The Journal of Neuroscience, July 1, 2002, 22(13):5271-5276
BRIEF COMMUNICATION
Absence of Long-Term Depression in the Visual Cortex of Glutamic
Acid Decarboxylase-65 Knock-Out Mice
Se-Young
Choi1, *,
Bernardo
Morales1, *,
Hey-Kyoung
Lee2, and
Alfredo
Kirkwood1
1 Department of Neuroscience and 2 Howard
Hughes Medical Institute, Mind Brain Institute, Johns Hopkins
University, Baltimore, Maryland 21218
Long-term depression (LTD) is widely considered a mechanism for
experience-induced synaptic weakening in the brain. Recent in
vivo studies on glutamic acid decarboxylase [GAD 65 (
/
)] knock-out mice indicates that GABAergic synaptic inhibition is also
required for the normal weakening of deprived inputs in the visual
cortex. To better understand how GABAergic inhibition might control
plasticity, we assessed the status of synaptic inhibition and LTD in
visual cortical slices of GAD 65 knock-out mice. We found the
following: (1) the efficacy of GABAergic synapses during repetitive
activation is reduced in GAD 65 (
/
) mice; (2) the induction of LTD
is impaired in the visual cortex of GAD 65 (
/
) mice; and (3)
chronic, but not acute, treatment with the benzodiazepine agonist
diazepam restores LTD in GAD 65 (
/
) mice. These results suggest
that a certain inhibitory tone is required for the induction of LTD in
visual cortex. We propose that the lack of visual cortical LTD in GAD
65 (
/
) may account for the lack of experience-dependent plasticity
in these mice.
Key words:
critical period; synaptic plasticity; GABA; neocortex; IPSC; synaptic inhibition
*
S.-Y.C. and B.M. contributed equally to this work.