Cortisol, hypothermic, and behavioral responses to ipsapirone in patients with bipolar depression and normal controls

• Published in: Neuropsychobiology Vol. 38; no. 1; p. 6
• Main Authors: Shiah, I S, Yatham, L N, Lam, R W, Tam, E M, Zis, A P
• Format: Journal Article
• Language: English
• Published: Switzerland 01-01-1998
• Subjects: Adult; Analysis of Variance; Behavior - drug effects; Bipolar Disorder - blood; Bipolar Disorder - drug therapy; Blood Pressure - drug effects; Body Temperature - drug effects; Female; Heart Rate - drug effects; Humans; Hydrocortisone - blood; Hypothermia - chemically induced; Male; Pain Measurement; Psychiatric Status Rating Scales; Pyrimidines - pharmacology; Pyrimidines - therapeutic use; Serotonin Receptor Agonists - pharmacology; Serotonin Receptor Agonists - therapeutic use; Statistics, Nonparametric
• ISSN: 0302-282X
• DOI: 10.1159/000026510

To examine if 5-HT1A receptor function is involved in the pathophysiology of bipolar depression, we measured the cortisol, hypothermic and behavioral responses to ipsapirone, a 5-HT1A receptor agonist, in 8 patients with bipolar depression and 26 normal controls. After obtaining blood samples for baseline cortisol levels and measuring baseline body temperature, a single dose of 0.3 mg/kg of ipsapirone was administered orally to all the subjects, and further blood and temperature readings were obtained every 30 min for 3 h. The results showed that the administration of ipsapirone led to a significant increase in cortisol release and a significant decrease in body temperature both in bipolar depressed patients and normal controls. There was no significant difference in the cortisol or hypothermic responses to ipsapirone between groups. However, there was a significant positive correlation between the Hamilton Depression Rating (HAMD) scores and the hypothermic response in the depressed patients, while the HAMD scores were not significantly correlated with the cortisol response. Comparing our findings with those of previous studies, we suggest that the alterations in 5-HT1A receptor sensitivity in depressed patients may be related to the severity of depression, and they may only occur in more severely depressed patients.