Related Experiment Video
Updated: May 2, 2026

The Fibular Nerve Injury Method: A Reliable Assay to Identify and Test Factors That Repair Neuromuscular Junctions
Published on: August 11, 2016
Coupling of serotonergic input to NMDA receptor-phosphorylation following peripheral nerve injury via rapid, synaptic
Zigor Aira1, Itsaso Buesa1, Diego Rada2
1Department of Neurosciences, School of Medicine and Dentistry, University of the Basque Country, PO Box 699, 48080 Bilbao, Spain.
Abstract:
Evidence implicates serotonergic input to spinal dorsal horn neurons in shifting the NMDA receptor (NMDAR) into a high functional output profile after spinal nerve ligation (SNL). We investigated the involvement of adaptor protein NADH dehydrogenase subunit 2 (ND2) in NMDAR-phosphorylation and spinal hyperexcitability secondary to peripheral nerve injury. Immunofluorescence for ND2 was found in dorsal horn neurons immunopositive for NMDAR subunit NR1. Co-localization of ND2 with postsynaptic marker PSD-95 was significantly increased 60min after SNL (Rr 0.77 vs Rr 0.06 in sham controls; z=-242.85; p<0.01 at Fisher's exact test). Western blot analyses confirmed ND2 up-regulation both in cytoplasmic (S2) and synaptic (P3) compartments (p<0.01 at the Student's t test). SNL was followed by increased co-localization of ND2 with the phosphorylated form (serine 896) of NR1 (pNMDA). Spinal superfusion with ND2 inhibitor rotenone prevented up-regulation of ND2 (Rr 0.06 after rotenone vs Rr 0.78 in vehicle-treated controls, z=-253.22, p<0.01) and pNR1 in P3. C fiber-evoked dorsal horn field potentials were increased 60min after SNL by superfusion with NMDA agonist cis-ACPD at 100nM (p<0.01 at the Bonferroni test), however cis-ACPD was effective only at 10μM following prior administration of rotenone. Rotenone also abolished enhancement of evoked potentials induced by simultaneous stimulation of NMDA and 5-HR2B receptors in uninjured rats. Increased postsynaptic up-regulation of ND2/pNMDAR 60min after SNL was prevented by prior administration of selective 5-HT2B antagonist SB204741. These results support a pivotal role for ND2 in coupling serotonergic input to NMDAR-activation during neuropathic pain.
More Related Videos
07:11Examination of Anatomical Features of Retinal Ganglion Cells Under N-methyl-D-aspartic Acid (NMDA)-induced Excitotoxicity
Published on: September 19, 2025
05:08Mouse Sciatic Nerve Transection/Resuture Procedure for Studying Nerve Repair and Functional Recovery
Published on: January 16, 2026
Related Concept Videos
Secondary Spinal Cord Injury llI: Pathophysiology
Adrenergic Neurons: Neurotransmission
Synthesis: Catecholamine synthesis requires tyrosine, which...
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Neurogenesis and Regeneration of Nervous Tissue
Nociception
Integration of Synaptic Events