Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence suggests that the volume of the amygdala is significantly reduced in patients with post-traumatic stress disorder (PTSD), and that this may be related to neuronal apoptosis. However, the precise molecular mechanism of this decrease in amygdala volume during PTSD remains unclear. In this study, we investigated the relationship between the activity of the 5-HT1A receptor and amygdala neuronal apoptosis. Rats were exposed to a single-prolonged stress (SPS) procedure to create a PTSD rat model, with or without prior treatment with WAY100635, a 5-HT1A receptor antagonist. The expression of Bax, a pro-apoptotic protein, and Bcl-2, an anti-apoptotic protein, was examined by Western Blotting. TUNEL staining and flow cytometry (FCM) were employed for the detection of apoptotic cells in the amygdala. Our results indicate that SPS induces amygdala neuronal apoptosis, which was partially inhibited by WAY100635, and suggest that this apoptosis may be related to the activity of the 5-HT1A receptor.
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PMID:Activity of 5-HT1A receptor is involved in neuronal apoptosis of the amygdala in a rat model of post-traumatic stress disorder. 2146 66

Mechanisms underlying stress-induced depression and antidepressant drug action were shown to involve alterations in serotonergic (5-HT) neurotransmission and expression of genes coding for proteins associated with neurotrophic signaling pathways and cell-survival in the hippocampus and cortex. Expression of these genes in the brainstem containing 5-HT neurons may also be related to vulnerability or resilience to stress-related psychopathology. Here we investigated 5-HT markers and expression of genes for Brain-Derived Neurotrophic Factor (BDNF) and apoptotic proteins in the brainstem in relation to swim stress-induced behavioral despair. We found that anti-apoptotic Bcl-xL gene is sensitive to stress during the course of fluoxetine administration. Responsiveness of this gene to stress appeared concomitantly with an antidepressant-like effect of fluoxetine in the forced swim test. Bcl-xL transcript levels showed negative correlations with duration of immobility in the test and 5-HT turnover in the brainstem. In contrast, BDNF and pro-apoptotic protein Bax mRNA levels were unchanged by either fluoxetine or stress, suggesting specificity of Bcl-xL gene responses to these treatments. We also found that the levels of mRNAs for tryptophan hydroxylase-2 (TPH2) and 5-HT transporter (5-HTT) were significantly down-regulated following prolonged treatment with fluoxetine, but were not affected by stress. Unlike TPH2 and 5-HTT, 5-HT1A receptor mRNA levels were not altered by fluoxetine but significantly increased in response to swim stress. These data show that long-term fluoxetine treatment leads to changes in 5-HT and Bcl-xL responses to stress associated with antidepressant-like effects of the drug. This article is part of a Special Issue entitled 'Anxiety and Depression'.
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PMID:Stress-induced activation of the brainstem Bcl-xL gene expression in rats treated with fluoxetine: correlations with serotonin metabolism and depressive-like behavior. 2174 Sep 20