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. 2005 Jun 20;102(26):9365–9370. doi: 10.1073/pnas.0503777102

Fig. 6.

Fig. 6.

RIM1α is required for L-LTP induced by synaptic capture. (A) Diagram illustrating the placement of stimulating and recording electrodes for synaptic-capture experiment shown in B and C. Stim 1 was placed in the stratum radiatum to stimulate the Schaffer collateral fiber input from CA3 neurons. Stim 2 was placed in the alveus to stimulate antidromically the axons of the CA1 pyramidal neurons. (B) The role of RIM1α in synaptic capture. Four trains of 100-Hz antidromic stimulation (1 s, *) were applied to Stim 2, located in the alveus, 1 h before the application of a single 100-Hz tetanus to Stim 1, located in the stratum radiatum. In wild-type mice, the single train (*) applied to Stim 1, primed with four trains of tetanus to Stim 2, induced a long-lasting synaptic potentiation (open circles). In RIM1α-knockout mice, the synaptic potentiation was reduced to baseline in 1.5–2 h (filled circles). (Insets) Sample traces 10 min before and 3 h after the LTP. (Scale bars: 10 ms, 2 mV.) (C) The baseline EPSPs elicited by Stim 1 were not significantly changed in wild-type or RIM1α-/- mice for up to 3 h when the four trains of 100-Hz tetanic stimulation to Stim 2 (alveus) were delivered in the absence of the single 100-Hz tetanus to the Schaffer collaterals (Stim 1) (n = 4). Open squares, wild type; filled squares, RIM1α-/-.