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Depression antidepressants and neurogenesis, chronic fatigue syndrome fibromyalgia - Try Out

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Increased neurogenesis after chronic antidepressant treatment may influence fundamental properties of the dentate gyrus such as pattern separation as well as dentate gyrus excitability. This journal is a member of and subscribes to the principles of the Committee on Publication Ethics. While TMS continues to help more and more patients, the precise mechanisms of its actions remain a mystery. Neurogenesis is detected by injecting the subject with the cell proliferation marker bromodeoxyuridine (BrdU), which is taken during DNA formation. Risk for major depression is typified through biological factors such as genetic risk, drug abuse, or medical conditions and environmental factors such as parental neglect or psychosocial stress (Karel, 1997). Animal models of depression entail exposing subjects to chronic stress until they develop symptoms of depression such as anhedonia (loss of interest in play, food, or socialization) and chronic anxiety disorders, such as learned helplessness. Hippocampal biopsies and postmortem studies in depression patients show decreases in neurotrophic factors (Lucassen et al 2010) and volume loss in the anterior dentate gyrus (Boldrini et al 2013).
Hippocampal shrinkage in animal models of depression appear to be arrested by antidepressants, through the stimulation of neurogenesis in the dentate gyrus, and prevention of cell death or dendritic atrophy in the CA3 region in rats, tree shrews, and monkeys (Duman et al 1999, Czeh et al, 2001, Perera et al, 2011). Several groups have shown that rTMS improves hippocampal function including short-term and episodic memory, and performance on hippocampus-dependent cognitive tasks (Avery et al 1999, Padberg et al, 1999, Martis et al, 2003, Holtzheimer 2004, Fitzgerald et al, 2006, review by Luber, Lisanby et al, 2013). The untreated stressed group (Stress-Placebo) developed depression related behaviors (anhedonia and subordinance) and reduced neurogenesis.

Across all groups, depressive behavior levels inversely correlated with neurogenesis rates but this correlation was significant only for new neurons in the anterior dentate gyrus consistent with the role of the anterior hippocampus in mediating affective behavior.
Based on the evidence presented in this article we propose that the stimulation of neurogenesis in the hippocampus is necessary but not always sufficient for treating most, but not all patients with unipolar depression. The Clinical TMS Society advocates with insurance carriers about policy and authorization processes. Access to member-only section of the Clinical TMS Society website where you can find useful information and download helpful forms.
Efficacy and safety of transcranial magnetic stimulation in the acute treatment of major depression: a multisite randomized controlled trial. Daily left prefrontal transcranial magnetic stimulation therapy for major depressive disorder: a sham-controlled randomized trial. Durability of clinical benefit with transcranial magnetic stimulation (TMS) in the treatment of pharmacoresistant major depression: assessment of relapse during a 6-month, multisite, open-label study. Transcranial magnetic stimulation (TMS) for major depression: a multisite, naturalistic, observational study of quality of life outcome measures in clinical practice. Antidepressants may also modulate the activity of brain regions downstream of the dentate gyrus such as the prefrontal cortex, nucleus accumbens, amygdala and hypothalamus directly or indirectly through enhancing dentate gyrus function by increasing neurogenesis. In this review we will argue that hippocampal neurogenesis plays a pivotal role in the therapeutic effects of rTMS, that it is the magic bullet.

Mature neurons stained in DAPI (Blue) in the hippocampus of control rat and two rats (P1 and P5) treated with 2 weeks of deep magnetic stimulation. Consequently, it is no surprise that rTMS robustly stimulates neurogenesis (Ueyma et al, 2011).
These continue to divide symmetrically as they mature into Type-3 cells (neuroblasts) and migrate into the granule cell layer. Neurogenesis is possible elsewhere in the neocortex but mainly in the context of brain damage. The neuro-suppressive effects of stress are mediated through a final common pathway that includes activation of the HPA axis and the subsequent increase in adrenal steroid hormones and NMDA receptor activation (Cameron et al., 1998). In line with this, postmortem human studies have not shown any greater reduction in hippocampal precursor proliferation in patient depression at the time of death compared to those that were successfully treated.
Stimulation of neurogenesis is a mechanism of antidepressant action that encompasses a disparate array of treatments ranging from all classes of medications, to brain stimulation in the PFC to exercise to cognitive behavior therapy (CBT), (which can be viewed as a form of learning that stimulates neurogenesis). Decreased neurogenesis may provide a medium of vulnerability to depression stemming from a vast array of risk factors including genes, maternal neglect, psychosocial stress, emotional deprivation, drug abuse, and medical conditions.

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