Altered parcellation of neocortical somatosensory maps in N-methyl-D-aspartate receptor-deficient mice.

The body map in the parietal neocortex is built by inputs from the brainstem and thalamic somatosensory nuclei. Receptor density in the sensory periphery and neural activity play a major role in allocation of cortical tissue to different components of the somatosensory body map. Here we present evidence that neural activity mediated via N-methyl-D-aspartate (NMDA) receptors plays a major role in parcellation of the cortical body map subdivisions. In mice with genetically lowered NMDA receptor function along the trigeminal pathway, subcortical trigeminal nuclei shrink and, consequently, the face representation area of the primary somatosensory cortex diminishes in size. In contrast, dorsal column subcortical paw representation areas that are not as severely affected by the genetic manipulation of NMDA receptors do not show any areal changes, yet their cortical projection zones expand. Our findings indicate that both subcortical and cortical mechanisms contribute to cortical parcellation of body map subdivisions in an NMDA receptor-dependent manner. Copyright (c) 2005 Wiley-Liss, Inc.