Pharmacology, biochemistry, and behavior
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Pharmacol. Biochem. Behav. · May 1994
Evidence of a role for N-methyl-D-aspartate (NMDA) receptors in the facilitation of tail withdrawal after spinal transection.
Peripheral injury produces a characteristic excitation of spinal cord dorsal horn cells (wind-up) which is associated with a facilitation of spinal nociceptive reflexes (hyperalgesia). These phenomena are believed to be mediated by a trauma-induced increase in the release of excitatory amino acids (EAAs). A similar increase in the activity of dorsal horn neurons and spinal reflexes occurs after spinal transection. ⋯ However, both systemic and intrathecal ketamine significantly increased TF latencies in spinal, relative to intact rats. These results indicate that ketamine did not prevent the development of spinal reflex facilitation, but it selectively reduced this reaction once it was established in spinal rats. The data support an involvement of EAAs in reflex facilitation produced by spinal transection.
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Pharmacol. Biochem. Behav. · May 1994
Effects of valine, leucine, isoleucine, and a balanced amino acid solution on the seizure threshold to picrotoxin in rats.
During infusion of branched-chain amino acids (BCAAs) in humans, changes in ventilatory drive, sleeping pattern, and appetite have been reported. The mechanism by which BCAA exerts their effects on CNS remains unclear. ⋯ A balanced amino acid solution (Vamin-Glucose) had no effect on the seizure threshold. Thus, these CNS effects are specific for BCAAs and occur with all three.
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Pharmacol. Biochem. Behav. · Apr 1994
Serotonergic neurotoxic lesions facilitate male sexual reflexes.
The effects of the neurotoxin 5,7 dihydroxytryptamine (5,7 DHT) on the urethrogenital reflex was examined in anesthetized male rats. Both ICV and intrathecal administration of 5,7 DHT produced a marked depletion (92%) of spinal 5-hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HT IAA) levels. ICV but not intrathecal administration of 5,7 DHT also caused a moderate reduction in 5-HT and 5-HT IAA levels in the medulla and hypothalamus (40-48%). ⋯ In spinally intact, vehicle-treated rats the urethrogenital reflex could not be evoked. However, the urethrogenital reflex could be evoked in rats pretreated with either ICV or intrathecal 5,7 DHT prior to section of the spinal cord. These data support the hypothesis that 5-HT mediates the descending inhibition of male sexual reflexes.
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Pharmacol. Biochem. Behav. · Mar 1994
Dihydropyridine-sensitive calcium channels and barbiturate tolerance and withdrawal.
We have shown previously that the dihydropyridine calcium channel antagonist nitrendipine, given chronically, prevents the development of ethanol tolerance and physical dependence. The present study examines the effects on barbiturate tolerance and physical dependence. Nitrendipine, given acutely during withdrawal, provided little protection against barbiturate withdrawal, as measured by convulsive behaviour on handling. ⋯ Acute nitrendipine significantly increased the latency of seizures in response to the partial benzodiazepine inverse agonist FG7142 during barbiturate withdrawal, but there was no effect on the seizure incidence in response to bicuculline. Chronic treatment with nitrendipine did not alter the development of tolerance to the ataxic or general anaesthetic actions of barbiturates, but evidence was found of a possible interaction between nitrendipine and pentobarbitone, which may have been pharmacokinetic. The results suggest that neuronal calcium channels may be involved to some degree in the development of the changes responsible for barbiturate withdrawal, but to a less extent than found previously for ethanol dependence.
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Pharmacol. Biochem. Behav. · Sep 1993
Naloxone-induced analgesia: involvement of kappa-opiate receptors.
Rats treated with an acute high dose (30 mg/kg) or 4 days with a lower dose (5 mg/kg) of naloxone or naltrexone show an analgesic response at the hot-plate test. This paradoxical analgesic effect of the two mu-opiate receptor antagonists is blocked by the kappa opiate receptor antagonist MR 1452, and is modulated by the kappa opiate receptor agonist U 50-488. Our results suggest that kappa opiate receptors are involved in naloxone-induced analgesia and are consistent with a high degree of plasticity of the opiatergic system.