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Intracellular calcium release resulting from mGluR1 receptor activation modulates GABA sub(A) currents in wide-field retinal amacrine cells: a study with caffeine
The modulatory action of calcium (Ca super(2+)) released from intracellular stores on GABA sub(A) receptor-mediated current was investigated in wide-field amacrine cells isolated from the teleost, Morone chrysops, retina. Caffeine, ryanodine or inositol 1,4,5-triphosphate (IP sub(3)) markedly inhibi...
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Published in: | The European journal of neuroscience 2003-06, Vol.17 (11), p.2237-2248 |
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Main Authors: | , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | The modulatory action of calcium (Ca super(2+)) released from intracellular stores on GABA sub(A) receptor-mediated current was investigated in wide-field amacrine cells isolated from the teleost, Morone chrysops, retina. Caffeine, ryanodine or inositol 1,4,5-triphosphate (IP sub(3)) markedly inhibited the GABA sub(A) current by elevating [Ca super(2+)] sub(i). The inhibition resulted from the activation of a Ca super(2+) arrow right Ca super(2+)/calmodulin arrow right calcineurin cascade. Long (>12s) exposure to glutamate mimicked the caffeine effect, i.e. it inhibited the GABA sub(A) current by elevating [Ca super(2+)] sub(i) through mGluR1 receptor activation and consequent IP sub(3) generation. This pathway provides a 'timed' disinhibitory mechanism to potentiate excitatory postsynaptic potentials in wide-field amacrine cells. It occurs as a result of the suppression of GABA-mediated conductances as a function of the duration of presynaptic excitatory input activity. This is much like some forms of long-term potentiation in the central nervous system. In a local retinal circuit this will selectively accentuate particular excitatory inputs to the wide-field amacrine cell. Similar to other neural systems, we suggest that activity-dependent postsynaptic disinhibition is an important feature of the signal processing in the inner retina. |
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ISSN: | 0953-816X 1460-9568 |
DOI: | 10.1046/j.1460-9568.2003.02652.x |