https://link.springer.com/article/10.1007/s12035-017-0732-y
Abstract
Approximately,
1.7 million Americans suffer a TBI annually and TBI is a major cause of
death and disability. The majority of the TBI cases are of the mild
type and while most patients recover completely from mild TBI (mTBI)
about 10% result in persistent symptoms and some result in lifelong
disability. Anxiety disorders are the second most common diagnosis
post-TBI. Of note, TBI-induced anxiety disorders are difficult to treat
and remain a chronic condition suggesting that new therapies are needed.
Previous work from our laboratory demonstrated that a mild TBI induced
an anxiety-like phenotype, a key feature of the human condition,
associated with loss of GABAergic interneurons and hyperexcitability in
the basolateral amygdala (BLA) in rodents 7 and 30 days after a
controlled cortical impact (CCI) injury. We now confirm that animals
display significantly increased anxiety-like behavior 30 days after CCI.
The anxiety-like behavior was associated with a significant loss of
GABAergic interneurons and significant reductions in the frequency and
amplitude of spontaneous and miniature GABAA-receptor-mediated
inhibitory postsynaptic currents (IPSCs) in the BLA. Significantly,
subchronic treatment with alpha-linolenic acid (ALA) after CCI prevents
the development of anxiety-like behavior, the loss of GABAergic
interneurons, hyperexcitability in the BLA and reduces the impact
injury. Taken together, administration of ALA after CCI is a potent
therapy against the neuropathology and pathophysiological effects of
mTBI in the BLA.
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