Abstract

N-ethylmaleimide-sensitive fusion (NSF) protein is a homohexameric ATPase that binds to the GluR2 subunit of α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid (AMPA) receptors. The stability and movement of AMPA receptors at synapses are important factors that control synaptic strength. NSF is involved in the surface expression regulation of AMPA receptors and consequently synaptic activity. Reduced expression of NSF or reduced interaction of NSF with GluR2 leads to a number of neurological disorders. Using a rat model of L5 spinal nerve ligation (SNL), we investigated the temporal and spatial expression of NSF in injured L5 and uninjured L4 dorsal root ganglion (DRG) neurons during mechanical allodynia. L5 SNL led to a significant decrease of NSF in both L4 and L5 DRGs observed at 3, 7, and 14 days after injury. In particular, NSF expression in calcitonin gene-related peptide (CGRP)-immunoreactive (IR) and IB4-IR neurons was reduced, whereas NSF expression in NF-200-IR neurons remained unaltered. These results indicate a role for NSF in CGRP-IR and IB4-IR neurons in SNL, with reduced NSF expression possibly contributing to SNL derived neuropathic pain.

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