Effects of delta opioid receptors activation on a response inhibition task in XXXX .

@entity2227 @entity146 @entity935 @entity19 @entity5172 @entity969 @entity13847 @entity750 @entity1286 @entity35 @entity1063
RATIONALE: Response inhibition, a primary symptom of many @entity146 , is mediated through a complex neuropharmacological network that involves @entity935 , @entity750 , @entity2227 , @entity1063 , and cannabinoid mechanisms. Recently, we identified an opioidergic contribution to response inhibition by showing that deletion of mu or delta opioid receptors in @entity19 alters motor impulsivity. OBJECTIVES: We investigated this phenomenon further by testing whether pharmacological activation of opioid receptors disrupts the ability to inhibit a motor response. METHODS: Long-Evans @entity35 were trained to withhold a lever-pressing response for @entity969 until a discriminative stimulus (lever light) was presented. The delay to the discriminative stimulus (1 to 60  s) was varied, so animals could not predict, on any given trial, the length of the pre-response phase. Motor impulsivity was assessed as the inability to inhibit lever pressing prior to the discriminative stimulus. @entity35 were tested following an injection of the mu opioid receptor agonist @entity1286 (0, 0.5, 1, 2, 4, 6, 8, or 10  mg/kg) or the delta receptor agonist @entity13847 (0, 2.5, 5, or 10  mg/kg). RESULTS: @entity13847 (10  mg/kg) increased premature responses and locomotor activity, but had no effect on the speed of responding or non-reinforced presses. The @entity13847 -induced decrease in accuracy was blocked by the delta opioid receptor antagonist @entity5172 . @entity1286 had no effect on accuracy but increased locomotor activity (2  mg/kg). CONCLUSIONS: These findings point to a role for delta, but not mu, opioid receptors in disinhibition as measured in the response inhibition task. The results appear to contradict those of previous opioid receptor deletion studies; possible sources of these discrepant results are discussed.
