The is evidence that some of the actions of both endogenous and exogenous
opioids (e.g., stimulation of
prolactin release) are mediated by interaction with catecholaminergic systems.
Morphine (1.67, 5, and 15 mg/kg of
body weight, intraperitoneally) altered
dopamine turnover as measured by the
alpha-methyl-p-tyrosine method 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 accelerated in the neostriatum. In the frontal cortex all doses were effective in decreasing
dopamine turnover; however, in the median eminence the lowest dose of
morphine did not significantly alter
dopamine turnover. All three doses accelerated
dopamine turnover in the neostriatum.
Naloxone effectively reversed the effects of
morphine at all doses in all brain areas, whereas it had no effect on turnover when given alone. In the median eminence, neostriatum, and frontal cortex,
intraventricular injection of [D-Ala2,D-Leu5]-
enkephalin (25 micrograms) or
beta-endorphin (15 micrograms) produced the same effects on
dopamine turnover as
morphine. The actions of these
peptides were blocked by
naloxone. It is hypothesized that
opiates and
opioid peptides increase
prolactin release by reducing the activity of the tuberoinfundibular dopaminergic system.