30 views
Of the spinal dorsal horn in na e (b) and 7 days after SNI (c). Solid arrowheads indicate the positive cells. Scale bar 25Kiyoyuki et al. Mol Pain (2015) 11:Page 3 of(AMPA) receptor-mediated excitatory synaptic transmission, LTB4 (10 M) was dissolved in Krebs solution and was applied by perfusion for 1 min. When the cell membrane is fixed at -70 mV, N-methyl-d-aspartate (NMDA) receptors are blocked by Mg2+. The frequency and amplitude of sEPSC were not affected by application of LTB4 in dorsal horn neurons (n = 14) of na e rats (Fig. 2a). The frequency and the amplitude were, respectively, 116.1 ?7.4 (n = 14, P > 0.05) of control (1.2 ? 0.4 Hz) and 105.2 ? 3.9 (n = 14, P > 0.05) of control (8.5 ?1.8 pA, Fig. 2b). The frequency and amplitude of sEPSC also were not affected by the application of LTB4 in dorsal horn neurons (n = 19) of spared nerve injury (SNI) model rats (Fig. 2c, d). The frequency and the amplitude were, respectively, 112.6 ?9.7 (n = 19, P > 0.05) of control (1.8 ? 0.4 Hz) and 103.5 ? 3.6 (n = 19, P > 0.05) of control (7.1 ?0.2 pA, Fig. 2d). These results indicate that LTB4 does not affect AMPA receptor-mediated sEPSC of dorsal horn neurons in either na e or SNI rats. Next, we investigated whether LTB4 affects AMPAinduced currents in dorsal horn neurons. Exogenous application of AMPA (10 M) for 30 s induced inward currents at a holding potential of -70 mV. After 30 s pretreatment of LTB4 (10 M) in na e rats, AMPAinduced PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26599718 inward currents did not change Chloroquinoxaline sulfonamide (n = 11, Fig. 3a). The average peak amplitude of AMPA-induced currents was 100.1 ?4.9 of the control (24.5 ?3.6 pA, Fig. 3b). Next, we examined LTB4 effects in SNI model rats. AMPA-induced currents of SNI model rat also did not change (n = 13, Fig. 3c). The average peak amplitude of AMPA-induced currents was 102.9 ?7.4 of the control (24.5 ?3.6 pA, Fig. 3d). The application of LTB4 did not affect AMPA-induced currents of dorsal horn neurons in either na e or SNI rats.LTB4 enhanced postsynaptic NMDA currents in spinal dorsal horn neurons of SNI model ratsreceptor antagonist, and strychnine (2 M), a glycine receptor antagonist, to distinguish it from IPSCs and AMPA receptor-mediated sEPSCs. In na e rats the average increases in NMDA receptor-mediated sEPSC frequency and amplitude mediated by LTB4 (10 M) were 104.1 ? 7.2 and 99.8 PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/26648081 ? 13.4 (n = 5), respectively (Fig. 4b). These values were not significantly different from control (P < 0.05). However, we found that LTB4 slightly enhanced the amplitude of NMDA receptormediated sEPSCs in SNI model rats (Fig. 4a). The average increases in NMDA receptor-mediated sEPSC frequency and amplitude mediated by LTB4 were 107.8 ?7.0 and 109.6 ?2.6 (n = 5), respectively (Fig. 4c). This increase in amplitude was significantly large compared to control (P < 0.05). These results suggest LTB4 enhanced postsynaptic NMDA receptor actions in the neuropathic pain model. Therefore, we examined whether LTB4 affects postsynaptic NMDA currents in dorsal horn neurons. Exogenous application of NMDA (30 M) for 30 s induced inward currents at a holding potential of -50 mV. After 30 s pretreatment of LTB4 (10 M) in na e rats, NMDA-induced inward currents did not change (n = 28, Fig. 5a). The average peak amplitude of NMDA-induced currents was 103.6 ?3.9 of the control (8.8 ?1 pA, Fig. 5b). In the dorsal horn neurons of SNI model rats, we found that NMDA-induced currents increased in the presence of.
Be the first person to like this.