Cortisol and Prolactin Responses to Buspirone in Alcoholism / 신경정신의학

OBJECTIVES: The purpose of this study was to evaluate the prolactin and cortisol responses to 5-HT 1A receptor activation by buspirone in alcoholics. METHODS: The subjects were twenty two male alcoholic patients meeting the DSM-IV criteria for alcohol dependency and abstaining for more than 3 months. Patients were free from overt anxiety and depressive symptoms. Controls were fifteen male normal volunteers, with no psychiatric and medical illness. Blood samples for the measurement of serum cortisol and prolactin levels were drawn 0, 30, 60, 90, 120, 150 minutes after oral administration of 30mg buspirone hydrochloride at 9:00 a.m. RESULTS: The baseline cortisol levels were not significantly different between alcoholics and controls. Serum cortisol levels of controls after buspirone administration were significantly increased over time(p<0.01), but those of alcoholics did not increased. After 60 minutes following buspirone administration, cortisol levels were significantly lower in alcoholics than in controls(p<0.05). Prolactin responses to buspirone were not significantly different between the two groups. CONCLULSION: Our results suggested that 5-HT 1A receptor function is decreased in alcoholic patients.

Neurobiology of Depression

At the beginning, researches on the biology of depression or affective illness have focused mainly on the receptor functions and neuroendocrine activities. And the studies of the past years did not break new theoretical background, but the recent advances in the research on the molecular mechanisms underlying neural communication and signal transduction do add some insights to many established ideas. This article will overview some of the more recent advances in the clinical researches of depression. Our major concerns to be presented here include the following : (1) alterations in the post-synaptic neural transduction ; (2) changes in the neurons of hypothalamic neuropeptides ; (3) decreased peptidase enzyme activities : (4) associations of hypothalamic-pituitary-adrenal axis abnormalities with serotonin neurotransmission ; (5) role of serotonin transporter ; (6) changes in the responsiveness of intracellular calcium ion levels ; (7) the inositol deficiency theory of lithium and depression ; (8) the transcription factors including immediate early genes ; (9) recent genetic studies in some families. This brief overview will suggest that changes in DNA occur during antidepressant therapy. These changes at the DNA level initiating a cascade of events underlying antidepressant modality will give us the insight on the molecular biological basis of the pathogenesis of depression and cues for a new class of antidepressants.