Of Stress And Glucocorticoids

The mechanisms that underlie the influence of stress and glucocorticoid exposure are likely to involve multiple cellular actions, as well as regulation of different neurotransmitter and neuroendocrine factors. Some of the best characterized effects that are relevant to neuronal damage are discussed in this section. The primary mechanism by which glucocorticoids influence cellular function is via binding to their cytoplasmic receptors, referred to as mineralocorticoid or glucocorticoid...

Adenylyl Cyclase In Alzheimers Disease

In contrast to the multiple deficits seen in the phosphoinositide hydrolysis pathway, it appears that disrupted AC signaling see Fig. 2 for the scheme in Alzheimer's disease brain is more circumscribed in that it occurs primarily at the level of neurotransmitter receptor-Gs-protein-enzyme coupling. Somewhat analogous to the deficit in acetylcholine muscarinic Ml receptor-Gq-protein coupling described earlier, it has been shown using radioligand binding techniques that P adrenoceptor coupling to...

Influence Of Antidepressant Treatments On Neuronal Morphology And Survival

If neuronal atrophy and survival play a significant role in the effects of stress that eventually lead to depression, it is conceivable that treatments for depression may reverse these neuronal deficits or, at the very least, prevent further damage. Although this area of research is still being studied, early reports have provided evidence that antidepressant treatments are capable of influencing synaptic plasticity and neuronal morphology. The results of these studies are briefly discussed....

Postmortem Brain Studies

Significantly higher levels of Gaq 11 and a moderate elevation in the Gaq 11-regulated phospholipase C-P1 isozyme PLC-P1 have been reported in the occipital cortex of BD subjects compared with matched controls 78 . The increases in Gaq 11 and PLC-P1 appeared to be regionally specific, as no significant differences were found between BD and control subjects in the cerebral frontal and temporal cortex 15,78 . In addition, Gaq 11 levels, expressed as a percent of respective postmortem delay and...

And the Late Phase of LTP

Like the study of mice lacking the R1 subunit of the NMDA receptor only in hippocampal area CA1, the study of other genetically modified mice has focused on the early, transient phase of LTP E-LTP in area CA1 that lasts about 1 h. These studies have shown that genetic manipulation of any one of several kinases interferes with not only E-LTP but also short-term memory 61,62 . The study of amnesiac patients and experimental animals has revealed, however, that the role of the hippocampus in memory...