Delta opioid inhibition of light-induced phase advances in hamster circadian activity rhythms.
A master neuronal pacemaker located within the suprachiasmatic nucleus in the ventral hypothalamus generates circadian activity rhythms in hamsters. The circadian pacemaker receives afferent input from many brain regions, one of which is the intergeniculate leaflet of the thalamus. This thalamic input to the suprachiasmatic nucleus in hamsters contains enkephalins, neuropeptide Y, neurotensin, and GABA. The role of enkephalins in modulating light-induced phase shifts of hamster activity rhythms has not been reported. Therefore, in this study, we examined the ability of enkephalin-mimetic and other opioid compounds to modulate light-induced phase advances in hamster circadian activity rhythms. The delta opioid agonists SNC 80 and BW373U86 both inhibited light-induced phase advances of hamster circadian activity rhythms. Neither the mu opioid agonist morphine, nor the kappa opioid agonist U50488H had any effect on light-induced phase shifts. The antagonists naltrindole, naltrexone, and nor-binaltorphimine, selective for delta, mu, and kappa opioids respectively, were also without effect on light-induced phase advances. Therefore, we found that only delta opioid agonists modulate light-induced phase advances in hamster circadian activity rhythms. These results imply that enkephalins released from the intergeniculate leaflet onto components of the suprachiasmatic pacemaker may be capable of inhibiting the responsiveness of the pacemaker to photic input arriving from the retina. The inability of antagonists to modulate light-induced phase advances suggests that endogenous opiate systems are not tonically active in generating circadian activity rhythms, but rather that enkephalins are probably used by the circadian system to modulate responses only under certain conditions or time of day.
Tierno
Antonio
A
Department of Biology, Dowling College, Oakdale, NY 11769, USA.
Fiore
Paul
P
Gannon
Robert L
RL
D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer / Q000494:pharmacology; D000818:Animals; D001549:Benzamides / Q000494:pharmacology*; D001683:Biological Clocks / Q000187:drug effects* / Q000502:physiology; D002940:Circadian Rhythm / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D006224:Cricetinae; D004745:Enkephalins / Q000502:physiology; D008027:Light; D008297:Male; D008647:Mesocricetus; D009020:Morphine / Q000494:pharmacology; D009043:Motor Activity / Q000187:drug effects / Q000502:physiology; D009271:Naltrexone / Q000031:analogs & derivatives* / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009419:Nerve Tissue Proteins / Q000502:physiology*; D018847:Opioid Peptides / Q000502:physiology; D010879:Piperazines / Q000494:pharmacology*; D017465:Receptors, Opioid, delta / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology*; D017473:Receptors, Opioid, kappa / Q000187:drug effects / Q000502:physiology; D017450:Receptors, Opioid, mu / Q000187:drug effects / Q000502:physiology; D013493:Suprachiasmatic Nucleus / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects
D001549:Benzamides; D004745:Enkephalins; D009292:Narcotic Antagonists; D009419:Nerve Tissue Proteins; D018847:Opioid Peptides; D010879:Piperazines; D017465:Receptors, Opioid, delta; D017473:Receptors, Opioid, kappa; D017450:Receptors, Opioid, mu; C083877:BW 373U86; C088464:4-(alpha-(4-allyl-2,5-dimethyl-1-piperazinyl)-3-methoxybenzyl)-N,N-diethylbenzamide; C051844:norbinaltorphimine; D009271:Naltrexone; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D009020:Morphine; C055382:naltrindole