Fig. 5

Changes of neurotransmission, neuroplastic, and neuromodulatory molecules in injured spinal cords. IRL of calcitonin gene-related peptide (CGRP, a pain-related neurotransmitter) and p75 neurotrophin receptor (p75NTR, a regulator of nociceptive neurons) were significantly higher in spinal cord sections 5 mm rostral to the epicenter (i.e., ~ T8 spinal cord; SCI group; A and B/CGRP; C and D/p75NTR), compared to T10 level of the control (A₁/CGRP; C₁/p75NTR); the IHC signals were primarily located in Rexed Laminae (RL) I and II (CGRP: right inset in A; p75NTR: inset in C) and deeper zones of DH (CGRP: left inset in A) and in the dorsal roots (CGRP: H₁, J; p75NTR: H₂, J₁; I/control; p < 0.01, n = 4/group, Student’s t test). Also disclosed by IHC analysis were significantly increased mean IRL of Homer-1a, a marker of DH neuronal plasticity (E, G) and serotonin (5HT), a neuromodulator (E₁, G₁) in RL-I & II of the SCI group, relative to the control group (F; p < 0.05, n = 4/group, Student’s t test). Furthermore, statistical linear regressions uncovered that IRL of CGRP and p75NTR were negatively correlated with the sensitivity threshold (unit: second) of the bilateral hot plate test (CGRP: p = 0.02, R² = 0.83, K; p75NTR: p < 0.01, R² = 0.94, L) in the SCI group; changes in IRL of Homer-1α and 5HT also correlated negatively with the sensitivity threshold of the bilateral hot plate test in SCI animals (Homer-1α: p < 0.01, R² = 0.72, M; 5HT: p < 0.01, R² = 0.85, N; scale bars: 100 µm)