was first employed to demonstrate the capability of L-glutamate, in addition to structurally-associated amino acids, to destroy nerve cells, a process which has been suggested to occur in acute and chronic health issues of the central nervous system (CNS). Excitotoxicity is caused by the excess stimulation of iGluRs into a characteristic loss of cell bodies and dendrites as well as post-synaptic structures. There is a substantial degree of variation in the sensitivity of nerve cells compared to the variety of iGluRs which is associated with the specific receptors demonstrated on the nerve cells and their metabolisms. The susceptibility of neurons to excitotoxicity can be affected with age. �
Acute excitotoxic nerve cell death is believed to occur in reaction to a number of severe insults, including cerebral ischemia, traumatic brain injury (TBI), hypoglycemia, and status epilepticus. However, what about neurodegenerative diseases, such as Alzheimer’s disease? Does chronic excitotoxicity also occur? Could exposure of nerve cells to low but above-average concentrations of L-glutamate, or even glutamatergic neurotransmission through a variety of molecules be involved as previously mentioned, within an extended time period also significantly result in neural cell death? The purpose of the article below is to demonstrate the concepts of acute and chronic glutamate toxicity on the health and wellness of the brain. �
Acute and Chronic Glutamate Toxicity
Excitotoxicity was initially studied in animals, however, so as to comprehend the mechanisms underlying this procedure, cell culture models were developed. The basic cell culture model of acute excitotoxicity involves the treatment of principal neurons in accordance with L-glutamate or particular iGluRs for a brief time interval (min) and then analyzing downstream events in the time point which is most relevant for the research study. By way of instance, cell death is frequently determined after 24 hours. While these types of research studies are proven to be quite useful for understanding the pathways involved in acute excitotoxicity, it has demonstrated to be far more difficult to evaluate chronic excitotoxicity in culture partially because it is not completely clear how to specify “chronic” in the context of cell culture. Does consistent imply a minimal dose supplied for 24 hours instead of a maximum dose supplied for 5 to 10 minutes or is it more complicated than that? �
Among the few research studies which tried to come up with a model of chronic excitotoxicity, it was revealed that it is indeed more complicated with acute and chronic excitotoxicity appearing to be different processes. In this research study, the researchers utilized pure cultures of primary cortical neurons developed from day 14 mouse embryos and treated them after seven and 14 days in culture (DIV). For constant excitotoxicity, the neurons were exposed to L-glutamate or NMDA for 24 hours and for severe excitotoxicity for 10 minutes. In both circumstances, cell death was measured after 24 hours. Surprisingly, the EC50s in their toxicity of L-glutamate were lower for acute toxicity, particularly in the 7 DIV cultures, when compared with the EC50s for chronic toxicity. Additionally, it was discovered that a high cell culture density increased the cells’ sensitivity into excitotoxicity that was acute but not chronic. Further research studies indicated that the lower sensitivity of these neurons to L-glutamate in the chronic excitotoxicity paradigm was due to the stimulation of mGluR1, associated with earlier data on the neuroprotective effects of mGluR1 stimulation, among other important processes. �
Further Research Studies for Glutamate Toxicity
An alternative approach for understanding chronic glutamate toxicity used organotypic spinal cord cultures in conjunction with L-glutamate uptake inhibitors. These spinal cord cultures, which had been prepared from 8-day-old rat pups, were kept in culture for up to 3 months. Persistent inhibition of L-glutamate uptake utilizing two varieties of uptake inhibitors caused a consistent increase of L-glutamate in the cell culture medium and time period as well as a concentration of dependent motor neuron cell death. The highest concentration of uptake inhibitor increased extracellular L-glutamate levels at least 25-fold and began to kill the cells within 1 week whereas a five-fold lower concentration raised extracellular L-glutamate levels eight-fold and cell death only began after 2 to 3 weeks of treatment. The toxicity was obstructed with non-NMDA but not NMDA receptors as well as by inhibitors of L-glutamate synthesis or release. These research studies ultimately indicate that moderately increased L-glutamate concentrations can also induce toxicity as well as a variety of other health issues. �
In vivo approaches to studying excitotoxicity have relied on an approach analogous to that utilized with the spinal cord cultures. In the wide variety of the research studies, a single or multiple EAATs were transiently or permanently genetically eliminated and the effects on brain function were evaluated. During the first few research studies, which utilized rats, chronic intraventricular administration of antisense RNA was utilized to eliminate every one of the 3 primary EAATs (EAAT1, EAAT2, and EAAT3). The loss of either of the glial L-glutamate transporters (EAAT1 and EAAT2) but not the neuronal transporter (EAAT3) caused large increases in extracellular L-glutamate concentrations in the striatum following 7 days as demonstrated by microdialysis (EAAT2, 32-fold increase; EAAT1, 13-fold increase). Treatment with the EAAT1 or EAAT2 antisense oligonucleotides caused a progressive motor impairment whereas epilepsy was produced by the EAAT3 antisense oligonucleotide. The loss of any of the 3 transporters demonstrated clear evidence of neuronal damage in the striatum and hippocampus after 7 days of treatment although the effects of the EAAT1 and EAAT2 antisense oligonucleotides were far more dramatic, consistent with the substantial increases in extracellular L-glutamate brought about by treatment. �
Particularly different results were demonstrated with homozygous mice deficient in EAAT2 or EAAT1. Mice deficient in EAAT2 demonstrated sudden and normally deadly seizures with 50 percent dead by 6 weeks of age. Approximately 30 percent of these mice demonstrated selective degeneration in the CA1 area at 4 to� 8 weeks of age. L-glutamate amounts in the CA1 region of the hippocampus measured by microdialysis were three-fold greater in the mutant mice as compared with the wild type mice. In contrast, heterozygous EAAT2 knock-out mice have an average lifespan and do not reveal hippocampal CA1 atrophy. However, they exhibit several behavioral abnormalities suggestive of moderate glutaminergic hyperactivity. While mice deficient in EAAT1, that is expressed in cerebellar astrocytes, didn’t reveal changes in cerebellar arrangement or obvious indicators of cerebellar impairment, such as ataxic gait, they had not been able to adapt to difficult motor tasks like rapidly running the rotorod. When taken collectively, these results imply that disruptions in homeostasis which are glutamatergic have a greater impact when they occur in the animal rather than when they are found from conception. �
Other Health Issues in Glutamate Toxicity
Tuberous sclerosis complex (TSC) is a multi-system genetic disease caused by the mutation of both TSC1 or TSC2 genes, where it is characterized by severe neurodegenerative diseases. Mice with inactivation of the TSC1 gene in glia have a less than 75 percent reduction in the expression and function of EAAT1 and EAAT2 as well as to cause seizures. At 4 weeks of age, prior to the development of seizures in these mice, there was a 50 percent increase in extracellular L-glutamate in the hippocampus of the mutant mice, as determined by microdialysis, which correlated with increases in markers of cell death in neurons in both hippocampus and cortex. Utilizing slices from mice that were 2 to 4 week old, impairments in long-term potentiation were determined, which translated into deficits when mice were analyzed for contextual and spatial memory in the Morris water maze and fear conditioning assays. Further research studies are still necessary for outcome measures. �
In the majority of the research studies described above, there was a large increase in extracellular L-glutamate that, when analyzed, caused adverse effects on the role of specific neuronal populations. To ascertain the long-term effects of more moderate increases in extracellular glutamate, further research studies created transgenic (Tg) mice with extra copies of this gene for Glud1, especially in neurons. Mitochondrial 2-oxoglutarate from Glud1 is transported into the cytoplasm of nerve terminals in which it’s converted back into L-glutamate and kept in synaptic vesicles thus leading to the pool of synaptically releasable L-glutamate. Nine-month-old Glud1 Tg mice demonstrated a 10 percent boost in L-glutamate in the hippocampus and striatum relative to wild type mice as determined to utilize magnetic resonance spectroscopy. In addition, 50 percent caused increased L-glutamate release in the striatum. At 12 to 20 months of age, the Glud1 Tg mice revealed significant decreases in the numbers of neurons in the CA1 area of the hippocampus and granule cell layer of the dentate gyrus in addition to an age-dependent loss of the two dendrites and dendritic spines in the hippocampus. There was also a drop in long-term potentiation after high frequency stimulation in hippocampal slices in the mice when compared with the wild type mice. Evaluation of the transcriptome of those Glud1 Tg mice in comparison with wild type mice indicated that long-term moderate increases in cerebral L-glutamate ultimately caused both rapid aging in the level of gene expression combined with compensatory reactions which protected against pressure and/or promoted recovery, among other capabilities. �
Conclusion
Brain function and nerve cell survival can be affected by excitotoxicity. The results appear to be highly dependent on the degree of L-glutamate increase, however, even a 10 percent growth appears to influence nerve cell survival, particularly in the context of aging indicating that chronic excitotoxicity may be associated with neurodegenerative diseases. �
Several toxins which connect to iGluRs and that have also been demonstrated to cause excitotoxicity in cell culture may cause slowly growing neurological health issues in both animals and humans. Surprisingly, each toxin appears to target a particular type of neuron, an effect which may be associated with the pharmacokinetics and ADME properties of the toxins, which have not been analyzed to any great extent. The data from these types of toxins supports the idea that excitotoxicity may play a fundamental role in neurodegenerative diseases as well as in other health issues which exist in humans. �
Because iGluRs are demonstrated both from the synapse and in extra-synaptic locations, there has been a great deal of effort devoted to discovering if the region of the receptors impacts the toxicity of molecules. An influential research study with primary neuronal cultures indicated that synaptic and extrasynaptic NMDA receptors have counteracting effects on cell survival with neural cell death being primarily controlled by extrasynaptic NMDA receptors. Nonetheless, these outcome measures have not been reproduced in brain slices or in vivo. Furthermore, many more recent research studies utilizing the exact same primary neuronal culture preparation protocol as the prior research study found either no difference between synaptic and extrasynaptic NMDA receptors in boosting excitotoxicity or discovered that both receptors were needed for cell death. Finally, a variety of research studies that supported the idea that extrasynaptic NMDA receptors promote excitotoxicity relied on the NMDA receptor inhibitor memantine that was originally believed to specifically act on extrasynaptic NMDA receptors. However, more recent research studies demonstrate that memantine can inhibit both synaptic and extrasynaptic NMDA receptors. These results strongly imply that synaptic and extrasynaptic NMDA receptors may contribute to excitotoxicity but the contribution of each depends on the experimental and/or pathological conditions. �
Glutamate is the primary excitatory neurotransmitter in the brain. Although it plays a fundamental role in the overall structure and function of the central nervous system, excessive amounts of glutamate can ultimately cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurodegenerative diseases. Acute and chronic excitotoxicity treatment currently focuses on decreasing or restricting glutamate receptors or extracellular glutamate. The article above summarizes the available research studies for glutamate toxicity in neurodegenerative diseases. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
Excitotoxicity demonstrates the capability of L-glutamate, as well as structurally-associated amino acids, processes which have been suggested to occur in acute and chronic excitotoxicity. Excitotoxicity is caused by the excess stimulation of iGluRs in cell bodies and dendrites as well as post-synaptic structures. There is a substantial degree of variation in nerve cells compared to iGluRs associated with the receptors demonstrated on the nerve cells and their metabolisms. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
Formulas for Methylation Support
XYMOGEN�s Exclusive Professional Formulas are available through select licensed health care professionals. The internet sale and discounting of XYMOGEN formulas are strictly prohibited.
Proudly,�Dr. Alexander Jimenez makes XYMOGEN formulas available only to patients under our care.
Please call our office in order for us to assign a doctor consultation for immediate access.
If you are a patient of Injury Medical & Chiropractic�Clinic, you may inquire about XYMOGEN by calling 915-850-0900.
�
For your convenience and review of the XYMOGEN products please review the following link.*XYMOGEN-Catalog-Download �
* All of the above XYMOGEN policies remain strictly in force.
Hormone testing can now be done by using top of the line integrative methods and techniques. There are multiple reasons and benefits for an individual to complete a hormone test. These tests have the ability to help a patient understand their cycle, testosterone/ estrogen levels, why they are tired upon waking or throughout their day, and more.
Precision Analyical, Inc. has discovered a way to use scientists who have extensive experience and coupled them with the most advanced analytical methods and instruments. This allows them to achieve the best results when it comes to the dutchtest.
What is D.U.T.C.H?
D.U.T.C.H stands for ” Dried Urine for Comprehensive Hormones” and is comprised of multiple tests designed by Precision Analytical Inc. Dried urine samples allow scientists to see an entire day of hormones and measure multiple different aspects. There are different D.U.T.C.H tests that can be completed depending on the patient’s needs.�
Dutch Complete– This is a comprehensive assessment of sex and adrenal hormones and their metabolites. This test measures progesterone, androgen, estrogen metabolites, cortisol, cortisone, cortisol metabolites, creatine, DHEA-S.�
Dutch Sex and Hormone Metabolites– This test is focused on testing progesterone, androgen, estrogen metabolites
Dutch Adrenal– This is important to measure because it controls the stress hormone and the levels in the body to help with energy upon waking. This test specifically measures cortisol, cortisol metabolites, creatinine, DHEA-S
Dutch OATS “Organic Acid Tests”-� This test will give insights to symptoms such as mood and fatigue. This test measures 9-OHdG, melatonin.
Dutch Plus– This test uses 5 saliva samples to provide the up and down pattern of cortisol and cortisone throughout the day. This test adds salivary cortisol measurements of the cortisol awakening response (CAR) to the dutch complete to bring another important piece of the HPA axis into focus
Dutch Test Cycle Mapping– This test maps the progesterone and estrogen pattern throughout the menstrual cycle. It provides the full picture of a woman’s cycle to answer important questions for patients with month-long symptoms, infertility, and PCOS. This test is targeted to measure 9 estrogens and progesterone that are taken throughout the cycle to characterize the follicular, ovulatory, and luteal phases.�
How Does It Work?
One of the reasons that many practicing offices are starting to use the D.U.T.C.H tests is because they have an extremely simple sample collection. Patients will collect just 4-5 dried urine samples over a period of 24 hours. This makes transportation and collection of the sample hassle-free. The dried urine samples provide excellent results due to the fact that the collections offer a span of the entires day hormones. The time of testing looks as follows:
The patient obtains the first sample at approximately 5pm ( dinnertime)
The� second sample is to be taken around 10 pm ( bedtime)
This next sample is dependent upon each individual, but if the patient wakes to urinate during the night, a sample is to be collected at this time.
The third sample should be collected within 10 minutes of rising. It is very important that the patient does not lay in bed after waking and they collect this sample within those allotted 10 minute time frame.
Once the patient has collected their third sample upon rising, they should set an alarm for 2 hours, as this is when the fourth and final sample is to be collected.
As one can see above, these urine samples will be dry when sent off to the lab. Studies show that dried urine samples are stable for weeks and will give an accurate representation of the hormone levels that are being assessed. From here, the results are gone over with a team of clinicians from Precision Analytical with the doctor who ordered the test. This ensures that the best treatment protocol is created for the patient.��
What Is The Purpose?�
With the turn around time being just 7-10 business days, individuals can gain control fairly quickly. As mentioned, Precision Analytical uses the most advanced instruments to achieve the best results for patients. The main purpose is to create an understanding of what is going on inside the patient’s body and allows the treatment to be more specific and targeted to the individual’s needs. As Chiropractic Health Month approaches, there is no better time than now to get started!�
�I highly recommend the D.U.T.C.H test. Knowing and understanding your hormones and the times that they are rising and falling throughout the day opens so many doors. It allows an individual to have an understanding of why they are so tired or why they can not fall asleep and take distinctive steps towards correcting that issue, rather than shooting in the dark. In addition, it allows patients to have knowledge of what is occurring when it comes to their sex hormone metabolites. This test gives the ordering doctor a complete look at the patient’s hormones and ensures they can be confident in creating a treatment protocol. – Kenna Vaughn, Senior Health Coach
The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
For anyone that has dealt with mold knows that it is mostly found in fresh produce when it hasn’t been eaten. It is even there is a new damp spot in the house, and it�s left untreated. Mold is a type of fungus that is presented everywhere, including the air. It can actually cause someone highly sensitive to mold exposure to have chronic raspatory illnesses like asthma and bronchitis.
Studies show that the most common species of mold is Stachybotrys chartarum or black mold. This type of fungus thrives in warm, moist environments, including the basement, the bathroom, and the kitchen. It releases toxins in the air that is irritating or harmful to individuals with existing health conditions and becoming mycotoxin.
What is Mycotoxin?
A mycotoxin is a secondary metabolite being produced by organisms of the fungal kingdom. It can move in and out of cells in the body, causing inflammation when it is indigested. Researchers suggest that mycotoxin can link to serious health problems to people who live in contaminated buildings, and it can have long-term results. In most cases, mycotoxin can cause problems in the gut by consuming moldy food; causing leaky gut and destroying the gut microflora.
Here are some of the symptoms of mycotoxin:
Aches and pains
Mood changes
Headaches
Brain fog
Asthma
Watery, red eyes
Runny or blocked nose
Gut inflammation
Sore throat
They are teratogenic, mutagenic, nephrotoxic, immunosuppressive, and carcinogenic. They can cause DNA damage, cancer, immune suppression, neurological issues, and a variety of adverse health effects on the human body. With mycotoxins, they have spores and pieces of hyphae that releases toxins into the air. They are tiny, but they are not easily detectable in the bloodstream since they can attach themselves to enzymes that are involved in insulin receptors. This results in dysfunction the in cells ability to intake and process glucose in the gut.
When mycotoxin is in the gut, it damages the intestinal barrier. It can cause malabsorption of food and disrupts the protein synthesis. When that happens, the individual�s autoimmunity will rise up, causing their bodies to go into overdrive to fight the problem.
Mycotoxin can actually grow in grains such as rice. The fungal mycotoxin has been known to cause liver damage since the contaminated food is being consumed by people, and it creates a rise in inflammation. When this happens, individuals start being sensitive to the contaminated foods that they are consuming. There is still more research to mycotoxin that is being produced to create a resistance to mycotoxin exposure.
Diagnosing Mycotoxin
Mycotoxin can�t be diagnosed by the symptoms themselves, doctors can perform one of these tests to determine the severity of mycotoxins in individuals.
Blood test: Physicians can take a patient�s blood sample and send it to a testing lab to test. This is to see if there is a reaction of specific antibodies in the patient�s immune system. A blood test can even check the individual�s biotoxins in their blood to see if mycotoxin present.
Skin prick test: Healthcare professionals can take tiny amounts of mold and use a small needle to apply it onto the patient�s skin. This is to determine if the individual is breaking out in bumps, a rash or hives, then they are allergic to any mold species.
Diagnosing mycotoxin is known by many names, but it is mostly called mast cell disorder. Even though they are different and have different manifestations, diagnosing them in the body is essential to help individuals to heal their ailments. With technology getting better, healthcare physicians can detect mycotoxins in the body much faster.
Treating Mycotoxin
There are many ways to treat mycotoxin. Options include:
Avoiding the mold whenever possible.
A nasal rinse to flush out the mold spores that are in the nose.
Antihistamines to stop the itchiness, runny noses, and sneezing due to mold exposure.
A short term remedy for congestion is using decongestant nasal spray.
Montelukast is an oral medication to reduce the mucus in a patent�s airways to lower the symptoms for both mold allergies and asthma.
Doctors can recommend patients an allergy shot to build up the patient�s immunity to mycotoxin if the exposure is long term.
How to check for mycotoxin?
When individuals are checking for mycotoxins in their environment, it is best to hire professionals to help identify and remove it. A lot of individuals can look for black clusters growing in warm, moist rooms and can search for the causes of mold growth like any leaks, old food, papers, or wood. People can throw away the items that are affected by mold or that are contributing to mold growth. They can also remove the things that are not affected by mold exposure.
Wearing a mold-resistant suit, mask, gloves, and boots can protect individuals as they are getting rid of mildew and mold from their environment. Even purchasing a HEPA air purifier can help get rid of the spores to ensure that no allergens will affect the body�s immune system. When individuals are removing the mold exposure out of the affected area, they can cover the non-affected surfaces with bleach or a fungicidal agent. Then let it dry to prevent the mold from reproducing on the same area it has infected.
Conclusion
Since researchers are still doing a test on mycotoxin, mold exposure is still all around the world and in many forms. It can even contaminate food and places where it can thrive and grow. Individuals can prevent it from locating the source and can take precautions when they are exposed to the spores. If the individual is exposed to mycotoxin, going to the doctors to get tested is the best route to go. The scope of our information is limited to chiropractic, musculoskeletal, and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 .
References
Borchers, Andrea T, et al. �Mold and Human Health: a Reality Check.� Clinical Reviews in Allergy & Immunology, U.S. National Library of Medicine, June 2017, www.ncbi.nlm.nih.gov/pubmed/28299723.
Do�en, Ina, et al. �Stachybotrys Mycotoxins: from Culture Extracts to Dust Samples.� Analytical and Bioanalytical Chemistry, Springer Berlin Heidelberg, Aug. 2016, www.ncbi.nlm.nih.gov/pmc/articles/PMC4939167/.
Gautier, C, et al. �Non-Allergenic Impact of Indoor Mold Exposure.� Revue Des Maladies Respiratoires, U.S. National Library of Medicine, June 2018, www.ncbi.nlm.nih.gov/pubmed/29983225.
Hurra�, Julia, et al. �Medical Diagnostics for Indoor Mold Exposure.� International Journal of Hygiene and Environmental Health, U.S. National Library of Medicine, Apr. 2017, www.ncbi.nlm.nih.gov/pubmed/27986496.
Jewell, Tim. �Black Mold Spores and More.� Black Mold Exposure, 1 June, 2018, www.healthline.com/health/black-mold-exposure.
Leonard, Jayne. �Black Mold Exposure: Symptoms, Treatment, and Prevention.� Medical News Today, MediLexicon International, 17 Sept. 2019, www.medicalnewstoday.com/articles/323419.php.
Pitt, John I, and J David Miller. �A Concise History of Mycotoxin Research.� Journal of Agricultural and Food Chemistry, U.S. National Library of Medicine, 23 Aug. 2017, www.ncbi.nlm.nih.gov/pubmed/27960261.
Sun, Xiang Dong, et al. �Mycotoxin Contamination of Rice in China.� Journal of Food Science, U.S. National Library of Medicine, Mar. 2017, www.ncbi.nlm.nih.gov/pubmed/28135406.
Sciatica doesn�t have to prevent you from being able to travel.
Sometimes a journey can create a series of challenges for people with sciatic nerve pain in the low back and leg.
A common issue among individuals is to prevent sciatica from flaring up when on the road or in the air.
A solution for this is to find ways to keep moving. However, easier said than done, but it can be done!
Flying and driving often mean long periods of sitting and sitting in a position typically not friendly with sciatic pain.
“When we drive or fly for an extended trip, it means long sitting times, and sitting in a position that can cause sciatica to flare up at any time,” says Dr. Alexander Jimenez, D.C. in El Paso, Texas, and member of the American Chiropractic Association (ACA).
Dr. Jimenez shares some basic tips for keeping mobility up, all the while pain-free, when flying and driving with sciatica.
He also offers additional advice to keep radiating pain from starting, upon arrival.
Flying with Sciatica
Sciatica pain radiates through the lower body meaning:
The low back
Hips
Buttocks
Legs
So when a flight anchors you to a seat, this can aggravate the area and cause pain.
The first thing to consider is the seat choice.
An aisle seat allows you the easiest access out of the seat, allowing you to move more during the flight.
Also when flying with sciatica, tell the flight crew about your condition.
When the seatbelt off light comes on, get up, stretch your legs and move around anywhere you can find room.
With a good portion of the population suffering from sciatica, most crews have seen people with this condition, and will usually let you do some stretching if they’re not busy.
A good sciatica stretch is to put your hands on something stable and do some deep knee bends.
This will use the upper body weight to stretch the lumbar spine comfortably.
Do a few and make sure you feel and return to your seat stretched and refreshed.
When taking a long flight, do this every hour to feel better when landing.
Sciatica Road Trip
Road trips, on the other hand, are easier to stop and move around. However, it can also create over-concentration on the drive and forgetting how much you are hurting until the pain is unbearable.
Dr. Jimenez advises frequentstops, if possible every hour is best to prevent pain.
On the stops walk two or three laps around the car/Suv/truck.
Rear bumper stretching prop
Place one foot on the bumper, and the other a few feet behind, lean into the bumper and square the hips with the lead foot.
This is like a hurdle stretch.
Stretch both legs on each break.
Regular stretching helps relieve the pressure on the low back so you can drive comfortably.
Arrival
Packing light is a healthy tip because hauling heavy luggage will aggravate sciatic nerve pain.
There are a few things that Dr. Jimenez recommends packing or getting upon arrival.
Gel ice pack you can keep in the refrigerator or freezer in a hotel.
Apply the cold pack to the low back for 20-minute increments will go a long way toward relieving pain.
Topical agent/cream/gel that has menthol or camphor, that you can apply to any area of tenderness or pain before the ice gel pack.
This increases the ice pack’s power by helping relax muscles and decreasing pain.
Supportive shoes or custom foot orthotics
People with sciatica should choose footwear or orthotics that support all three arches of the foot.
Leg length is usually not equal on each side, and proper arch supports can be custom made for you by your chiropractor to compensate for the difference.
Even a 5mm difference can cause chronic back pain.
And if possible, ask your chiropractor or primary physician if they can recommend a chiropractor, physical/massage therapist,� or acupuncturist that you can see in case you need emergency treatment.
This can give you some peace of mind.
Keep Your Exercise/Stretching Routine When Traveling
When we travel especially on vacations it can be easy to let healthy lifestyle habits you practice at home slide.
All are sciatica�s natural enemies make sure to bring these healthy practices with you to your destination.
Use the same good sense when you travel just like at home getting:
Get plenty of rest
Drink plenty of water
Don’t overeat
You will need more rest when you travel and don’t forget when you travel to:
Walk
Stretch
Stay mobile
Difference Foot Orthotics Make to *REDUCE FOOT PAIN* & Correct Posture | El Paso, TX (2019)
Custom made foot orthotics can help control foot motion and posture. Healthcare professionals prescribe custom foot orthotics to help patients focus on their foot posture and mobility control. Research studies have ascertained that using custom foot orthotics for posture and mobility control can help fix excessive foot pronation and supination to prevent a variety of foot health problems. The subsequent video describes how custom foot orthotics will help control foot posture and mobility to improve health and wellness.
NCBI Resources
Sciatica is generally caused by the compression of lumbar or sacral nerves or by compression of the sciatic nerve. When sciatica is caused by compression of a dorsal nerve root, it’s known as lumbar radiculopathy. This can occur because of a spinal disk bulge or spinal disk herniation (a herniated intervertebral disc), or by roughening, enlarging, or misalignment (spondylolisthesis) of the fascia, or as a consequence of degenerated discs which can reduce the diameter of the lateral foramen by which nerve roots exit the spine.
L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the following article, we will discuss the general principles of L-glutamate signaling in the brain. Then, we will demonstrate this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discuss their possible physiological functions in the human brain. �
Glutamate Signaling in the Brain
According to research studies, the human brain has about a 6 to 7 ?mol/g wet weight of L-glutamate. L-glutamate, together with glutamine, is one of the most abundant free amino acids in the central nervous system (CNS). More than five decades ago, several research studies demonstrated that L-glutamate has an excitatory response on nerve cells. Since then, its role as an excitatory neurotransmitter as well as its cerebral metabolism has been evaluated in numerous research studies. �
L-glutamate is commonly found throughout synaptic vesicles in the presynaptic terminal through the process of vesicular glutamate transporters. Additionally, several of the L-glutamate in the vesicles may develop by a vesicle-associated aspartate amino-transferase from 2-oxoglutarate utilizing L-aspartate as the amino group donor. During the depolarization of the presynaptic membrane, L-glutamate is released into the synaptic cleft and connects to ionotropic glutamate receptors, known as iGluRs, at the postsynaptic membrane, as shown in Figure 1. According to research studies, iGluRs are characterized as ligand-gated ion channels which include receptors of the ?-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA), kainate, and N-methyl-D-aspartic acid (NMDA) types. While AMPA and kainate receptors primarily regulate and maintain sodium influx, NMDA receptors actually have a high calcium conductivity. Moreover, the activation of NMDA receptors plays a fundamental role in synaptic plasticity and learning. In contrast to the other iGluRs, the activity of NMDA receptors is ultimately restricted by an Mg+2 block at the regular membrane potential, however, the ion channel is immediately unblocked by membrane depolarization which eliminates Mg+2 from the pore. Furthermore, NMDA receptors are tetramers that have two NR1 subunits and two NR2 or NR3 subunits, according to several research studies. �
Additionally to iGluRs, there are also eight isoforms of metabotropic glutamate receptors (mGluRs) which belong to the family of G-protein-coupled receptors, where they don’t develop ion channels but instead signal through a variety of second messenger systems. L-glutamate-associated depolarization causes a postsynaptic excitatory potential which eases the development of an action potential at the axon hillock. The glutamatergic synapse is activated by astrocytic processes that demonstrate high levels of excitatory amino acid transporters (EAATs). There are five different EAATs, EAAT1 to 5, of which EAAT1 and 2 are the primary astrocytic EAATs, whereas EAAT3 shows a predominantly neuronal expression. Approximately 90 percent of the L-glutamate transport is regulated and maintained by EAAT2 such as GLT-1 in rodent models. These transporters then co-transport 2 or 3 molecules of Na+ and a proton with each molecule of L-glutamate or L-aspartate together with the counter-transport of a K+ ion. Therefore, by utilizing the electrochemical gradient of these ions throughout the plasma membrane as an energy source, the transporters are able to safely and effectively accumulate L-glutamate and L-aspartate in cells against their sudden intra- to extracellular concentration gradients. This allows the brain to control a very low extracellular L-glutamate concentration in the low micromolar range. It is generally believed that L-glutamate taken up by astrocytes is turned to glutamine by the enzyme glutamine synthetase, the glutamine is then released, taken up by neurons and turned to L-glutamate, where it is ultimately utilized once again for neurotransmission. �
Extrasynaptic Glutamate in the Brain
Aside from the essential role of L-glutamate as the primary excitatory neurotransmitter released from glutamatergic presynapses, as previously mentioned above, it has become evident that L-glutamate receptors outside the synaptic cleft also play an essential role in brain physiology. In the cerebellum, it was demonstrated by evaluating AMPA receptor-mediated currents in Bergmann glia that synaptically released L-glutamate concentrations can reach extrasynaptic concentrations of up to 190 ?M while concentrations in the synaptic cleft can exceed 1 mM. Moreover, several mGluRs have been shown to demonstrate a different localization in proximity to the postsynaptic density which would allow them to immediately recognize L-glutamate escaping from the synaptic cleft, as shown in Figure 1. However, current research studies have demonstrated that iGluRs, especially of the NMDA type, are also found at extrasynaptic regions in the neuronal cell membrane. Utilizing light and electron microscopy, other research studies also demonstrated that extrasynaptic NMDA receptors gather at different regions of close contact in the dendritic shaft with axons, axon terminals, or astrocytic processes. The proportion of extrasynaptic NMDA receptors was estimated to be as high as 36 percent of the dendritic NMDA receptor pool in rat hippocampal slices. Although extrasynaptic NMDA receptors were associated with similar scaffolding proteins as synaptic NMDA receptors, an in vitro research study suggested that extrasynaptic and synaptic NMDA receptors may ultimately activate different downstream signaling pathways with a variety of results, including the suppression of CREB activity by extrasynaptic NMDA receptor activation as well as activation by synaptic NMDA receptors. Furthermore, NMDA receptors localized extrasynaptically on dendritic shafts connect extrasynaptic L-glutamate as well as regulate and maintain Ca2+ influx during the elimination of the Mg+2 block by dendrite depolarization throughout the backfiring of action potentials. Research studies demonstrated that L-glutamate release from astrocytes can activate slow inward currents through extrasynaptic NMDAR receptors in CA1 neurons which can also be ultimately synchronized. The mechanisms through which glial cells release L-glutamate as well as how the extrasynaptic L-glutamate concentrations are controlled are vital towards understanding how the activity of extrasynaptic NMDA receptors is controlled. �
Different mechanisms through which astrocytes can release L-glutamate have been suggested, including vesicular L-glutamate release and non-vesicular release through anion channels as well as connexin hemichannels and release through the cystine/glutamate antiporter system x?c. Several research studies strongly suggest that vesicular release from astrocytes plays a minor role because the Ca+2-associated release of L-glutamate was still present in astrocytes created from dominant-negative SNARE mice where vesicular release can be blocked by doxycycline withdrawal. System x?c is a cystine/glutamate antiporter which is characterized as heterodimeric amino acid transporters, made up of xCT as the specific subunit and 4F2hc as the promiscuous heavy chain. This transporter is demonstrated in the brain, especially in astroglial and microglial cells, as shown in Figure 1. The fact that extrasynaptic L-glutamate levels in different regions of the human brain are downregulated by approximately 60 percent to 70 percent in xCT knock out mice, research studies demonstrated that system x?c releases L-glutamate into the extrasynaptic space and suggests that this transporter is essential in the regulation of extrasynaptic L-glutamate levels. This is further supported by the observation that when measured by in vivo microdialysis, the increase in extrasynaptic L-glutamate developed by EAAT inhibitors is neutralized by blocking system x?c while blocking neuronal vesicular L-glutamate release is ineffective. Further research studies are still required. �
Taken together, glutamatergic neurotransmissions don’t simply happen through classical excitatory synapses but also through extrasynaptic L-glutamate receptors, as shown in Figure 1. Finally, the levels of extrasynaptic L-glutamate are determined, at least partially, by glial non-vesicular L-glutamate release, as also shown in Figure 1. However, the regulation of extrasynaptic L-glutamate levels, as well as its temporal-spatial dynamics and its effect on neuronal function, neurodegeneration, and behavior, are far from being fully understood by researchers, healthcare professionals, and patients. �
Glutamate, together with aspartate, is one of the main excitatory neurotransmitters in the human brain. Although it plays a fundamental role in the overall structure and function of the nervous system, excessive amounts of glutamate can ultimately cause excitotoxicity which may lead to a variety of health issues, such as Alzheimer’s disease and other types of neurological diseases. The following article describes the role of glutamate in the human brain. – Dr. Alex Jimenez D.C., C.C.S.T. Insight
L-glutamate is one of the main excitatory neurotransmitters in the human brain and it plays an essential role in practically all activities of the nervous system. In the article above, we discussed the general principles of L-glutamate signaling in the brain. Then, we demonstrated this scheme by describing the different pools of extracellular glutamate, including the synaptic, the perisynaptic, and the extrasynaptic, resulting from vesicular and non-vesicular sources or abnormally located glutamate receptors outside of synapses as well as discussed their possible physiological functions in the human brain. The scope of our information is limited to chiropractic, musculoskeletal and nervous health issues as well as functional medicine articles, topics, and discussions. We use functional health protocols to treat injuries or chronic disorders of the musculoskeletal system. To further discuss the subject matter above, please feel free to ask Dr. Alex Jimenez or contact us at 915-850-0900 . �
Curated by Dr. Alex Jimenez �
References �
Lewerenz, Jan, and Pamela Maher. �Chronic Glutamate Toxicity in Neurodegenerative Diseases-What Is the Evidence?� Frontiers in Neuroscience, Frontiers Media S.A., 16 Dec. 2015, www.ncbi.nlm.nih.gov/pmc/articles/PMC4679930/.
Additional Topic Discussion: Chronic Pain
Sudden pain is a natural response of the nervous system which helps to demonstrate possible injury. By way of instance, pain signals travel from an injured region through the nerves and spinal cord to the brain. Pain is generally less severe as the injury heals, however, chronic pain is different than the average type of pain. With chronic pain, the human body will continue sending pain signals to the brain, regardless if the injury has healed. Chronic pain can last for several weeks to even several years. Chronic pain can tremendously affect a patient’s mobility and it can reduce flexibility, strength, and endurance.
Neural Zoomer Plus for Neurological Disease
�
Dr. Alex Jimenez utilizes a series of tests to help evaluate neurological diseases. The Neural ZoomerTM Plus is an array of neurological autoantibodies which offers specific antibody-to-antigen recognition. The Vibrant Neural ZoomerTM Plus is designed to assess an individual�s reactivity to 48 neurological antigens with connections to a variety of neurologically related diseases. The Vibrant Neural ZoomerTM Plus aims to reduce neurological conditions by empowering patients and physicians with a vital resource for early risk detection and an enhanced focus on personalized primary prevention. �
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