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J Neurophysiol 82: 3298-3306, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 6 December 1999, pp. 3298-3306
Copyright ©1999 by the American Physiological Society

Internal Calcium Modulates Apparent Affinity of Metabotropic GABA Receptors

Wen Shen and Malcolm M. Slaughter

Departments of Physiology and Biophysics and Ophthalmology, School of Medicine, State University of New York, Buffalo, New York 14214

Shen, Wen and Malcolm M. Slaughter. Internal Calcium Modulates Apparent Affinity of Metabotropic GABA Receptors. J. Neurophysiol. 82: 3298-3306, 1999. The metabotropic GABA receptor (GABABR) regulates calcium influx in neurons. Whole cell voltage-clamp techniques were employed to determine the effects of internal calcium on the activity of GABABRs. GABABR receptor apparent affinity was maximal when bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA) maintained internal calcium below 70 nM. Apparent affinity was reduced as internal calcium increased. EGTA did not produce similar effects, suggesting that localized increases in calcium influenced GABABR apparent affinity. Confocal imaging disclosed relatively high internal calcium just below the plasma membrane of isolated neurons. BAPTA, but not EGTA, reduced this ring of high calcium. Heparin, dantrolene, and ryanodine increased GABABR apparent affinity, effects similar to that of BAPTA. Calmodulin inhibitors also increased receptor apparent affinity. These results suggest that internally released calcium activates calmodulin, which reduces GABABR apparent affinity. This identifies a reciprocal system in which the metabotropic GABA receptor can reduce calcium influx, but internal calcium can suppress this receptor pathway. Metabotropic glutamate receptors linked to inositol 1,4,5 trisphosphate (InsP3) raised internal calcium and suppressed the action of GABABRs. Thus negative feedback systems control the balance between excitatory and inhibitory metabotropic receptor pathways in retinal neurons.




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