TY - JOUR
T1 - Developmental plasticity of inhibitory circuitry
AU - Pallas, Sarah L.
AU - Wenner, Peter
AU - Gonzalez-Islas, Carlos
AU - Fagiolini, Michela
AU - Razak, Khaleel A.
AU - Kim, Gunsoo
AU - Sanes, Dan
AU - Roerig, Birgit
PY - 2006/10/11
Y1 - 2006/10/11
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33749838128&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33749838128&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.3516-06.2006
DO - 10.1523/JNEUROSCI.3516-06.2006
M3 - Article
C2 - 17035517
AN - SCOPUS:33749838128
SN - 0270-6474
VL - 26
SP - 10358
EP - 10361
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 41
ER -