GABAergic inhibition in visual cortical plasticity.
Experience is required for the shaping and refinement of developing neural circuits during well defined periods of early postnatal development called critical periods. Many studies in the visual cortex have shown that intracortical GABAergic circuitry plays a crucial role in defining the time course of the critical period for ocular dominance plasticity. With the end of the critical period, neural plasticity wanes and recovery from the effects of visual defects on visual acuity (amblyopia) or binocularity is much reduced or absent. Recent results pointed out that intracortical inhibition is a fundamental limiting factor for adult cortical plasticity and that its reduction by means of different pharmacological and environmental strategies makes it possible to greatly enhance plasticity in the adult visual cortex, promoting ocular dominance plasticity and recovery from amblyopia. Here we focus on the role of intracortical GABAergic circuitry in controlling both developmental and adult cortical plasticity. We shall also discuss the potential clinical application of these findings to neurological disorders in which synaptic plasticity is compromised because of excessive intracortical inhibition.
Sale
Alessandro
A
Institute of Neuroscience Consiglio Nazionale delle Ricerche Pisa, Italy.
Berardi
Nicoletta
N
Spolidoro
Maria
M
Baroncelli
Laura
L
Maffei
Lamberto
L
Neuroscience. 2002;111(4):815-35
12031406
Nat Rev Neurosci. 2005 Nov;6(11):877-88
16261181
J Neurosci. 1999 Nov 15;19(22):RC40
10559430
Eur J Neurosci. 2008 Jun;27(12):3342-50
18557922
Neuron. 2004 Dec 16;44(6):1031-41
15603745
Nat Neurosci. 2007 Apr;10(4):411-3
17322876
Behav Brain Res. 2003 Jan 22;138(2):121-31
12527443
Neuropharmacology. 2004 Oct;47(5):649-60
15458836
Curr Biol. 2008 Jul 22;18(14):1067-71
18635353
Proc Natl Acad Sci U S A. 2002 May 28;99(11):7717-21
12032349
Proc Natl Acad Sci U S A. 2006 May 30;103(22):8517-22
16709670
Cell. 1999 Sep 17;98(6):739-55
10499792
J Neurosci. 2004 May 19;24(20):4840-8
15152044
Brain Res. 1995 Aug 21;689(2):172-82
7583320
Behav Genet. 2004 Jan;34(1):105-19
14739701
Nat Neurosci. 2000 Apr;3(4):303-4
10725911
Vision Res. 1994 Mar;34(6):709-20
8160387
Behav Neurosci. 2004 Dec;118(6):1196-205
15598129
Neurosci Biobehav Rev. 2002 Jun;26(4):471-83
12204193
Science. 1998 Nov 20;282(5393):1504-8
9822384
Nat Neurosci. 2007 Jun;10(6):679-81
17468749
Trends Neurosci. 2007 Oct;30(10):497-503
17825437
Proc Natl Acad Sci U S A. 2003 Oct 14;100(21):12486-91
14514885
Science. 2008 Apr 18;320(5874):385-8
18420937
Trends Neurosci. 2009 Apr;32(4):233-9
19268375
Curr Opin Neurobiol. 2008 Feb;18(1):101-7
18534841
PLoS One. 2007 May 30;2(5):e475
17534425
Cell. 2008 Aug 8;134(3):508-20
18692473
Am J Med Genet. 2002 Feb 1;107(4):317-24
11840489
Biol Psychiatry. 2010 Apr 1;67(7):657-65
20172507
Behav Brain Res. 2002 Aug 21;134(1-2):185-200
12191805
Nat Neurosci. 2007 Sep;10(9):1134-6
17694050
Nat Rev Neurosci. 2000 Dec;1(3):191-8
11257907
Proc Natl Acad Sci U S A. 2005 Aug 30;102(35):12560-5
16116096
J Child Neurol. 2006 Mar;21(3):210-3
16901422
Nat Genet. 1999 Oct;23(2):185-8
10508514
Science. 2002 Nov 8;298(5596):1248-51
12424383
Science. 2003 Oct 31;302(5646):885-9
14593183
Ann Neurol. 1983 Oct;14(4):471-9
6638958
Neurobiol Dis. 2006 Jan;21(1):217-27
16087343
J Neurosci. 2006 Mar 15;26(11):2951-5
16540572
Neuron. 2006 Feb 2;49(3):341-8
16446138
J Physiol. 1970 Feb;206(2):419-36
5498493
Gene. 2003 Oct 30;318:137-47
14585506
Neuroimage. 2006 Sep;32(3):1216-20
16809053
Cereb Cortex. 2003 Jul;13(7):758-64
12816891
Neuron. 2007 Mar 1;53(5):747-59
17329213
Nat Neurosci. 2004 Mar;7(3):215-6
14966527
Science. 2005 Sep 30;309(5744):2222-6
16195464
J Neurosci. 2010 Jan 6;30(1):361-71
20053917
Science. 2004 Mar 12;303(5664):1681-3
15017002
Nature. 2000 Mar 9;404(6774):183-6
10724170
Neuron. 2004 Dec 16;44(6):1021-30
15603744
Nat Neurosci. 2007 Dec;10(12):1569-77
18026099