Developmental plasticity of inhibitory circuitry

• Type of Material: Article
• Authors: Sarah L. Pallas, Georgia State University; Peter Wenner, Emory University; Carlos Gonzalez Islas, Emory University; Michela Fagiolini, RIKEN Brain Science Institute; Khaleel A. Razak, Georgia State University; Gunsoo Kim, University of Pittsburgh; Dan Sanes, New York University; Birgit Roerig, Sucampo Pharmaceuticals
• Language: English
• Date: 2006-10-11
• Publisher: Lippincott, Williams & Wilkins
• Publication Version: Final Published Version
• Copyright Statement: Copyright © 2006 Society for Neuroscience.
• License: Creative Commons Attribution 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1523/JNEUROSCI.3516-06.2006
• Title of Journal or Parent Work: Journal of Neuroscience Nursing
• ISSN: 0888-0395
• Volume: 26
• Issue: 41
• Start Page: 10358
• End Page: 10361
• Grant/Funding Information: This work was supported by National Institutes of Health Grants NS046510 (P.W.), EY12696 (S.L.P.), EY12702 (B.R.), DC006864 (D.S.), DC05202 (to Zoltan Fuzessery), and DC4199 (to Karl Kandler), and National Science Foundation Grants IBN-0078110 (S.L.P.) and IOB-0616097 (P.W.).
• Keywords: SPINAL NETWORKS; Life Sciences & Biomedicine; HIPPOCAMPAL PYRAMIDAL CELLS; DEVELOPING AUDITORY-SYSTEM; NEURAL MECHANISMS; VISUAL-CORTEX; Neurosciences; Science & Technology; GABA(A) RECEPTORS; SYNAPTIC-TRANSMISSION; Neurosciences & Neurology; LATERAL SUPERIOR OLIVE; DEPOLARIZATION-INDUCED SUPPRESSION; CEREBRAL-CORTEX
• Research Categories: Health Sciences, Opthamology; Biology, Neuroscience

Abstract

A growing body of evidence suggests that plasticity at GABAergic synapses is of critical importance during development and aging. A balance between excitation and inhibition maintains homeostasis at the neuronal and circuit levels, and inhibitory plasticity can function to drive a perturbed system toward homeostasis. Activity-dependent modification of inhibitory synaptic strength must be non-Hebbian, however, because the interaction between an inhibitory neuron and its target prevents them from firing together. Mechanisms that may underlie inhibitory plasticity will be discussed, including the possibility that it is limited to the early period when GABA/glycine release is excitatory (Ben-Ari, 2002) or that corelease of another substance alters synapses that produce inhibition (Gillespie et al., 2005). Alternatively, inhibitory synapses may decline in strength through long-term depression (Kotak et al., 2001; Chang et al., 2003), or an as-yet undiscovered mechanism may be responsible. Whatever the mechanism, it is clear that inhibitory plasticity plays an important role in activity-dependent modification of developing circuits.