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L-type voltage-dependent Ca2+ channels mediate expression of presynaptic LTP in amygdala


The molecular mechanisms underlying the expression of postsynaptic long-term potentiation (LTP) at glutamatergic synapses are well understood. However, little is known about those that mediate the expression of presynaptic LTP. We found that presynaptic LTP at cortical inputs to the mouse lateral amygdala was blocked and reversed by L-type voltage-dependent Ca2+ channel (L-VDCC) blockers. Thus, a persistent increase in L-VDCC–mediated glutamate release underlies the expression of presynaptic LTP in the amygdala.

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Figure 1: Differential role of distinct VDCC subtypes in synaptic transmission and plasticity.
Figure 2: L-VDCC mediate expression of presynaptic LTP.


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We thank J. Letzkus and all members of the Lüthi laboratory for helpful discussions and comments on the manuscript. This study was supported by the Agence Nationale pour la Recherche, the European Neuroscience Institutes Network, the Eucor Learning and Teaching Mobility Program, the Swiss National Science Foundation, the Austrian Science Fund and the Novartis Research Foundation.

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E.F., F.G, G.C., B.P., Y.H. and A.L. designed the study. E.F., F.G., G.C. and Y.H. carried out the experiments. E.F., F.G., G.C., B.P., Y.H. and A.L. analyzed the data. E.F., G.C., B.P., Y.H. and A.L. wrote the manuscript.

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Correspondence to Andreas Lüthi.

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Fourcaudot, E., Gambino, F., Casassus, G. et al. L-type voltage-dependent Ca2+ channels mediate expression of presynaptic LTP in amygdala. Nat Neurosci 12, 1093–1095 (2009).

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