Transduction of light in the suprachiasmatic nucleus: evidence for two different neurochemical cascades regulating the levels of Per1 mRNA and pineal melatonin.
The suprachiasmatic nucleus (SCN) contains a circadian clock and regulates melatonin synthesis in the pineal gland. Light exposure during the subjective night acutely increases the mRNA levels of the Period (Per)1 gene in the SCN and acutely suppresses melatonin levels in the pineal gland. Activation of N-methyl-D-aspartate (NMDA) receptors in the SCN has been demonstrated to phase-shift the circadian clock in a manner similar to light. We tested the hypothesis that activation of excitatory amino acid (EAA) receptors in the SCN mediates the acute effects of light on Per1 mRNA levels and pineal melatonin. NMDA, injected into the SCN of Syrian hamsters during the night, acutely suppressed melatonin levels in the pineal gland. Both the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5) and the alpha-amino-3-hydroxy-5-methylisoxazoleproprionic acid (AMPA)/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) inhibited the light-induced increase of Per1 mRNA levels in the SCN. In the same animals, however, these antagonists had no effect on the ability of light to suppress pineal melatonin. These results support the hypothesis that EAA receptor activation in the SCN is necessary for the acute effects of light on Per1 mRNA levels. They also indicate that NMDA receptor activation in the SCN is sufficient but may not be necessary for the acute effects of light on pineal melatonin. These data suggest that there may be at least two different neurochemical cascades that transduce the effects of light in the SCN
Paul
K N
KN
Center for Behavioral Neuroscience, Department of Biology, Georgia State University, 24 Peachtree Center Avenue, P.O. Box 4010, Atlanta, GA 30302-4010, USA.
Fukuhara
C
C
Tosini
G
G
Albers
H E
HE
D000818:Animals; D001345:Autoradiography; D006224:Cricetinae; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000528:radiation effects*; D008027:Light; D008297:Male; D008550:Melatonin / Q000378:metabolism*; D008845:Microinjections; D016202:N-Methylaspartate / Q000494:pharmacology; D009687:Nuclear Proteins / Q000235:genetics / Q000378:metabolism*; D010870:Pineal Gland / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D011810:Quinoxalines / Q000494:pharmacology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000528:radiation effects; D011863:Radioimmunoassay; D013493:Suprachiasmatic Nucleus / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D009687:Nuclear Proteins; D011810:Quinoxalines; D012333:RNA, Messenger; C056723:FG 9041; D016202:N-Methylaspartate; C056639:2-amino-5-phosphopentanoic acid; D014633:Valine; D008550:Melatonin