THE Trauma of voices. Body Mentalists.

L-Glatumine Depression/Anxiety

trauma of Depression and Psychological Anxiety. A vast majority of brain neurons and Synaptic connections are Glutamatergic, and Glutamate Synaptic transmission largely mediates both Psychosocial sublime Peripheral sensation to cognition and the resultant Neurochemical sublime feelings and emotion, two brain functions that seem to be inextricably linked together between the Parasympathetic and Sympathetic nerves. Moreover, compelling evidence from clinical studies suggests Glutamate transmission is abnormally regulated in a number of the limbic/cortical areas in the brain of Psychologically traumatized clinically depressed patients. Furthermore, increasing evidence suggests that the Glutamatergic signaling is associated with maladaptive changes in the structure and the function of Excitatory circuitry as an imbalance in the Parasympathetic Rest and Digest and a lack of Psychosocial Disassociation in the Excitatory Sympathetic nerve.
A whole wealth of data and knowledge from animal models of stress have shown that the different types of Psychosocial environmental stress enhance Glutamate release, reduce glial-mediated Glutamate cycling, and then alter Synapse connection transmission in limbic/cortical areas. Stress also induces powerful effects on structure and morphology in a rat's brain, inducing Dendritic remodeling, Synaptic spine reductions, glial loss, and also the possibility of volumetric reductions resembling those seen in the Psychological trauma of Parasympathetic nerve of the depressed patients. So, while it is well-established that Monoaminergic transmission has a primary role in the modulation of Psychosocial emotions and feelings and the resultant cognition of Psychological trauma of mood swing disorders, the time has come for us to recognize and posit that Excitatory transmission plays a key role in negotiation of the Sympathetic and Parasympathetic nerves and their Psychosocial interaction in the complex emotional and resultant cognitive changes associated with traumatic Depression and the Psychological trauma of Anxiety Disorders. In all likelihood, it also has representation in the actual final common pathway of any therapeutic treatments for Psychological Depression and other traumatic Anxiety Disorders. It should also be taken into research that while all Antidepressant agents available to patients have a Monoamine-based mechanism or at least a Monoamine-based Neurochemistry, there actually are no approved Antidepressant agents that directly target the Glutamatergic system of the body/brain barrier. Currently, only about 50–60% of the depressive Disorder patients respond to first-line Antidepressant treatment medicament therapies. And less than a third of the patients actually achieve a remission in the largest open-label study conducted so far to date. This means there is room for an improvement in the dealing of Psychiatric experimentation into Antidepressant medications. And that is, if non-Monoamine targets are taken into account and that there are new compounds developed that target directly Glutamate Neurotransmitter or related pathways such as the Nutraceutical supplemental called L-Glutamine.
Glutamate was not recognized as a neurotransmitter until the early 1980s, which is later than the monoaminergic transmitters. Glutamate is now accepted as the major Sympathetic nerve Excitatory neurotransmitter – by me - in the nervous system. Glutamate is the fast Excitatory transmission in the brain, but Aminobutyric acid (GABA), which is another amino acid Neurotransmitter and this mediates the vast majority of fast Parasympathetic nerve Inhibitory transmissions where the Ignorance kicks into Psychosocial Peripheral sublime interaction. It has been estimated that in the whole of the brain, there are approximately two to three hundred thousand Serotonergic neurons of the hundred billion total neurons which also negotiates the Psychological traumas of Sympathetic Anxiety and traumatic Parasympathetic Depression, but also Bipolar Disorder. Modern stereological methods have estimated that about 80% of neurons in the neocortex are from the effects of the Sympathetic Excitatory system and form 85% of all synaptic connections. While about 20% of the neurons are smooth and of the Parasympathetic Inhibitory affect and forming 15% of the synapses. These data indicate that Glutamate neurons and synapses outnumber all other Neurotransmitter systems in the brain via the Vagus nerve and its Medulla Oblongata affects of the Sympathetic and Parasympathetic nerves. The only exception of the GABAergic system comes to the body/brain barrier of the Vagus nerve leading to the Glossopharyngeal nerve and Psychological traumas of mood swings. In other words the brain, from the point of view of chemical Neurotransmission, is largely a Psychological Glutamatergic Sympathetic Excitatory action of negotiation, regulated by the smaller GABA reaction in the Parasympathetic Inhibitory component of Rest and Digest and the Inner Experience of thoughtfulness and is modulated by a much smaller number of neurons that release a variety of other neurotransmitters (including the Monoamines). It is well-known that Monoamines, by regulating fast Peripheral Sympathetic chemical neurotransmission, modulate all forms of brain function. This includes sleep/wakefulness, biological drive from negotiation activities mediated by the hypothalamus from the Glossopharyngeal nerve via the Inner thoughtfulness Experiences of the emotional/motivational trauma of Psychological mood swing. These activities are negotiated by limbic circuitry and value-based Rest and Digest Harmony behaviours in the neocortex that counteracts Fight or Flight from the Sympathetic nervous system. It is via the Inner Experience of Psychosocial Ignorance to Anxiousness. These changes to Sympathetic Excitatory transmission in the Central Nervous System of the body/brain interaction are with the Peripheral Nervous System of sublime interaction that is counterbalanced by the Parasympathetic Inhibitory component and that causes these functions in the Medulla Oblongata and its Glossopharyngeal nerve which leads to the Hypothalamus.
Increasing evidence that pathophysiological changes with the Amino acid Neurotransmitter systems are now being associated with the Psychosocial emotional mood and cognitive Psychological trauma of Sympathetic and Parasympathetic nerve imbalances of Anxiety dysfunctions. Reports of dysfunctions in the GABA content in patients with Psychosocial mood disorders, Glutamatergic dysfunctions have been demonstrated in the blood plasma, Cerebrospinal Fluid (CSF) and the Autonomic Nervous System of individuals afflicted with Psychological mood disorders such as traumatic clinical Depression Disorders, the Psychological trauma of Anxiety and the trauma of Bipolar Disorder.
Several studies have shown levels of higher Glutamate, and a Fashion Trend for decreased blood plasma Glutamine/Glutamate ratios in the blood of depressed patients. This is when compared to healthy people. Some other studies have provided some evidence that treatment with Antidepressant agents may decrease the plasma Glutamate levels in Psychologically traumatized Depressed patients. However, blood platelets possess a large level of Glutamate uptake in the system and are known to express the same amount of Glutamate transmitters that become present in the brain. A fact that Glutamate transport by human blood platelets appears as an indication of a variety of mental health illnesses that can be associated with the Glutamate impairment transmitters. This gives the suggestion that an alteration to blood platelet Glutamate uptake in Psychologically depressed patients takes place.
And yet it is seen as inconsistent with the theory and study of Bipolar Disorder patients in an emotional Psychological elation or mania dysfunction that have shown to have increased rates of Glutamate uptake in blood platelets towards the Sympathetic nerve. One study of depressed subjects has shown that blood platelet Glutamate levels to be numerically higher. However not significantly in traumatized depressed subjects compared to healthy people. There have been some attempts to directly compare the Central Nervous System tissue (meat) Glutamate content between mood disorder patients and the Norm of Society. Studies examining CSF from Psychological emotionally dysfunctional mood disorder patients are extremely limited.
One study has reported that reduced CSF Glutamate content in a mixture of patients with the Psychological trauma of major depressive and Bipolar Disorder and also an earlier study of CSF samples was unable to measure the Glutamate levels. It did, however, find that significantly higher CSF Glutamine concentrations in patients with the Psychological symptoms of major clinical depression disorder. The only study examining neurosurgical samples from chronically traumatized depressed patients failed to find any significance in the Frontal Cortex Glutamate concentrations. And yet a more recent post-mortem (autopsy) study of the frontal cortex showed a large increase in tissue Glutamate levels in individuals with Psychologically traumatizing major depressive and the trauma of Bipolar Disorders after controlling for post-mortem interval. This is then consistent with this examination of a recent analytic post-mortem Dorsolateral Prefrontal Cortex meat tissue that also revealed higher Glutamate levels in the trauma of Psychological Bipolar Disorder patients.

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