Molecular Mechanisms Involved in Depotentiation and Their Relevance to Schizophrenia.
Molecular mechanisms involved in depotentiation and their relevance to schizophrenia.
Filed under: Depression Treatment
Chonnam Med J. 2012 Apr; 48(1): 1-6
Sanderson TM
Long-term potentiation (LTP) and long-term depression (LTD) of synaptic transmission are forms of synaptic plasticity that have been studied extensively and are thought to contribute to learning and memory. The reversal of LTP, known as depotentiation (DP) has received far less attention however, and its role in behavior is also far from clear. Recently, deficits in depotentiation have been observed in models of schizophrenia, suggesting that a greater understanding of this form of synaptic plasticity may help reveal the physiological alterations that underlie symptoms experienced by patients. This review therefore seeks to summarize the current state of knowledge on DP, and then put the deficits in DP in models of disease into this context.
HubMed – depression
Approaches to understanding and addressing treatment-resistant depression: a scoping review.
Filed under: Depression Treatment
Depress Res Treat. 2012; 2012: 469680
Jenkins E, Goldner EM
Treatment-resistant depression is associated with significant disability and, due to its high prevalence, results in substantive economic and societal burden at a population level. The objective of this study is to synthesize extant literature on approaches currently being applied to understand and address this condition. It is hoped that the findings can be used to inform practitioners and guide future research. A scoping review of the scientific literature was conducted with findings categorized and charted by underlying research paradigm. Currently, the vast majority of research stems from a biological paradigm (81%). Research on treatment-resistant depression would benefit from a broadened field of study. Given that multiple etiological mechanisms likely contribute to treatment-resistant depression and current efforts at prevention and treatment have substantial room for improvement, an expanded research agenda could more effectively address this significant public health issue.
HubMed – depression
Neonatal SSRI Exposure Programs a Hypermetabolic State in Adult Mice.
Filed under: Depression Treatment
J Nutr Metab. 2012; 2012: 431574
Kummet GJ, Haskell SE, Hermann GM, Ni C, Volk KA, Younes AK, Miller AK, Roghair RD
Background. Selective serotonin reuptake inhibitor (SSRI) therapy complicates up to 10% of pregnancies. During therapy, SSRIs exert pleiotropic antidepressant, anorexigenic, and neurotrophic effects. Intrauterine SSRI exposure has been modeled by neonatal administration to developmentally immature rodents, and it has paradoxically elicited features of adult depression. We hypothesized neonatal SSRI exposure likewise programs a rebound hypermetabolic state in adult mice. Methods. C57BL/6 pups were randomized to saline or sertraline (5?mg/kg/d) from P1-P14. Because estrogen increases tryptophan hydroxylase 2 (TPH2) expression, a subset of female mice underwent sham surgery or bilateral ovariectomy (OVX). Metabolic rate was determined by indirect calorimetry. Results. In both male and female mice, neonatal SSRI exposure increased adult caloric intake and metabolic rate. SSRI-exposed female mice had significantly decreased adult weight with a relative increase in brain weight and melatonin excretion, independent of ovarian status. Cerebral cortex TPH2 expression was increased in SSRI-exposed male mice but decreased in OVX SSRI-exposed female mice. Conclusions. SSRI exposure during a critical neurodevelopmental window increases adult caloric intake and metabolic rate. Ovarian status modulated central TPH2 expression, but not adult energy balance, suggesting programmed neural connectivity or enhanced melatonin production may play a more important role in the post-SSRI hypermetabolic syndrome.
HubMed – depression
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This digital document is an article from NWHRC Health Center – Depression, published by Thomson Gale on December 12, 2006. The len…
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