The recovery of acetylcholinesterase activity and the progression of neuropathological and pathophysiological alterations in the rat basolateral amygdala after soman-induced status epilepticus: Relation to anxiety-like behavior

What is it about?

here we provide evidence examining the long term alterations to the amygdala after a nerve agent exposure, and how these changes are associated with increases in anxiety-like behavior.

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Why is it important?

We previously demonstrate that seizures may initiate in the amygdala after a nerve agent exposure. Here we demonstrate that up to 30 days after the exposure, pathology still exists, including a significant loss of neurons and GABAergic interneurons, which lead to hyperexcitability in the amygdala. We provide evidence of the hyperexcitability and impairments to cellular mechanisms of learning and memory (i.e., long-term potentiation of synaptic transmission). Importantly, our data also demonstrate that the loss of acetylcholinesterase, which leads to seizure generation, recovers more quickly in the amygdala than in other regions.