Involvement of dopamine D2 receptors in the induction of long-term potentiation in the basolateral amygdala–dentate gyrus pathway of anesthetized rats

We have previously found that synaptic pathway from the basolateral amygdala (BLA) to the dentate gyrus (DG) displays N-methyl-d-aspartate (NMDA) receptor-independent form of long-term potentiation (LTP), which should be a valuable model for elucidating neural mechanisms linking emotion and memory. To explore its cellular mechanisms, we investigated possible involvement of the β-adrenergic, muscarinic cholinergic and dopaminergic systems on LTP in this pathway of anesthetized rats. The induction of BLA–DG LTP was not affected by administration of the β-adrenoceptor antagonist propranolol (50–150 nmol, i.c.v.), the muscarinic receptor antagonist scopolamine (2–6 mg/kg, i.p.), the cholinesterase inhibitor physostigmine (50 nmol, i.c.v.) or the dopamine D1 receptor antagonist SCH23390 (100 nmol, i.c.v.), but significantly inhibited by the dopamine D2 receptor antagonists, chlorpromazine (15 nmol, i.c.v.) and haloperidol (0.15–0.5 mg/kg, i.p.), and significantly promoted by the dopamine D2 receptor agonist quinpirole (78 nmol, i.c.v.). Furthermore, lesioning with 6-hydroxydopamine of the ventral tegmental area (VTA), the origin of mesolimbic dopaminergic neurons, resulted in attenuated BLA–DG LTP. These results suggest that the D2-dopaminergic system, but not the β-adrenergic, muscarinic or D1-dopaminergic system, is involved in the induction of BLA–DG LTP. In addition, inhibition of BLA–DG LTP by haloperidol or VTA lesion was abolished by blockade of GABAergic inhibition with picrotoxin. It is probable that the D2-dopaminergic system promotes the induction of BLA–DG LTP by suppressing GABAergic inhibition.