Changes in intracellular chloride concentration, mediated by chloride influx through GABAA receptor-gated channels, may modulate GABAB receptor-mediated inhibitory postsynaptic potentials (GABAB IPSPs) via unknown mechanisms. Recording from CA3 pyramidal cells in hippocampal slices, we investigated the impact of chloride influx during GABAA receptor-mediated IPSPs (GABAA IPSPs) on the properties of GABAB IPSPs. At relatively positive membrane potentials (near -55 mV), mossy fiber-evoked GABAB IPSPs were reduced (compared with their magnitude at -60 mV) when preceded by GABAA receptor-mediated chloride influx. This effect was not associated with a correlated reduction in membrane permeability during the GABAB IPSP. The mossy fiber-evoked GABAB IPSP showed a positive shift in reversal potential (from -99 to -93 mV) when it was preceded by a GABAA IPSP evoked at cell membrane potential of -55 mV as compared with -60 mV. Similarly, when intracellular chloride concentration was raised via chloride diffusion from an intracellular microelectrode, there was a reduction of the pharmacologically isolated monosynaptic GABAB IPSP and a concurrent shift of GABAB IPSP reversal potential from -98 to -90 mV. We conclude that in hippocampal pyramidal cells, in which "resting" membrane potential is near action potential threshold, chloride influx via GABAA IPSPs shifts the reversal potential of subsequent GABAB receptor-mediated postsynaptic responses in a positive direction and reduces their magnitude.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Neurophysiology|
|State||Published - 2001|
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