AMPA and GABA(A/B) receptor subunit expression in the cortex of adult squirrel monkeys during peripheral nerve regeneration

• Published in: Brain research 2013-07, Vol.1520, p.80-94
• Main Authors: Mowery, Todd M, Walls, Sarah M, Garraghty, Preston E
• Format: Article
• Language: English
• Subjects: Aging; Animals; Immunohistochemistry; Median Nerve - injuries; Nerve Crush; Nerve Regeneration - physiology; Neuronal Plasticity - physiology; Protein Subunits - biosynthesis; Receptors, AMPA - biosynthesis; Receptors, GABA - biosynthesis; Saimiri; Somatosensory Cortex - physiology
• ISSN: 1872-6240
• DOI: 10.1016/j.brainres.2013.04.032

The primate somatosensory neuroaxis provides a highly translational model system with which to investigate adult neural plasticity. Here, we report immunohistochemical staining data for AMPA and GABAA/B receptor subunits in the area 3b cortex of adult squirrel monkeys one and five months after median nerve compression. This method of nerve injury was selected because it allows unique insight into how receptor expression changes during the regeneration of the peripheral nerve. One month after nerve compression, the pattern of subunit staining provides evidence that the cortex enters a state of reorganization. GABA α1 receptor subunits are significantly down-regulated in layer IV, V, and VI. Glur2/3 AMPA receptor subunits and postsynaptic GABABR1b receptor subunits are up and down regulated respectively across all layers of cortex. After five months of recovery from nerve compression, the pattern of AMPA and GABAA/B receptor subunits remain significantly altered in a layer specific manner. In layer II/III, GluR1, GluR2/3, and GABA α1 subunit expression is significantly up-regulated while post synaptic GABABR1b receptor subunits are significantly down regulated. In layer VI, V, and VI the GluR2/3 and presynaptic GABABR1a receptor subunits are significantly up-regulated, while the postsynaptic GABABR1b receptor subunits remain significantly down-regulated. Taken together, these results suggest that following nerve injury the cortex enters a state of reorganization that has persistent effects on cortical plasticity even after partial or total reinnervation of the peripheral nerve.