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Ionotropic receptors of γ-aminobutyric acid (GABA A Rs) produce two forms of inhibitory signaling: phasic inhibition triggered by activation of synaptic GABA A Rs at GABAergic synapses, and tonic inhibition generated in large part through persistent activation of extrasynaptic GABA A Rs. It has recently been demonstrated that tonic inhibition may also involve spontaneously opening GABA A Rs (s-GABA A Rs) whose activation does not require binding of γ-aminobutyric acid (GABA). Here, we examine intracellular mechanisms modulating GABA A Rs’ tonic effects in rat dentate gyrus granule cells (DGCs). Cellular control of s-GABA A Rs-delivered tonic current appears to involve signaling inputs from G-protein-dependent and -independent molecular cascades, whereas tonic GABA-dependent current in DGCs is regulated by protein kinase C. The intracellular agents that modulate s-GABA A R-generated inhibition could thus represent a generic mechanism controlling signal integration in central neural circuits.

Selective modulation of tonically active GABAA receptor functional subgroups by G-proteins and protein kinase C

Selective modulation of tonically active GABA_A receptor functional subgroups by G-proteins and protein kinase C