ABSTRACT
Objective To investigate the modulatory effect of different dosage of sufentanil on I GABA in rat dorsal root ganglion neurons. Methods The rat root ganglion neurons were enzymatically dissociated. The whole-cell patch clamp techniquewas applied to record the effect of 0.02 , 0.1, 0.5, 2.5 μmol/L sufentanil and 0.5 mol/L sufentanil + 1 nmol/L Naloxone, a non-specific ityopioid receptor antagonist on IGABA. Results 0.02, 0.1, 0.5, 2.5 μmol/L sufentanil potentiated IGABA to (108.7 ± 6.7)%,(122.0 ± 2.3)%, (146.7 ± 7.9)% and (130.1 ± 5.6)%, respectively (n = 10; *P < 0.05, **P < 0.01). The potentiation role of 0.1,0.5, 2.5 μmol/L sufentanil on IGABA lasted 10 to 20 min The potentiation could be blocked by Naloxone (n = 7; *P < 0.05, **P < 0.01). Conclusion Sufentanil activates μ opioid receptor and potentiates the action of GABAA receptor, and the potentiation could be blocked by Naloxone. The enhancement of currents by sufentanil may increase GABA A receptor-mediated presynaptic inhibition at the spinal cord level.
ABSTRACT
Objective To investigate the effects of morphine and tramadol pre-emptive use on the expressions of substance P mRNA (SPmRNA) and calcitonin gene-related peptide mRNA (CGRPmRNA) in dorsal root ganglia (DRG) following acute myocardial ischemia in the rats. Method Twenty-four adult male SD rats weighing 270 to 300 g were randomly (random number) divided into four groups (n = 6, in each): group Ⅰ(sham operation), group Ⅱ (myocardial ischemia), group Ⅲ (morphine pre-emptive use) and group Ⅳ (tramadol pre-emptive use). The left anterior descending branch of coronary artery was occluded (CAO) for 3 hours in rats of group Ⅱ and Ⅳ.In group Ⅲ morphine 1.25 mg·kg-1 was injected through caudal vein 15 minutes before CAO.In group Ⅳ,tramadol 12.5 mg·kg-1 was daministered via caudal vein 15 minutes before CAO.In 3 hours after myocardial ischemia, the tissue of DRG (T1-5) were taken for detecting the expressions of SPmRNA and CGRPmRNA by using RT-PCR. One-way ANOVA was used for statistical analysis. Results In the tissue of DRG, the expressions of SPmRNA(0.93±0.02) ,α-CGRP mRNA(0.98±0.02) and β-CGRP mRNA(0.83 ± 0.02)were up-regulated in group Ⅱ compared with those in group Ⅰ (0.84±0.04),(0.86±0.01),(0.45±0.03) (P ＜0.05),and decreased markedly in group Ⅲ (0.88 ± 0.03) ,(0.90 ± 0.02), (0.67 ± 0.02) (P ＜ 0.05) and group Ⅳ (0.88±0.04) ,(0.90 ± 0.01),(0.66±0.01) (P ＜ 0.05), but showed no difference between group Ⅲ and Ⅳ (P ＞ 0.05). Conclusions Morphine and tramadol pre-emptive use can significantly inhibit the expressions of SPmRNA and CGRPmRNA in rat's dorsal root ganglia after CAO.
ABSTRACT
It was reported that nerve fibers were present in the inner part of lumbar intervertebral discs from patients with discogenic pain. Because there are no nerve fibers in the inner part of annulus fibrosus in normal condition, this finding suggests nerve ingrowth into the disc may be a cause of discogenic pain. Disc degeneration is often asymptomatic, thus, to understand the differences between symptomatic and asymptomatic disc, it is necessary to understand the pathogenesis of discogenic pain. We recently revealed that over 90% of the nociceptive dorsal root ganglion (DRG) neurons innervating the disc are sensitive to nerve growth factor (NGF), which is related to inflammatory pain. This indicates that discogenic pain is closely related to inflammation and NGF may play a key role. The increase of inflammatory mediators in symptomatic discs has been reported; we therefore studied the effects of disc inflammation and found that it induces sensitization of disc-innervating neurons and nerve ingrowth into the disc. More recently, it was shown that annular rupture induces nerve ingrowth, an increase of inflammatory mediators in the disc, and upregulation of calcitonin gene-related peptide, a pain-related molecule in DRGs. These findings led us to believe that annular rupture triggers inflammation and nerve ingrowth, inflammatory mediators then further promote nerve ingrowth into the disc and sensitization of disc-innervating neurons, and discogenic pain finally becomes chronic. NGF, found in symptomatic discs, may act as a key factor in generating chronic discogenic pain by sensitizing disc-innervating neurons and stimulating nerve ingrowth into the disc.