@article{ref1,
title="The neuroscience of suicide",
journal="Brain and nerve",
year="2012",
author="Arita, Hideho",
volume="64",
number="8",
pages="929-935",
abstract="Abstract<br/> Various postmortem brain studies have provided evidence that reduced serotonin (5-HT) transmission in the ventrolateral prefrontal cortex (vlPFC) is associated with depression-related suicide. Suicide victims have fewer 5-HT transporter sites and a large number of postsynaptic 5-HT<sub>1A</sub> and 5-HT<sub>2A</sub> receptors in the vlPFC, which are implicated in behavioral inhibition and impulsivity. These could be compensatory changes in response to 5-HT hypofunction in depression and suicide. Selective serotonin reuptake inhibitors (SSRIs) are commonly used for the treatment of depression and suicidal ideation. 5-HT innervation of the PFC arises predominantly from 5-HT neurons in the brainstem dorsal raphe nucleus (DRN). In the DRN of suicide cases, 5-HT<sub>1A</sub> autoreceptors are increased and the levels of 5-HT biosynthetic enzyme, tryptophan hydroxylase (TPH), are reduced. Reduced 5-HT<sub>1A</sub> feedback inhibition and increased TPH may reflect compensatory changes in response to 5-HT hypofunction in depression-related suicide. Genetic polymorphisms in TPH, 5-HT transporter (5-HTTLPR allele), and 5-HT<sub>2A</sub> receptor were examined for their association with depression-related suicide, but no consistent associations were found. Stress is a risk factor for depression and is linked to hyperactivity of the hypothalamo-pituitary-adrenal axis and suicide. Corticotropin-releasing factor (CRF)-immunoreactive varicose fibers were detected in the DRN of suicide victims, suggesting that CRF neurons in the paraventricular nucleus of the hypothalamus and 5-HT neurons in the DRN may form a circuit in stress-induced depression. Alcoholics are at a significantly greater risk of suicide than the general population. Alcoholism is associated with alterations in the 5-HT system.<p /> <p>Language: ja</p>",
language="ja",
issn="1881-6096",
doi="",
url="http://dx.doi.org/"
}