Nucleus accumbens μ opioid receptors mediate immediate postictal decrease in locomotion after an amygdaloid kindled seizure in rats

Postictal movement dysfunction is a common symptom in patients with epilepsy. We investigated the involvement of opioid receptors in the nucleus accumbens (NAC) in amygdaloid kindling-induced postictal decrease in locomotion (PDL) in rats. Seizures were induced by daily electrical stimulation of the basolateral amygdala until four consecutive stage 5 seizures were elicited. Locomotion was quantified before and after infusion of an opioid receptor antagonist or saline into the NAC. Whereas PDL was induced after a stage 5 seizure in saline-infused rats, pre-infusion of the μ opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 5 μg/1 μL/side) into the NAC prevented PDL. Pre-infusion of δ (naltrindole, 30 μg/1 μL/side), κ (nor-binaltorphimine, 1.8 μg/1 μL/side), or nonselective (naloxone, 10 μg/1 μL/side) opioid receptor antagonists did not block PDL, but late postictal hyperactivity was blocked by naltrindole. None of the antagonists affected amygdaloid evoked afterdischarge duration. It is suggested that μ opioid receptors in the NAC participate in amygdaloid seizure-induced PDL without affecting seizure duration.