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T1 - Serotonin Hypothesis of Autism

This neurotransmitter is responsible for controlling fundamental physiological aspects of the body.

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These serotonin drugs are used for depression with some success.

In this paper, they work to deconstruct our indoctrination around serotonin as a “happy chemical”, and elucidate its complex role in redirecting energy production when a creature is under duress. It is only when we perturb the system with medication that the body’s response can sometimes result in a chemically adaptive state, that is temporary, at best (accounting for , while on medication, of up to 60%). Even this analysis is a theoretical offering in the service of challenging the dominant paradigm.

This reversal of antidepressant effects lends additional evidence to the indoleamine hypotheses.

The study in question was designed to compare the efficacy of MAO-I's and TCA's on the reduction of depression. A placebo group was used but was not the focus, i.e., the placebo was not a viable therapeutic option.

Serotonin and depression | The BMJ

T1 - The serotonin hypothesis of myoclonus from the perspective of neuronal rhythmicity.

I begin by raising five important methodological problems about this typical experiment. First, there is not a great difference in improvement rate of the clinically depressed patients between and among the three groups (61.8% for moclobemide, 66.4% for imipramine, and 37.3% for the placebo groups). True, the main purpose of the study was to the efficacy of moclobemide and imipramine in relieving clinical depression. However, from a philosophical, theoretical or even methodological perspective, what is missing or consistently overlooked in these studies is an adequate and rigorous account of the interpretation of the data in terms and, in particular, in terms of . The monoamine hypothesis is an attempt to explain-in terms of anatomy, physiology and biochemistry-the cause of clinical depression. But as I shall note in my subsequent questions, a close examination of the hypothesis and the experimental data reveals serious weaknesses about both the hypothesis itself and about the scientific and experimental methodology involved. Second, all these comparative studies leave unanswered the precise, detailed mechanism of the causal nature of the placebo. If the drug imipramine, for example, is considered causally efficacious for the 66.8% who improved, why is not also considered equally causally efficacious for the 37.3% who also improved?

AB - A quantitative analysis of two rat syndromes of myoclonus are presented, modeling myoclonic epilepsy and postanoxic myoclonus. Like the human conditions, both of the models benefit therapeutically from drugs that act on the serotonin system. The rat model of myoclonic epilepsy is associated with a profound loss of serotonin throughout the brain (except in the striatum) and is generated by an oscillator that is synchronized around the midline. The rat model of posthypoxic myoclonus does not demonstrate a significant reduction in serotonin in any location of its brain and is generated by a non-oscillating circuit in the medulla. Although some forms of myoclonic epilepsy may benefit from serotonin drugs because they are caused by a decrease in brain serotonin, our data indicate that posthypoxic myoclonus is not caused by a decrease in the serotonergic innervation of any region of the brain. That the raphe nuclei do not degenerate after global brain ischemia was noted by C. David Marsden in a discussion of the histologic findings of three of his human cases of posthypoxic myoclonus (page 117 of reference 10) and led him to question the hypothesis that posthypoxic myoclonus was due to a loss of serotonin neurons. Our data confirm his observation in the rat, but also indicate that density of serotonin fibers and terminals throughout the brain is not reduced by the brain ischemia that produces posthypoxic myoclonus. It remains to be determined whether the physiologic responsiveness of serotonin neurons is altered by global brain ischemia and whether changes in serotonin release or serotonin receptor properties are associated with posthypoxic myoclonus. The stability of the serotonin system in posthypoxic myoclonic rats is remarkable when one considers the wide range of disorders that is produced by the prolonged brain ischemia. The inability of the most severely posthypoxic myoclonic rats to perform 7-Hz tongue protrusions indicates substantial physiologic disruption of brainstem motor function. Moreover, the posthypoxic myoclonic rat suffers from ataxia, seizures, retrograde amnesia, and impaired ability to learn. The wide spectrum of these deficits is sharply constrasted by its apparently intact serotonin system. We have identified the inferior olive as a locus that may generate the rhythmic components of tremor and myoclonus in syndromes that are truly associated with a dramatic loss of brainstem serotonin. Serotonin acts within the inferior olive to constrain its rhythmic firing. Without intraolivary serotonin, olivary neurons are predisposed to oscillate continuously, providing a substrate upon which sustained rhythmic spiking may be superimposed. It is clear that such unconstrained rhythmicity produces synchronized whole-body tremor at 10 Hz (33, 41-43). The effects of serotonin to suppress olivocerebellar rhythmicity are mediated by postsynaptic 5-HT2 receptors that reduce the magnitude of the low-threshold calcium conductance, IT. It is notable that dysregulation of this conductance has been associated with hyper-rhythmic states in the thalamus underlying cognitive disorders ranging from depression to tinnitus (49), indicating a common mechanism underlying a variety of neurologic conditions. The identification of a specific brainstem locus (inferior olive), serotonin receptor 5-HT2, and ionic current IT involved in a form of rhythmic myoclonus may provide multiple clues toward which future pharmacotherapies can be directed.

Is the Link Between Depression and Serotonin a Myth? …

Upon stimulation of the serotonin system, the hormones, prolactin and growth hormone are released.

Based on what I have shown in this paper, I think that it is a fair inference to say that the association between abnormal serotonin systems, more specifically, serotonin deficiencies, and patients suffering from major depression is indeed significant.

In this study, 490 patients were enrolled in a double-blind, prospective, randomized, 6-week multi-center study. Participants were men and non-pregnant and non-lactating women, aged 18 to 65. A requirement for inclusion was meeting the DSM-III (Diagnostic and Statistical Manual of Mental Disorders, third edition) criteria for Major Depressive Episode and to have a minimum baseline score of 17 on the 21-item Hamilton Rating Scale for Depression (HRSD). Patients were randomly assigned to a study center and given either moclobemide (n=164), imipramine (n=164), or placebo (n=162). All patients received capsules of identical appearance and taste.

This finding supports the evidence that serotonin function is abnormal in depression.
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    These figures are incredible, so finding the root of the problem when it comes to depression is extremely important.

  • Low Serotonin Levels Don't Cause Depression

    "Alterations in serotonin metabolism may be an important factor in the etiology and treatment of depression." .

  • A serotonin hypothesis of schizophrenia - ScienceDirect

    Serotonin's action in the synapses is terminated by reuptake of the neurotransmitter by the presynaptic cell.

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Central fatigue: the serotonin hypothesis and beyond …

These studies have led to a series of hypotheses concerning the mechanism of the action of antidepressant treatments, as well as pathophysiology of depression, that have focused on alterations in brain levels of serotonin and norepinephrine or their receptors.

Death to the Serotonin Hypothesis | The Phineas Gage …

Your comments are not completely without ignorance. God is not a cure for mental illness any more than other ailments or diseases. My uncle has severe schizophrenia and he is one of the most righteous, good, god fearing people I have ever known. I do believe that much depression and other mild mental disorders do have a lot to do with attitude and faith. However, some of these illnesses are serious and cannot be cured with our way of thinking, or even by our faith.

The Neurotransmitter Hypothesis of Schizophrenia - …

Changes in beta-adrenergic receptor density, serotonin autoreceptor sensitivity, and serotonin turnover all struggle to compensate for the assault of the medication.

The Neurotransmitter Hypothesis of ..

DST was suggested as test for diagnosis of major depressive disorder, since increased function of HPA axis can be expressed in reduced decrease of ACTH and cortisol levels after dexamethasone administration.

The Neurotransmitter Hypothesis of Schizophrenia ..

So if we cannot confirm the role of serotonin in mood and we have good reason to believe that antidepressant effect is largely based on belief, then why are we trying to “boost serotonin”?

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