There is evidence that some of the actions of both endogenous and exogenous opioids (e.g. stimulation of prolactin release) are mediated via interaction with catecholaminergic systems. Morphine (1.67, 5 and 15 mg/kg i.p.) altered dopamine turnover as measured by the α-methylparatyrosine method (αMPT) in the median eminence, neostriatum and frontal cortex of male Sprague-Dawley rats. The turnover rate of dopamine was reduced in the median eminence and frontal cortex but accellerated in the striatum. In the frontal cortex all doses were effective in reducing turnover rate but only the two higher doses were effective in the median eminence. All three doses accelerated turnover in the striatum. In the nucleus accumbens, morphine (5 mg/kg i.p.) accelerated dopamine turnover. Naloxone effectively reversed the effects of morphine at all doses in all brain areas while having no effect on turnover given alone. In median eminence, neostriatum and frontal cortex, intraventricular injection of [D-Ala2,D-Leu5] enkephalin (25μg) and β-endorphin (15μg) produced the same effects on dopamine turnover as morphine. The actions of these peptides were also blocked by naloxone. It is hypothesized that opiates and opioid peptides increase prolactin release by reducing the activity of hypothalamic dopaminergic systems.
|Original language||English (US)|
|Pages (from-to)||No. 714|
|Issue number||3 I|
|State||Published - 1979|
ASJC Scopus subject areas