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Multimodal and Site-Specific Plasticity of Amygdala Parvalbumin Interneurons after Fear Learning.

Neuron | Aug 3, 2016

Stimulus processing in fear conditioning is constrained by parvalbumin interneurons (PV-INs) through inhibition of principal excitatory neurons. However, the contributions of PV-IN microcircuits to input gating and long-term plasticity in the fear system remain unknown. Here we interrogate synaptic connections between afferent pathways, PV-INs, and principal excitatory neurons in the basolateral amygdala. We find that subnuclei of this region are populated two functionally distinct PV-IN networks. PV-INs in the lateral (LA), but not the basal (BA), amygdala possess complex dendritic arborizations, receive potent excitatory drive, and mediate feedforward inhibition onto principal neurons. After fear conditioning, PV-INs exhibit nucleus- and target-selective plasticity, resulting in persistent reduction of their excitatory input and inhibitory output in LA but not BA. These data reveal previously overlooked specializations of amygdala PV-INs and indicate specific circuit mechanisms for inhibitory plasticity during the encoding of associative fear memories.

Pubmed ID: 27427462 RIS Download

Mesh terms: Amygdala | Animals | Conditioning (Psychology) | Fear | Interneurons | Male | Mice | Neural Pathways | Neuronal Plasticity | Neurons | Parvalbumins | gamma-Aminobutyric Acid

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Core facility that provides consultation on the use of viral vector technologies as well as custom design and production services for multiple vector types. The GT3 facilitates the use of these research tools by Salk researchers and others across diverse fields of study such as systems neuroscience, stem cell biology, metabolism, ageing, cancer biology and gene therapy. The GT3 core is a designated Cancer Center Council (C3) core facility. Cancer Center members from participating C3 institutes have preferential rates.


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