Intracellular calcium release resulting from mGluR1 receptor activation modulates GABAA currents in wide‐field retinal amacrine cells: a study with caffeine

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Abstract
The modulatory action of calcium (Ca2+) released from intracellular stores on GABAA 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 (IP3) markedly inhibited the GABAA current by elevating [Ca2+]i. The inhibition resulted from the activation of a Ca2+→ Ca2+/calmodulin → calcineurin cascade. Long (>12 s) exposure to glutamate mimicked the caffeine effect, i.e. it inhibited the GABAA current by elevating [Ca2+]i through mGluR1 receptor activation and consequent IP3 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.