Research Reports - Reduced GABAergic inhibition in the basolateral amygdala and the development of anxiety-like behaviors after mild traumatic brain injury

PLoS One. 2014 Jul 21;9(7)

Almeida-Suhett CP(1), Prager EM(2), Pidoplichko V(3), Figueiredo TH(3), Marini AM(4), Li Z(5), Eiden LE(6), Braga MF(7)

Traumatic brain injury (TBI) is a major public health concern affecting a large
number of athletes and military personnel. Individuals suffering from a TBI risk
developing anxiety disorders, yet the pathophysiological alterations that result
in the development of anxiety disorders have not yet been identified. One region
often damaged by a TBI is the basolateral amygdala (BLA); hyperactivity within
the BLA is associated with increased expression of anxiety and fear, yet the
functional alterations that lead to BLA hyperexcitability after TBI have not been
identified. We assessed the functional alterations in inhibitory synaptic
transmission in the BLA and one mechanism that modulates excitatory synaptic
transmission, the α7 containing nicotinic acetylcholine receptor (α7-nAChR),
after mTBI, to shed light on the mechanisms that contribute to increased
anxiety-like behaviors. Seven and 30 days after a mild controlled cortical impact
(CCI) injury, animals displayed significantly greater anxiety-like behavior. This
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). Decreases in
the mIPSC amplitude were associated with reduced surface expression of α1, β2,
and γ2 GABAA receptor subunits. However, significant increases in the surface
expression and current mediated by α7-nAChR, were observed, signifying increases
in the excitability of principal neurons within the BLA. These results suggest
that mTBI causes not only a significant reduction in inhibition in the BLA, but
also an increase in neuronal excitability, which may contribute to
hyperexcitability and the development of anxiety disorders.

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