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Nucleus accumbens mu opioid receptors mediate immediate postictal decrease in locomotion after an amygdaloid kindled
Jingyi Ma1, Richard Boyce, L Stan Leung
1Department of Physiology and Pharmacology, University of Western Ontario, London, ON, Canada.
Epilepsy & Behavior : E&B
|February 2, 2010
Summary
Mu opioid receptors in the nucleus accumbens (NAC) are key to postictal movement dysfunction after seizures. Blocking these receptors prevents decreased locomotion following amygdaloid kindling in rats.
Area of Science:
- Neuroscience
- Epilepsy Research
- Pharmacology
Background:
- Postictal movement dysfunction, specifically a decrease in locomotion, is a frequent occurrence in epilepsy patients.
- The nucleus accumbens (NAC) is implicated in motor control and reward pathways, making it a potential site for regulating postictal behaviors.
Purpose of the Study:
- To investigate the role of opioid receptors within the NAC in amygdaloid kindling-induced postictal decrease in locomotion (PDL) in a rat model.
- To determine which specific opioid receptor subtypes (mu, delta, kappa) in the NAC are involved in PDL.
Main Methods:
- Rats underwent amygdaloid kindling to induce stage 5 seizures.
- Locomotion was measured before and after seizure induction.
- Opioid receptor antagonists (mu, delta, kappa, nonselective) or saline were infused into the NAC.
Main Results:
- Infusion of a mu opioid receptor antagonist (CTAP) into the NAC prevented PDL.
- Delta, kappa, and nonselective opioid receptor antagonists did not block PDL, though naltrindole blocked late postictal hyperactivity.
- None of the tested antagonists altered the afterdischarge duration of amygdaloid-evoked seizures.
Conclusions:
- Mu opioid receptors located in the NAC play a critical role in mediating postictal decrease in locomotion following amygdaloid kindling-induced seizures.
- The involvement of mu opioid receptors in PDL appears independent of their effect on seizure duration.
