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Receptor autoradiographic correlates of deafferentation‐induced reorganization in adult primate somatosensory cortex
Author(s) -
Garraghty Preston E.,
Arnold Lori L.,
Wellman Cara L.,
Mowery Todd M.
Publication year - 2006
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.21018
Subject(s) - somatosensory system , neuroscience , ampa receptor , biology , nmda receptor , receptive field , glutamate receptor , inhibitory postsynaptic potential , neuroplasticity , stimulation , receptor , biochemistry
The primate somatosensory system provides an excellent model system with which to investigate adult neural plasticity. We have previously shown that transection of the median and ulnar nerves is followed by an expansion in the representation of radial nerve skin, and that this plasticity proceeds in stages. Immediately following nerve injury, new receptive fields are “unmasked” in a fraction of the affected cortex. The remaining deprived cortex regains responsiveness to tactile stimulation over the following days to weeks. Given these progressive changes, it has been suggested that different mechanisms might account for the earlier and later phases of reorganization. In the present experiments, we quantified receptor autoradiographic binding data for GABA A and GABA B , AMPA, and NMDA receptors in the primary somatosensory cortices of adult squirrel monkeys at four postnerve injury survival durations: immediately (1–3 hours), 3 days, 1 month, and 2 months. We found dramatic reductions in GABA A binding in layer IV within hours following nerve injury, and this reduction was maintained across all survival durations. This finding is consistent with the idea that the earliest reorganizational changes are due to a relaxation in tonic inhibitory mechanisms permitting the expression of formerly subthreshold receptive fields. GABA B receptor binding is decreased in layer IV by 1 month after nerve injury, while binding for AMPA receptors is increased in layer IV by this time. These findings are consistent with our previous suggestion that the second stage of reorganization proceeds via mechanisms comparable to those revealed to account for NMDA‐dependent long‐term potentiation in the hippocampus. J. Comp. Neurol. 497:636–645, 2006. © 2006 Wiley‐Liss, Inc.