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. Author manuscript; available in PMC: 2013 Jul 3.
Published in final edited form as: Eur J Neurosci. 2009 Oct 12;30(8):1462–1475. doi: 10.1111/j.1460-9568.2009.06944.x

Fig. 12. Theoretical model of glutamatergic light input signaling to the g-aminobutyric acid (GABA)ergic suprachiasmatic nucleus (SCN) network.

Fig. 12

The effect of GABA on membrane potential and [Ca2+]i is a balance, with excitatory and inhibitory effects of GABA neurotransmission within the network driven by the chloride gradient that is under control by the cotransporters, NKCC1 and KCC2. (A) Depolarization induced by external light input signaling to glutamate receptors (GluR) via the retinohypothalamic tract (RHT) is facilitated by GABA release from other SCN neurons (dashed circle) within the network to a SCN neuron (solid circle) with a high intercellular chloride concentration ([Cl-]i), where opening of GABAA receptors (GABAAR) moves Cl- out of the neuron, further depolarizing the membrane potential (Vm), opening voltage-dependent calcium channels (VDCC) and increasing [Ca2+]i. (B) In neurons with low baseline [Cl-]i, GABA released from the SCN network opens GABAAR and moves Cl- into the neuron hyperpolarizing the cell beyond the depolarizing effect of RHT signaling and decreasing [Ca2+]i. A balance may also occur between the depolarizing action of RHT light input signaling with a hyperpolarizing effect from GABA release within the network, and no change in membrane potential, firing frequency or [Ca2+]i occurs.