title: Basolateral amygdala D1- and D2-dopaminergic system promotes the formation of long-term potentiation in the dentate gyrus of anesthetized rats.
abstract: We have previously found that the induction of hippocampal long-term potentiation (LTP) is modulated by neuron activities in the basolateral amygdala (BLA). However, little is known about what neurotransmitter system in the BLA contributes to modulation of hippocampal LTP. In the present study, we investigated possible involvement of BLA dopaminergic system in the induction of LTP at the perforant path (PP)-dentate gyrus (DG) granule cell synapses of anesthetized rats. The induction of PP-DG LTP was significantly attenuated by intra-BLA injection of the D(1) receptor antagonist SCH23390 (2 or 6 nmol) or the D(2) receptor antagonists, chlorpromazine (30 or 100 nmol) or haloperidol (4.4 or 13.3 nmol). The effects of SCH23390 and haloperidol were abolished by concomitant intra-BLA injection of the D(1) receptor agonist SKF38393 (17 nmol) and the D(2) receptor agonist quinpirole (3 nmol), respectively. Furthermore, lesioning with 6-hydroxydopamine of the ventral tegmental area, the origin of the dopaminergic system projecting to the BLA, resulted in attenuated PP-DG LTP, which was restored by intra-BLA injection of SKF38393 or quipirole. These results suggest that the induction of PP-DG LTP is promoted by the BLA dopaminergic system via both D(1) and D(2) receptors.
authors.affiliation: Department of Pharmacology, School of Pharmacy, Hoshi University, Tokyo 142-8501, Japan. kazuabe@musashino-u.ac.jp
authors.forename: Kazuho
authors.initials: K
authors.lastname: Abe
authors.forename: Taiki
authors.initials: T
authors.lastname: Fujimoto
authors.forename: Tatsuhiro
authors.initials: T
authors.lastname: Akaishi
authors.forename: Miwa
authors.initials: M
authors.lastname: Misawa
mesh_terms: D018663:Adrenergic Agents / Q000633:toxicity; D000679:Amygdala / Q000187:drug effects / Q000293:injuries / Q000378:metabolism*; D000818:Animals; D001552:Benzazepines / Q000494:pharmacology; D001703:Biophysics; D002746:Chlorpromazine / Q000494:pharmacology; D018891:Dentate Gyrus / Q000502:physiology*; D018492:Dopamine Antagonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation / Q000379:methods; D017774:Long-Term Potentiation / Q000502:physiology*; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D016627:Oxidopamine / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar; D017447:Receptors, Dopamine D1 / Q000037:antagonists & inhibitors / Q000502:physiology*; D017448:Receptors, Dopamine D2 / Q000502:physiology*; D017557:Ventral Tegmental Area / Q000293:injuries / Q000502:physiology
chemical_list: D018663:Adrenergic Agents; D001552:Benzazepines; D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; C534628:SCH 23390; D016627:Oxidopamine; D002746:Chlorpromazine