阿部 和穂

モルモット気管平滑筋を弛緩させる南天実エキスの活性成分の同定を試み、それがヒゲナミンであり、β<SUB>2</SUB>受容体刺激によって気管拡張をおこすことを解明した。

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 UP 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 UP is promoted by the BLA dopaminergic system via both D(1) and D(2) receptors. (C) 2009 Elsevier Inc. All rights reserved.

We have previously found that the induction of long-term potentiation in the synaptic pathway from the basolateral amygdala to the dentate gyros (BLA-DG LTP) is regulated by L-type Ca2+ channels, dopamine D-2 receptors and GABAergic inhibition. In the present study, we investigated possible relations among the three mechanisms by using anesthetized rats. Blockade of GABAergic inhibition with picrotoxin abolished both the inhibitory effect of the dopamine D-2 receptor antagonist chlorpromazine and the promoting effect of the dopamine D-2 receptor agonist quinpirole on the induction of BLA-DG LTP. However, the inhibitory effect of the L-type Ca2+ channel blocker verapamil on BLA-DG LTP was not affected by picrotoxin. These results suggest that the role of dopamine D-2 receptors in the induction of BLA-DG LTP is modulatory and depends on GABAergic inhibition, whereas the role of L-type Ca2+ channels is fundamental. (C) 2009 Elsevier B.V. All rights reserved.

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 serotonergic 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 inhibited by intra-BLA injection of the 5-HT2 receptor antagonist cinanserin (25-50 nmol), but not by intra-BLA injection of the 5-HT1.7 receptor antagonist methiothepin (50 nmol), the 5-HT3 receptor antagonist ondansetron (50 nmol) or the 5-HT4 receptor antagonist RS23597-190 (100 nmol). In addition, intra-BLA injection of the 5-HT2C receptor agonist MK212 (50 nmol) facilitated the induction of PP-DG LTP. These results suggest that the induction of PP-DG LTP is promoted by activation of 5-HT2C receptors in the BLA. (C) 2008 Elsevier Ireland Ltd. All rights reserved.

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 beta-adrenergic, muscarinic cholinergic and dopaminergic systems on UP in this pathway of anesthetized rats. The induction of BLA-DG LTP was not affected by administration of the beta-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 D-1 receptor antagonist SCH23390 (100 nmol, i.c.v.), but Significantly inhibited by the dopamine D-2 receptor antagonists, chlorpromazine (15 nmol, i.c.v.) and haloperidol (0.15-0.5 mg/kg, i.p.), and significantly promoted by the dopamine D-2 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 D-2-dopaminergic system, but not the beta-adrenergic, muscarinic or D-1-dopaminergic system, is involved in the induction of BLA-DG LTR In addition, inhibition of BLA-DG UP by haloperidol or VIA lesion was abolished by blockade of GABAergic inhibition with picrotoxin. It is probable that the D-2-dopaminergic system promotes the induction of BLA-DG LTP by Suppressing GABAergic inhibition. (C) 2008 Elsevier Ltd. All rights reserved.