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Synaptic Plasticity

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Protein synthesis inhibitors do not block long-term depression (LTD) in CA1 field of hippocampal slices induced electrically or chemically in either juvenile or adult rats

  • P2-040
  • Abdul Karim Abbas:1 Sameh Mohammad:2 
  • 1:Inst. Neuroscience and Physiology, University of Gothenburg, Sweden 2:School of Life Sciences, Skövde University, Sweden  

We have previously reported that long-term depression (LTD), a proposed cellular model for processing and storing some forms of information, induced by stimulation of the metabotropic glutamate receptors in CA1 area of hippocampal slices obtained from neonatal or adult rats was maintained, in both normal slices and slices treated with protein synthesis inhibitors (PSI). To verify whether another form of LTD that is induced by stimulation of NMDA receptor exhibits different pattern of tendency we induced LTD either electrically or chemically. Electrically-induced LTD was conducted by introduction of a low-frequency stimulation (LFS). A robust LTD maintained for up to 10-12 h was observed in 12-21 days old rats. Treating slices with PSIs cycloheximide (100 μM) or anisomycin (40 μM) did not reveal a visible difference in LTD magnitude and duration between the two groups. To maximize NMDA receptors stimulation, we induced LTD by a brief application (3 min) of NMDA at concentration of 20 μM in hippocampal slices obtained from 12-18 weeks old rats, the method that is reported to be in principle similar to the electrically-induced LTD. Again a robust and long-standing (10 h) LTD was induced by such protocol, which was also insensitive to a continuous perfusion of slices by cycloheximide (100 μM). Given it is the first time in literature to observe such long-lasting LTD (10-12 h), the data confirm that LTD can be sustained for longer intervals without the requirement for triggered protein synthesis, a phenomenon that has already been shown with long-term potentiation (LTP). They also raise suspicion whether the prevalent notion in neuroscience of synaptic plasticity that entails it is divided into two temporal phases: an early, protein synthesis-independent, and a late, protein synthesis-dependent one is valid.

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