TY - JOUR
T1 - Presynaptic induction of heterosynaptic associative plasticity in the mammalian brain
AU - Humeau, Yann
AU - Shaban, Hamdy
AU - Bissière, Stephanie
AU - Lüthi, Andreas
N1 - Funding Information:
Acknowledgements We thank the Malagasy authorities and the University of Antananarivo Department of Animal Biology for their assistance. Fieldwork (C.J.R and R.A.N) was supported by Conservation International, Earthwatch, the National Geographic Society, the US National Science Foundation and the World Wide Fund for Nature. This work was supported by NASA and the Center for Biodiversity and Conservation at the American Museum of Natural History.
Funding Information:
Acknowledgements We thank B. Gähwiler, C. Heuss, A. Matus, B. Poulain and E. Seifritz for discussions and comments on the manuscript. This work was supported by the Borderline Personality Disorder Research Foundation, the Swiss National Science Foundation and the Novartis Research Foundation.
PY - 2003/12/18
Y1 - 2003/12/18
N2 - The induction of associative synaptic plasticity in the mammalian central nervous system classically depends on coincident presynaptic and postsynaptic activity. According to this principle, associative homosynaptic long-term potentiation (LTP) of excitatory synaptic transmission can be induced only if synaptic release occurs during postsynaptic depolarization. In contrast, heterosynaptic plasticity in mammals is considered to rely on activity-independent, non-associative processes. Here we describe a novel mechanism underlying the induction of associative LTP in the lateral amygdala (LA). Simultaneous activation of converging cortical and thalamic afferents specifically induced associative, N-methyl-D-aspartate (NMDA) -receptor-dependent LTP at cortical, but not at thalamic, inputs. Surprisingly, the induction of associative LTP at cortical inputs was completely independent of postsynaptic activity, including depolarization, postsynaptic NMDA receptor activation or an increase in post-synaptic Ca2+ concentration, and did not require network activity. LTP expression was mediated by a persistent increase in the presynaptic probability of release at cortical afferents. Our study shows the presynaptic induction and expression of heterosynaptic and associative synaptic plasticity on simultaneous activity of converging afferents. Our data indicate that input specificity of associative LTP can be determined exclusively by presynaptic properties.
AB - The induction of associative synaptic plasticity in the mammalian central nervous system classically depends on coincident presynaptic and postsynaptic activity. According to this principle, associative homosynaptic long-term potentiation (LTP) of excitatory synaptic transmission can be induced only if synaptic release occurs during postsynaptic depolarization. In contrast, heterosynaptic plasticity in mammals is considered to rely on activity-independent, non-associative processes. Here we describe a novel mechanism underlying the induction of associative LTP in the lateral amygdala (LA). Simultaneous activation of converging cortical and thalamic afferents specifically induced associative, N-methyl-D-aspartate (NMDA) -receptor-dependent LTP at cortical, but not at thalamic, inputs. Surprisingly, the induction of associative LTP at cortical inputs was completely independent of postsynaptic activity, including depolarization, postsynaptic NMDA receptor activation or an increase in post-synaptic Ca2+ concentration, and did not require network activity. LTP expression was mediated by a persistent increase in the presynaptic probability of release at cortical afferents. Our study shows the presynaptic induction and expression of heterosynaptic and associative synaptic plasticity on simultaneous activity of converging afferents. Our data indicate that input specificity of associative LTP can be determined exclusively by presynaptic properties.
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U2 - 10.1038/nature02194
DO - 10.1038/nature02194
M3 - Article
C2 - 14685239
AN - SCOPUS:0346096511
VL - 426
SP - 841
EP - 845
JO - Nature
JF - Nature
SN - 0028-0836
IS - 6968
ER -