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. Author manuscript; available in PMC: 2009 Jul 1.
Published in final edited form as: Neurobiol Learn Mem. 2008 Jan 7;90(1):275–279. doi: 10.1016/j.nlm.2007.11.004

Figure 2.

Figure 2

Cellular mechanisms of T→S LTP. All data are expressed as a ΔEPSP between an initial pretest and a posttest 60min later. T+ represents the tetanized T→S synapse, while T− represents the non-tetanized pathway. Under control conditions (saline (N=8) or methanol vehicle (N=4)), tetanization induces homLTP in the T+ pathway and hetLTD in the T− pathway. (A) Treatment with the mGluR antagonist, MCPG, blocked homLTP and homLTD was observed at the T+ synapse instead (N=7). MCPG did not affect hetLTD at T− and MCPG applied without tetanus did not alter synaptic transmission (N=4). (B) Treatment with the VDCC blocker, nimodipine, blocked homLTP and homLTD was observed at the T+ synapse instead (N=4). Nimodipine did not affect hetLTD at T− and nimodipine applied without tetanus did not alter synaptic transmission (N=3). (C) Treatment with the PKC antagonist, bisindolylmaleimide (BIS), blocked homLTP and homLTD was observed at the T+ synapse instead (N=4). BIS did not affect hetLTD at T− and BIS applied without tetanus did not alter synaptic transmission (N=4).