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演題詳細

Poster

シナプス
Synapse

開催日 2014/9/12
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

海馬歯状回の貫通線維-顆粒細胞間シナプス伝達における入力線維特異的なセロトニン の作用
Serotonin inhibits the excitatory inputs in the dentate granule cells from the lateral perforant path but not the medial perforant path

  • P2-025
  • 野﨑 香菜子 / Kanako Nozaki:1 久保 怜香 / Reika Kubo:1,2 古川 康雄 / Yasuo Furukawa: 
  • 1:広島大学 / Hiroshima University 

The hippocampus is a brain structure which contains the neural networks for learning and memory, and the dentate gyrus is a gateway for the hippocampal networks. Granule cells are primary neurons in the dentate gyrus, and receive excitatory inputs mainly from the entorhinal cortex via perforant-path.
Serotonin (5-HT) is known to modulate the activity of GABAergic interneurons in the dentate gyrus, which indirectly affects the excitatory inputs from the perforant-path. A possible direct modulation of the excitatory synapses by 5-HT is, however, not well examined.
In the present study, we examined the actions of 5-HT on the excitatory synapses in granule cells under the condition in which GABAergic inputs were blocked by picrotoxin. 5-HT (1 μM) decreased the input resistance (IR) of granule cells around 50 % and shortened the decay of EPSPs evoked by stimulation of the perforant-path. Computer simulation showed that such reduction of IR decreases EPSPs around 30 % at most. We, however, observed more than 50 % reduction of EPSPs evoked by the lateral perforant path (LPP) in some preparations. Moreover, the synaptic transmission failure and the paired-pulse ratio (PPR) were often increased by 5-HT, suggesting that 5-HT reduces the release probability of the LPP synapse. These effects were suppressed by a 5-HT1A receptor antagonist, WAY100635. On the other hand, 5-HT did not reduce the amplitude of EPSPs evoked by the medial perforant path (MPP) and the PPR was rather decreased, suggesting that 5-HT may enhance the release probability of the MPP synapse. These results suggest that 5-HT induces pathway-specific modulation of excitatory inputs to the dentate granule cells.

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