The Journal of Neuroscience, November 1, 2002, 22(21):9171-9175
BRIEF COMMUNICATION
Lesion-Induced Thalamocortical Axonal Plasticity in the S1
Cortex Is Independent of NMDA Receptor Function in Excitatory Cortical
Neurons
Akash
Datwani1, *,
Takuji
Iwasato2, 3, *,
Shigeyoshi
Itohara3, and
Reha S.
Erzurumlu1
1 Department of Cell Biology and Anatomy and
Neuroscience Center, Louisiana State University Health Sciences Center,
New Orleans, Louisiana 70112, 2 PRESTO, Japan Science and
Technology Corporation, and 3 Laboratory for Behavioral
Genetics, Brain Science Institute, RIKEN, Saitama 351-0198, Japan
Neural activity plays an important role in refinement and
plasticity of synaptic connections in developing vertebrate sensory systems. The rodent whisker-barrel pathway is an excellent model system
to investigate the role of activity in formation of patterned neural
connections and their plasticity. When whiskers on the snout or the
sensory nerves innervating them are damaged during a critical period in
development, whisker-specific patterns are altered along the trigeminal
pathway, including the primary somatosensory (S1) cortex. In this
context, NMDA receptor (NMDAR)-mediated activity has been implicated in
patterning and plasticity of somatosensory maps. Using CxNR1KO mice, in
which NMDAR1 (NR1), the essential NMDAR
subunit gene, is disrupted only in excitatory cortical neurons, we
showed that NMDAR-mediated activity is essential for whisker-specific patterning of barrel cells in layer IV of the S1 cortex. In CxNR1KO mice, thalamocortical axons (TCAs) representing the large whiskers segregate into rudimentary patches, but barrels as cellular modules do
not develop. In this study, we examined lesion-induced TCA plasticity
in CxNR1KO mice. TCA patterns underwent normal structural plasticity
when their peripheral inputs were altered after whisker lesions during
the critical period. The extent of the lesion-induced morphological
plasticity and the duration of the critical period were quantitatively
indistinguishable between CxNR1KO and control mice. We conclude that
TCA plasticity in the neocortex is independent of postsynaptic NMDAR
activity in excitatory cortical neurons, and that non-NMDAR-mediated
cortical activity and/or subcortical mechanisms must be operational in
this process.
Key words:
somatosensory cortex; thalamocortical synaptic
plasticity; conditional knock-out; barrels; whiskers; glutamatergic
transmission; Cre/loxP system
*
A.D and T.I. contributed equally to this work.
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