• Top page
  • Timetable
  • Per session
  • Per presentation
  • How to
  • Meeting Planner



Synaptic Plasticity

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

Activity-dependent reduction of Ca2+ responses through AL-MB synaptic transmission in the isolated Drosophila brain

  • P2-037
  • 佐藤 翔馬 / Shoma Sato:1 上野 耕平 / Kohei Ueno:2 坂井 貴臣 / Takaomi Sakai:1 
  • 1:首都大院理工学生命科学 / Department of Biological Sciences, Tokyo Metropolitan Univ., Tokyo, Japan 2:東京都医学総合研 / Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan 

Long-term potentiation (LTP) and long-term depression (LTD) are considered to be cellular models for learning and memory in the mammalian brain. In the fruitfly, Drosophila melanogaster, behavioral and genetic studies have been extensively used to elucidate the molecular and neural mechanisms in learning and memory. In Drosophila brain, neurons of the mushroom bodies (MBs), which are considered to be the memory center, receive sensory information via the dendritic calyx mainly from the antennal lobes (ALs). In 2013, facilitation of the synaptic activity known as long-term enhancement (LTE) of synaptic transmission between AL and MB was reported in Drosophila. In this current study, in an isolated cultured Drosophila brain, we report activity-dependent reduction of Ca2+ responses in the MB using electrical stimulation of AL (AL-stimulation). AL-stimulation induces Ca2+ responses in the MB via AL-MB synaptic transmissions. GCaMP3, which is a GFP-based calcium indicator, was used for measurement of Ca2+ responses in MB. After repetitive-stimulation of AL (more than 40 bursts with a 1 sec inter-burst interval, with 30 pulses at 100 Hz per burst), interestingly, Ca2+ responses in the MB were reduced. It is possible that this activity-dependent reduction of Ca2+ responses shares common molecular pathways in controlling LTP or LTD in the mammalian brain. One of the ionotropic glutamate receptor, NMDAR, is critically involved in hippocampal LTP and LTD, and Drosophila LTE is also NMDAR-dependent. In contrast to hippocampal LTD, administration of NMDAR antagonist (MK-801) enhanced the reduction of Ca2+ responses after repetitive-stimulation, suggesting that AL-stimulation-inducible Ca2+ influx in the MB neurons is predominantly mediated via the NMDAR after repetitive stimulation of AL. However, it seems unlikely that NMDAR contributes to the activity-dependent reduction of Ca2+ responses in MB like hippocampal LTD.

Copyright © Neuroscience2014. All Right Reserved.