Abstract:
:Entrainment of the dominant circadian pacemaker localised to the hypothalamic suprachiasmatic nuclei (SCN) is mediated partially via the indirect retino-geniculo-hypothalamic projection to the SCN, which is presumed to utilise enkephalin and other neurotransmitters, to modulate circadian rhythmicity. In the present study, we have investigated electrophysiologically the currently unknown functional effects of enkephalin, and another opioid receptor agonist morphine, on hamster SCN neuronal activity in vitro. Basal or N-methyl-D-aspartate-evoked firing rates of SCN neurones were generally unresponsive (86%) to the opioid receptor agonists leucine-enkephalin, methionine-enkephalin, or morphine. Washout of the enkephalins or morphine resulted in a rebound excitatory response ("withdrawal activation") in 39% of neurones 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 attenuated by the alpha2-adrenoceptor agonist clonidine, results which suggest a functional interaction exists between opioid receptors and alpha2-adrenoceptors in the SCN. Our observations show that opioid receptor agonists are largely devoid of actions on normal hamster SCN circadian pacemaker activity, while the occurrence of withdrawal responses may have implications on circadian function during withdrawal from opiate abuse.
journal_name
Brain Res Bulljournal_title
Brain research bulletinauthors
Cutler DJ,Mundey MK,Mason Rdoi
10.1016/s0361-9230(99)00069-6keywords:
subject
Has Abstractpub_date
1999-09-15 00:00:00pages
119-25issue
2eissn
0361-9230issn
1873-2747pii
S0361-9230(99)00069-6journal_volume
50pub_type
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