Short-term ionic plasticity at GABAergic synapses

Abstract

Fast synaptic inhibition in the brain is mediated by the pre-synaptic release of the neurotransmitter γ-Aminobutyric acid (GABA)and the post-synaptic activation of GABA-sensitive ionotropic receptors. As with excitatory synapses, it is being increasinly appreciated that a variety of plastic processes occur at inhibitory synapses, which operate over a range of timescales. Here we examine a form of activity-dependent plasticity that is somewhat unique to GABAergic transmission. This involves short-lasting changes to the ionic driving force for the post-synaptic receptors, a process referred to as short-term ionic plasticity. These changes are directly related to the history of activity at inhibitory synapses and are influenced by a variety of factors including the location of the synapse and the post-synaptic cell's ion regulation mechanisms. We explore the processes underlying this form of plasticity, when and where it can occur, and how it is likely to impact network activity.

Cation-chloride cotransporters in neuronal development, plasticity and disease

“…These mechanisms underlie the phenomenon of ionic plasticity 6,15,176,199,200 , a hallmark of GABA A R-mediated transmission that is based on the dynamic nature of DF GABA (REFS 100,201,202). …”

Postnatal maturation of GABAergic transmission in the rat basolateral amygdala

“…GABA A receptor desensitization is also known to contribute to shortterm depression (Overstreet et al 2000), although there is no precedent for a developmental change in this phenomenon. Finally, short-term depression of immature GABAergic IPSCs may involve ionic plasticity, a depolarization of the chloride reversal following strong GABA A activation (for review see Raimondo et al 2012). To better understand the maturation of STP we observed, future studies should differentiate the various interneuron subtypes found in the BLA, which play different roles in the network but were grouped in the population response used here.…”

Simultaneous two-photon imaging of intracellular chloride concentration and pH in mouse pyramidal neurons in vivo

“…In recent years, regulation of the intracellular Cl − concentration ([Cl − ] i ) in neurons has attracted lots of attention, because it is the main ion that carries current across GABA A (and also, glycine) receptors. Changes in [Cl − ] i exert an immediate effect on the reversal potential of GABAergic currents (E GABA ) and, thereby, on the properties of GABA A receptor-mediated transmission (2)(3)(4). The "ionic plasticity" of GABAergic signaling involves not only the passive flux of Cl − ions through membrane channels but also, a number of ion transporters that regulate [Cl − ] i .…”