A double-blind, placebo-controlled study of the effect of imipramine on TRH-induced urinary urgency in healthy men.

We studied the effect of imipramine (IMI) on thyroid releasing hormone (TRH)-induced urinary urgency as a way of investigating the mechanism of the beneficial effect of IMI on enuresis. In a double-blind study, 12 normal, healthy men between 21 and 39 yr of age ranked their urge to urinate at 30-sec intervals following IV injection of TRH (500 micrograms) or saline. The subjects then were randomly assigned to either IMI (1 mg/kg) or placebo groups for 10 days, and the procedure was repeated. Compared to saline, TRH produced a significant elevation in urinary urgency in all subjects. IMI did not significantly blunt TRH-induced urinary urgency. Thus, the mechanism by which IMI affects enuresis is likely not mediated at the level of the urinary urgency induced by TRH.     

Development of hypothalamic opioid neurons: a combined immunocytochemical and [3H]thymidine autoradiographic study

Using a combined technique of immunocytochemistry and [3H]thymidine autoradiography, we have determined the "birth-date" of opioid peptide containing neurons in three hypothalamic nuclei. These include proopiomelanocortin neurons (indicated by ACTH immunoreactivity) in the arcuate nucleus, dynorphin A neurons in the supraoptic nucleus, and [Leu]enkephalin neurons in the periventricular nucleus. Arcuate proopiomelanocortin neurons were born very early in embryonic development, with peak heavy [3H]thymidine nuclear labelling occurring on embryonic day E12. Supraoptic dynorphin A neurons were also labelled relatively early (peak at E13). By contrast, [Leu]enkephalin neurons in the periventricular nucleus exhibited peak heavy nuclear labelling on day E14. The results indicate a differential genesis of these three opioid peptide containing neuronal groups in three different hypothalamic nuclei.