Neuroscience letters
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Neuroscience letters · Jul 1995
Continuous infusion of acidified saline around the rat sciatic nerve produces thermal hyperalgesia.
Recent observations using both clinical and animal models have suggested that acidosis may initiate pain and sensitization. In the present study, we examined if changing the acidic environment around the rat sciatic nerve resulted in thermal hyperalgesia. ⋯ Unbuffered, acidified PFS significantly decreased the perineural pH (pH 6.9 +/- 0.15, P < 0.05), and decreasing perineural pH values were significantly correlated with increasing thermal hyperalgesia (r = 0.91) for individual rats. While it is likely that multiple factors play a role in the development of neuropathic pain, these data demonstrate that an acidic environment around the sciatic nerve will produce thermal hyperalgesia.
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Neuroscience letters · Jun 1995
Electrophysiological evidence for the antinociceptive effect of transcutaneous electrical stimulation on mechanically evoked responsiveness of dorsal horn neurons in neuropathic rats.
Using a rat model of peripheral neuropathy induced by a tight ligation of L5-6 spinal nerves, the effects of transcutaneous electrical stimulation on the mechanical responses of wide dynamic range (WDR) dorsal horn neurons were investigated. The responses of the WDR neurons to both the brush and pinch stimuli were found to be enhanced in the neuropathic rats compared to those in the normal rats. ⋯ The durations of the depressive effects on the brush responses ranged between 30 and 45 min and those on the pinch responses were 60-90 min. These results imply that the transcutaneous electrical stimulation used here produces an antinociceptive effect via a depressive action on the enhanced mechanical responsiveness of the spinal neurons in this rat model of peripheral neuropathy.
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Neuroscience letters · Jun 1995
Peri-administration of clonidine or MK801 delays but does not prevent the development of mechanical hyperalgesia in a model of mononeuropathy in the rat.
Following loose ligation of the sciatic nerve, rats develop a persistent hyperalgesia which mimics some of the features of traumatic neuropathy seen in man. Previously, we have shown that administration of MK801 or clonidine prior to and 30 min following loose ligation of the sciatic nerve prevented the development of hyperalgesia up to 30 days following surgery. In the current study, we have extended our observation and examined the effect of administration of clonidine (1 mg/kg, s.c.) or MK801 (0.3 mg/kg, s.c.) 30 min prior to and 6 h following loose ligation of the sciatic nerve on the development of hyperalgesia assessed at 9 time points between 16 and 150 days after loose ligation. ⋯ No significant difference between the 2 treatment groups was detected at any other time points during the study. Similarly, when compared with saline treated controls, the degree of hyperalgesia measured in animals following peri-administration of clonidine was significantly less when measured 16 and 28 days after surgery, but did not differ significantly at any of the time points tested between 42 and 150 days following surgery. Our results indicate that peri-administration of MK801 or clonidine significantly delay, but do not prevent, the onset of neuropathic hyperalgesia.
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Neuroscience letters · May 1995
Fucoidin, a polysaccharide inhibiting leukocyte rolling, attenuates inflammatory responses in experimental pneumococcal meningitis in rats.
It is presumed that adjuvant therapy rather than new antibiotics will improve the prognosis of pneumococcal meningitis. We investigated the effect of fucoidin, a polysaccharide inhibiting leukocyte rolling, on inflammatory changes in experimental meningitis in rats. ⋯ Fucoidin treatment in the meningitis group reduced all inflammatory changes, whereas fucoidin treatment of animals without meningitis increased blood white cell count, but had no effect on any other parameter. Our results confirm that selectins are involved in the early phase of pneumococcal meningitis and possibly are a target for adjunctive therapy.
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In mice, activation of sigma1 receptors antagonizes opioid analgesia. Sigma antagonists potentiate opioid analgesia, implying that the anti-opioid sigma system is tonically active. Co-administration of haloperidol with the mu opioid morphine, the kappa 1 analgesic U50,488H or the kappa 3 agonist naloxone benzoylhydrazone enhances the analgesic activity of all agents. The effect results from sigma receptor blockade since (-)sulpiride, a selective D2 antagonist which does not block sigma receptors, is inactive.