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• W2057482024 endingPage "125" @default.
• W2057482024 startingPage "119" @default.
• W2057482024 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." @default.
• W2057482024 created "2016-06-24" @default.
• W2057482024 creator A5006598488 @default.
• W2057482024 creator A5040786493 @default.
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• W2057482024 date "1999-09-01" @default.
• W2057482024 modified "2023-10-06" @default.
• W2057482024 title "Electrophysiological effects of opioid receptor activation on Syrian hamster suprachiasmatic nucleus neurones in vitro" @default.
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• W2057482024 doi "https://doi.org/10.1016/s0361-9230(99)00069-6" @default.
• W2057482024 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10535330" @default.
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