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. 2014 Feb 25;8:55. doi: 10.3389/fncel.2014.00055

Figure 4.

Figure 4

Interaction of the phasic and tonic inhibitory mechanisms in the glomerulus. Phasic and tonic inhibition are not independent but share a number of mechanisms and influence one each other in several ways. (1) GABA released by Golgi cell terminals during phasic inhibition contributes in increasing the level of ambient GABA, that activates extrasynaptic α6 containing GABA-A receptors, contributing to the tonic conductance (Diaz et al., 2013). (2) The tonic GABA level in the glomerulus is sufficient to activate pre-synaptic high affinity GABA-B receptors (GABABRs), that modulate release probability affecting phasic transmission (Mapelli et al., 2009). (3) GABA spillover from neighboring synapses increases the level of ambient GABA (giving a phasic contribution to tonic inhibition). (4) tonic and phasic sources of GABA (ambient and spillover) determine post-synaptic GABA-B receptors activation, modulating the K inward rectifier current and therefore granule cell excitability (Rossi et al., 2006).