Journal
NATURE NEUROSCIENCE
Volume 12, Issue 9, Pages 1093-1095Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2378
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Funding
- Agence Nationale pour la Recherche
- European Neuroscience Institutes Network
- Eucor Learning and Teaching Mobility Program
- Swiss National Science Foundation
- Austrian Science Fund
- Novartis Research Foundation
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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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