Mechanisms of GABAergic Homeostatic Plasticity

Homeostatic plasticity ensures that appropriate levels of activity are maintained through compensatory adjustments in synaptic strength and cellular excitability. For instance, excitatory glutamatergic synapses are strengthened following activity blockade and weakened following increases in spiking...

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Main Author: Peter Wenner
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Neural Plasticity
Online Access:http://dx.doi.org/10.1155/2011/489470
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spelling doaj-311d1375f8714b06adc69ebbf01237112020-11-24T22:05:29ZengHindawi LimitedNeural Plasticity2090-59041687-54432011-01-01201110.1155/2011/489470489470Mechanisms of GABAergic Homeostatic PlasticityPeter Wenner0Department of Physiology, Emory University, School of Medicine, 615 Michael Street, Room 601, Atlanta, GA 30322, USAHomeostatic plasticity ensures that appropriate levels of activity are maintained through compensatory adjustments in synaptic strength and cellular excitability. For instance, excitatory glutamatergic synapses are strengthened following activity blockade and weakened following increases in spiking activity. This form of plasticity has been described in a wide array of networks at several different stages of development, but most work and reviews have focussed on the excitatory inputs of excitatory neurons. Here we review homeostatic plasticity of GABAergic neurons and their synaptic connections. We propose a simplistic model for homeostatic plasticity of GABAergic components of the circuitry (GABAergic synapses onto excitatory neurons, excitatory connections onto GABAergic neurons, cellular excitability of GABAergic neurons): following chronic activity blockade there is a weakening of GABAergic inhibition, and following chronic increases in network activity there is a strengthening of GABAergic inhibition. Previous work on GABAergic homeostatic plasticity supports certain aspects of the model, but it is clear that the model cannot fully account for some results which do not appear to fit any simplistic rule. We consider potential reasons for these discrepancies.http://dx.doi.org/10.1155/2011/489470
collection DOAJ
language English
format Article
sources DOAJ
author Peter Wenner
spellingShingle Peter Wenner
Mechanisms of GABAergic Homeostatic Plasticity
Neural Plasticity
author_facet Peter Wenner
author_sort Peter Wenner
title Mechanisms of GABAergic Homeostatic Plasticity
title_short Mechanisms of GABAergic Homeostatic Plasticity
title_full Mechanisms of GABAergic Homeostatic Plasticity
title_fullStr Mechanisms of GABAergic Homeostatic Plasticity
title_full_unstemmed Mechanisms of GABAergic Homeostatic Plasticity
title_sort mechanisms of gabaergic homeostatic plasticity
publisher Hindawi Limited
series Neural Plasticity
issn 2090-5904
1687-5443
publishDate 2011-01-01
description Homeostatic plasticity ensures that appropriate levels of activity are maintained through compensatory adjustments in synaptic strength and cellular excitability. For instance, excitatory glutamatergic synapses are strengthened following activity blockade and weakened following increases in spiking activity. This form of plasticity has been described in a wide array of networks at several different stages of development, but most work and reviews have focussed on the excitatory inputs of excitatory neurons. Here we review homeostatic plasticity of GABAergic neurons and their synaptic connections. We propose a simplistic model for homeostatic plasticity of GABAergic components of the circuitry (GABAergic synapses onto excitatory neurons, excitatory connections onto GABAergic neurons, cellular excitability of GABAergic neurons): following chronic activity blockade there is a weakening of GABAergic inhibition, and following chronic increases in network activity there is a strengthening of GABAergic inhibition. Previous work on GABAergic homeostatic plasticity supports certain aspects of the model, but it is clear that the model cannot fully account for some results which do not appear to fit any simplistic rule. We consider potential reasons for these discrepancies.
url http://dx.doi.org/10.1155/2011/489470
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