Neuropeptides. 2007 Nov 5; [Epub ahead of print]
Rat brain opioid peptides-circadian rhythm is under control of melatonin.
Miguel Asai MA, Lilian Mayagoitia LM, David García DG, Gilberto Matamoros-Trejo GM, Marcela Valdés-Tovar MV, Phillipe Leff PL.
Laboratorio de Análisis Químicos, Instituto Nacional de Psiquiatría, Calzada México-Xochimilco #101, Col. San Lorenzo Huipulco, C.P. 14370, México D.F., Mexico.
Several experiments have revealed an Endogenous Opioid System (EOS)-circadian rhythm. The brain-borne hormone, melatonin (MEL) has been shown to regulate the organism photoperiodic activity and may be implicated in the EOS-circadian rhythm. To explore this hypothesis, we studied the effect of functional pinealectomy on the EOS-circadian rhythm by measuring the immunoreactive content of Met-Enkephalin, Leu-Enkephalin and Synenkephalin in both hypothalamus and hippocampus of the rat brain, using standard radioimmunoassay procedures. Experimental animals exposed to white fluorescent light (WFL) for 15days (<50lux), displayed a disruption of the EOS-circadian rhythm, showing that absence of MEL induced a significant decrease of tissue content of enkephalin peptides at 01:00h during the dark-phase of the 24-h circadian rhythm, when compared to control rats. Functional pinealectomized rats exposed to 4 or 6h period of darkness (used to revert the effects induced by the absence of melatonin) significantly increased the tissue content of ME-IR and LE-IR, when compared to both controls and non-exposed WFL-treated rats. In addition, subcutaneous administration of exogenous melatonin (10, 100, 150, 300, 600mug/kg), in WFL-treated animals produced significant dose-dependent increases of ME-IR in both brain regions tested. Finally, luzindole (melatonin receptor antagonist) administration, was not able to prevent the enkephalin tissue increase, induced with the MEL administration (150mug/kg). This data suggest that MEL not only regulates the EOS-circadian rhythm, but also appears to modulate their synthesis in the rat brain from their respective neurons.
PMID: 17988732 [PubMed - as supplied by publisher]
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