GABAergic neural activity involved in salicylate-induced auditory cortex gain enhancement.

GABAergic neural activity involved in salicylate-induced auditory cortex gain enhancement.
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DOI:
10.1016/j.neuroscience.2011.04.073
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发表时间:
2011-08-25
期刊:
影响因子:
3.3
通讯作者:
Sun, W.
Sun, W.
中科院分区:
医学3区
文献类型:
--
作者:
Lu, J.;Lobarinas, E.;Deng, A.;Goodey, R.;Stolzberg, D.;Salvi, R. J.;Sun, W.

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Although high doses of sodium salicylate impair cochlear function, it paradoxically enhances sound-evoked activity in the auditory cortex (AC) and augments acoustic startle reflex responses, neural and behavioral metrics associated with hyperexcitability and hyperacusis. To explore the neural mechanisms underlying salicylate-induced hyperexcitability and “increased central gain”, we examined the effects of γ-aminobutyric acid (GABA) receptor agonists and antagonists on salicylate-induced hyperexcitability in the AC and startle reflex responses. Consistent with our previous findings, local or systemic application of salicylate significantly increased the amplitude of sound-evoked AC neural activity, but generally reduced spontaneous activity in the AC. Systemic injection of salicylate also significantly increased the acoustic startle reflex. S-baclofen or R-baclofen, GABA-B agonists, which suppressed sound-evoked AC neural firing rate and local field potentials, also suppressed the salicylate-induced enhancement of the AC field potential and the acoustic startle reflex. Local application of vigabatrin, which enhances GABA concentration in the brain, suppressed the salicylate-induced enhancement of AC firing rate. Systemic injection of vigabatrin also reduced the salicylate-induced enhancement of acoustic startle reflex. Collectively, these results suggest that the sound-evoked behavioral and neural hyperactivity induced by salicylate may arise from a salicylate-induced suppression GABAergic inhibition in the AC.
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