Circadian Rhythmicity in AVP Secretion and GABAergic Synaptic Transmission in the Rat Suprachiasmatic Nucleus
: A variety of physiological and behavioral functions exhibit circadian changes and these circadian rhythms are driven by oscillatory expression of clock genes in the suprachiasmatic nuclei (SCN). It is still unknown how this molecular clockwork is controlled by extracellular neurohormones and neuro...
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Published in | Annals of the New York Academy of Sciences Vol. 1048; no. 1; pp. 103 - 115 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.06.2005
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Subjects | |
Online Access | Get full text |
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Summary: | : A variety of physiological and behavioral functions exhibit circadian changes and these circadian rhythms are driven by oscillatory expression of clock genes in the suprachiasmatic nuclei (SCN). It is still unknown how this molecular clockwork is controlled by extracellular neurohormones and neurotransmitters and which membrane receptors undergo circadian modulation. Circadian rhythm can be measured as a secretion of arginine vasopressin (AVP) in organotypic SCN culture for several weeks. Melatonin applied directly to the SCN late in the day induces a phase advance, when applied late at night or at the beginning of the day melatonin causes a phase delay. The time window for phase advance corresponds with the highest level of melatonin receptors in the SCN but the mechanism of melatonin‐induced phase delay is unknown. The principal neurotransmitter on SCN synapses is γ‐aminobutyric acid (GABA), which acts at postsynaptic GABAA receptors. Spontaneous release of GABA from presynaptic nerve terminals, recorded as miniature inhibitory postsynaptic currents in the presence of TTX, does not change, but zinc sensitivity of exogenous GABA‐induced currents varies during the day and night, possibly due to changes in subunit composition of GABAA receptors. We conclude that there is daily variation in the postsynaptic, but not presynaptic, function in the SCN. |
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Bibliography: | ark:/67375/WNG-KDHF1TFZ-D istex:82359DD104CB8562CCA10FC6353FE25CE7886E5F ArticleID:NYAS103 Section on Cellular Signaling, ERRB/NICHD/NIH, Bethesda, Maryland 20892‐4510. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0077-8923 1749-6632 |
DOI: | 10.1196/annals.1342.010 |