Depression pathophysiology

Cowen, P. J., Serotonin and Depression Pathophysiological Mechanism or Marketing Myth , Trends Pharmacol Sci, no. 9 (2008)... 

Seifritz E (2001) Contribution of sleep physiology to depressive pathophysiology. Neuropsychopharmacology 25 S85-S88... 

S100A10 was found to interact with the serotonin IB receptor increasing its presence at the cell membrane. S100A10 was found to be closely associated with the pathophysiology of depression. 

Explain the etiology and pathophysiology of major depressive disorder. 

While such models of depression are quite useful in conceptualizing the mechanisms behind antidepressant activity, they are assuredly an oversimplification of the actual pathophysiologic process of the disorder. Depression probably involves a complex dysregulation of monoamine systems, and these systems, in turn, modulate and are modulated by other neurobio-logic systems. Thus, the underlying cause of depression may well extend beyond dysfunction of the monoamine system.10... 

Charney DS. Monoamine dysfunction and the pathophysiology and treatment of depression. J Clin Psychiatry 1998 59(Suppl 14) 11-14. 

NEUROTRANSMITTER AND NEUROPEPTIDE SYSTEMS ARE IMPLICATED IN THE PATHOPHYSIOLOGY OF BIPOLAR AND MAJOR DEPRESSIVE DISORDERS 889... 

Quigley s group in Cork, Ireland, have concluded that normal aging is associated with changes in motility but the pattern is varied and no clear clinical consequence can be identified (67). More important in their view are the pathophysiological influences, including depression (and treatment with anti-cholinergics and opiates), hypothyroidism, and chronic renal failure. 

Willner (1995) provides evidence from many sources that increases or decreases of dopaminergic activity in the mesolimbic system may underpin the pathophysiology of mania and depression respectively. A key area involved may be the subgenual prefrontal cortex which receives extensive reciprocal dopaminergic projections from the ventral tegmental area and substantia nigra and influences dopamine release in the nucleus accumbens (Drevets et al., 1997 see Chapter 16). 

The results with tacl and NK1R mice in these models of depression strongly support the idea that the tachykinin system is involved in the pathophysiology of depression. 

Stress is thought to be an important factor in the pathophysiology of depression and anxiety disorders. It seems possible that the reduced stress reactivity of NKl receptor- and tael-deficient mice has contributed to the behavioral phenotypes observed in the animal models of anxiety and depression. 

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