4.7 Article

Coactivation of thalamic and cortical pathways induces input timing-dependent plasticity in amygdala

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NATURE NEUROSCIENCE
卷 15, 期 1, 页码 113-U145

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NATURE PUBLISHING GROUP
DOI: 10.1038/nn.2993

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  1. US National Institutes of Health [MH083011, MH090464, MH079079]
  2. National Alliance for Research on Schizophrenia and Depression
  3. Whitehall Foundation
  4. US Army [W81XWH-08-2-0126]

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Long-term synaptic enhancements in cortical and thalamic auditory inputs to the lateral nucleus of the amygdala (LAn) mediate encoding of conditioned fear memory. It is not known, however, whether the convergent auditory conditioned stimulus (CSa) pathways interact with each other to produce changes in their synaptic function. We found that continuous paired stimulation of thalamic and cortical auditory inputs to the LAn with the interstimulus delay approximately mimicking a temporal pattern of their activation in behaving animals during auditory fear conditioning resulted in persistent potentiation of synaptic transmission in the cortico-amygdala pathway in rat brain slices. This form of input timing-dependent plasticity (ITDP) in cortical input depends on inositol 1,4,5-trisphosphate (InsP(3))-sensitive Ca2+ release from internal stores and postsynaptic Ca2+ influx through calcium-permeable kainate receptors during its induction. ITDP in the auditory projections to the LAn, determined by characteristics of presynaptic activity patterns, may contribute to the encoding of the complex CSa.

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