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Circadian Modulation of the ClEquilibrium Potential in the Rat Suprachiasmatic Nuclei
Author(s) -
Javier Alamilla,
Azucena PérezBurgos,
Daniel Quinto,
Raúl AguilarRoblero
Publication year - 2014
Publication title -
biomed research international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 126
eISSN - 2314-6141
pISSN - 2314-6133
DOI - 10.1155/2014/424982
Subject(s) - excitatory postsynaptic potential , inhibitory postsynaptic potential , reversal potential , gabaergic , circadian rhythm , gabaa receptor , suprachiasmatic nucleus , endocrinology , chemistry , gamma aminobutyric acid , medicine , bumetanide , cotransporter , membrane potential , biophysics , neurotransmission , patch clamp , neuroscience , biology , electrophysiology , receptor , biochemistry , organic chemistry , sodium
The suprachiasmatic nuclei (SCN) constitute a circadian clock in mammals, where γ -amino-butyric acid (GABA) neurotransmission prevails and participates in different aspects of circadian regulation. Evidence suggests that GABA has an excitatory function in the SCN in addition to its typical inhibitory role. To examine this possibility further, we determined the equilibrium potential of GABAergic postsynaptic currents ( E GABA ) at different times of the day and in different regions of the SCN, using either perforated or whole cell patch clamp. Our results indicate that during the day most neurons in the dorsal SCN have an E GABA close to −30 mV while in the ventral SCN they have an E GABA close to −60 mV; this difference reverses during the night, in the dorsal SCN neurons have an E GABA of −60 mV and in the ventral SCN they have an E GABA of −30 mV. The depolarized equilibrium potential can be attributed to the activity of the Na(+)-K(+)-2Cl(−) (NKCC) cotransporter since the equilibrium potential becomes more negative following addition of the NKCC blocker bumetanide. Our results suggest an excitatory role for GABA in the SCN and further indicate both time (day versus night) and regional (dorsal versus ventral) modulation of E GABA in the SCN.

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