Electrophysiological effects of opioid receptor activation on Syrian hamster suprachiasmatic nucleus neurones in vitro

Entrainment of the dominant circadian pacemaker localised to the hypothalam ic suprachiasmatic nuclei (SCN) is mediated partially via the indirect reti no-geniculo-hypothalamic projection to the SCN, which is presumed to utilis e enkephalin and other neurotransmitters, to modulate circadian rhythmicity , In the present study, we have investigated electrophysiologically the cur rently unknown functional effects of enkephalin, and:another opioid recepto r agonist morphine, on hamster SCN neuronal activity in vitro. Basal or N-m ethyl-D-aspartate-evoked firing rates of SCN neurones were generally unresp onsive (86%) to the opioid receptor agonists leucine-enkephalin, methionine -enkephalin, or morphine. Washout of the enkephalins or morphine resulted i n a rebound excitatory response ("withdrawal activation") in 39% of neurone s tested. Withdrawal activation was also elicited by administration of the opioid receptor antagonist naloxone, following pre-exposure to morphine, in 59% of neurones tested. These withdrawal responses were blocked or attenua ted by the alpha(2)-adrenoceptor agonist clonidine, results which suggest a functional interaction exists between opioid receptors and alpha(2)-adreno ceptors in the SCN, Our observations show that opioid receptor agonists are largely devoid of actions on normal hamster SCN circadian pacemaker activi ty, while the occurrence of withdrawal responses may have implications on c ircadian function during withdrawal from opiate abuse. (C) 1999 Elsevier Sc ience Inc.