a | Somatic inhibition by fast-spiking parvalbumin-positive (PV+) cells (green) expressing the potassium channel Kv3.1 is mediated by the GABAA (γ-aminobutyric acid type A) α1-subunit, whereas axonal inhibition is mediated by the GABAA α2-subunit. Somatic inhibition is ideally situated for suppression, or 'editing' of unwanted spikes, preventing them from back-propagating through the cell body into the dendritic tree (red arrow). This is an 'instructive' model, as individual action potentials can produce long-term potentiation (LTP) or depression (LTD) based on precise spike-timing dependent windows at individual synapses of coincident pre- and postsynaptic activity123, 124. Notably, failure to regulate excess spiking at the axon initial segment can still be differentiated by fast-spiking inhibition at the cell body. b | Gap junctional coupling endows networks of parvalbumin-positive (PV+) interneurons with the ability to detect synchronous input128, 129, 130. Even a slight jitter in input timing (for example, between eyes) dampens network activity through reciprocal GABA-mediated contacts (enriched with GABAA-receptor α1-subunits131). Only synchronous open-eye input will produce maximal, activity-dependent release or uptake of 'permissive' factors for neurite growth (for example, tissue-type plasminogen activator78, 86 and brain-derived neurotrophic factor). Competition is determined extracellularly.

	Created by Cher Bachar over 11 years ago

Synaptic plasticity Note on Developmental plasticity, created by Cher Bachar on 09/05/2013.