The role of mu-, delta1- and delta2-opioid receptors in the nucleus accumbens in pivoting was investigated in freely moving rats. Unilateral injections of the mu-opioid receptor agonist, [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO, 1 and 2 microg) and the delta2-opioid receptor agonist, deltorphin II (1 and 2 microg), but not the delta1-opioid receptor agonist, [D-Pen(2,5)]-enkephalin (DPDPE, 1-4 microg), into the shell or the core of the nucleus accumbens significantly induced contraversive pivoting. The pivoting induced by DAMGO (2 microg) and deltorphin II (2 microg) was inhibited significantly by the mu-opioid receptor antagonist, D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Phe-Thr-NH2 (CTOP, 0.1 and 1 microg), and the delta2-opioid receptor antagonist, naltriben (NTB, 0.1 and 1 mg/kg, i.p.), respectively. The DAMGO (2 microg)- or deltorphin II (2 microg)-induced pivoting was also inhibited significantly by co-administration of the dopamine D1/D2 receptor antagonist, cis(Z)-flupentixol (1 and 10 microg). The pivoting induced by unilateral injections of a mixture of dopamine D1 (SKF 38393, 5 microg) and D2 (quinpirole, 10 microg) receptor agonists into the shell was significantly inhibited by cis(Z)-flupentixol (1 and 10 microg) or NTB (1 and 3 mg/kg, i.p.), but not CTOP (1 microg) or delta1-opioid receptor antagonist, (E)-7-benzylidenenaltrexone (1 mg/kg, i.p.). The contraversive pivoting elicited by the cholinergic agonist, carbachol (5 microg), into the core was inhibited by co-administration of the muscarinic M1 antagonist, pirenzepine (1 microg), but not cis(Z)-flupentixol (1 microg). The results suggest that unilateral activation of mu- or delta2-opioid, but not delta1-opioid, receptors in the core and/or shell of the nucleus accumbens elicits contraversive pivoting that requires intact dopamine D1/D2 receptors in the shell, but not intact muscarinic M1 mechanism in the core. The study also shows that delta2-opioid, but not mu- and delta1-opioid, receptors in the core and/or shell modulate the shell-specific, dopamine D1/D2 receptor mechanisms involved in the production of pivoting.