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Progressive elevations in AMPA and GABA A receptor levels in deafferented somatosensory cortex
Author(s) -
He Haiyan,
Rasmusson Douglas D.,
Quinlan Elizabeth M.
Publication year - 2004
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2004.02590.x
Subject(s) - ampa receptor , somatosensory system , neuroscience , excitatory postsynaptic potential , inhibitory postsynaptic potential , nmda receptor , cortex (anatomy) , glutamate receptor , gabaa receptor , receptive field , long term potentiation , ionotropic effect , sensory system , biology , chemistry , receptor , medicine
Restricted receptive fields (RFs), a hallmark of mature sensory systems, are actively maintained by a balance between ascending excitation and local inhibition in the cortex. Deafferentation disrupts this balance, allowing a sequence of changes in neuronal response properties that culminate in the reorganization of cortical RFs. To explore the molecular basis of deafferentation‐induced RF reorganization, we tracked changes in AMPA receptor (AMPAR), NMDA receptor (NMDAR) and GABA A receptor (GABA A R) levels in the deafferented somatosensory cortex of adult raccoons following single‐digit amputation. In synaptoneurosomes prepared from deafferented cortex, we observe a significant increase in AMPARs, but no change in NMDARs, 1–9 days post‐deafferentation, coincident with the appearance of new excitatory inputs and enlarged RFs. We observe a significant increase in GABA A Rs 2–7 weeks post‐deafferentation, coincident with a return of inhibitory input and shrinking RFs. These experience‐dependent changes in the levels of the major cortical ionotropic receptors were transient, returning to pre‐experimental baseline by ≥ 17 weeks post‐deafferentation, when RFs return to original size, but are remapped to different loci. This suggests that deafferentation‐induced cortical reorganization may be generated by activity‐dependent potentiation of weak excitatory synapses, followed by an increase in the strength of inhibitory synapses, resulting in finely tuned, remapped cortical RFs.