What is it about?

We provide a mechanism by which increases in anxiety-like behavior are observed after a nerve agent exposure. In particular we find that after a nerve agent exposure there is a significant loss of inhibitory neurons in the amygdala, which leads to long lasting reductions in inhibitory synaptic transmission, and enhanced excitatory synaptic transmission.

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Why is it important?

This work demonstrates that the loss of GABAergic interneurons leads to long lasting reductions in the basolateral amygdala, a very seizurogenic brain region. This leads to increased excitation, which may be observed as increased anxiety-like behavior and spontaneous recurrent seizures.

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This page is a summary of: Pathophysiological mechanisms underlying increased anxiety after soman exposure: Reduced GABAergic inhibition in the basolateral amygdala, NeuroToxicology, September 2014, Elsevier,
DOI: 10.1016/j.neuro.2014.08.007.
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