![]() ![]() Inhibitory neurotransmission is essential for accurate processing of acoustic information. These tinnitus-related changes in GABAergic function may be markers for tinnitus pathology in the MGB. In agreement with this hypothesis, we found tinnitus-related increases in tonic extrasynaptic GABA AR currents, in action potentials/evoked bursts, and in GABA AR δ-subunit gene expression. ![]() ![]() Tinnitus and chronic pain may reflect thalamocortical dysrhythmia, which results from abnormal theta-range resonant interactions between thalamus and cortex, due to neuronal hyperpolarization and the initiation of low-threshold calcium spike bursts ( Walton and Llinás, 2010). In summary, we found little evidence of tinnitus-related decreases in GABAergic neurotransmission. Tin rats showed significant increases in the number of spikes per burst evoked using suprathreshold-injected current steps. In situ hybridization studies found increased mRNA levels for GABA AR δ-subunits contralateral to the sound exposure. Months after a tinnitus-inducing sound exposure, gaboxadol-evoked tonic GABA AR currents showed significant tinnitus-related increases contralateral to the sound exposure. Tonic GABA AR currents were evoked using the selective agonist gaboxadol. Given that extrasynaptic GABA ARs control the firing mode of thalamocortical neurons, we examined tonic GABA AR currents in MGB neurons in vitro, using the following three groups of adult rats: unexposed control (Ctrl) sound exposed with behavioral evidence of tinnitus (Tin) and sound exposed with no behavioral evidence of tinnitus (Non-T). In thalamus, GABA mediates fast synaptic inhibition via synaptic GABA A receptors (GABA ARs) and persistent tonic inhibition via high-affinity extrasynaptic GABA ARs. Opposing hypotheses proposed either a pathologic decrease or increase of GABAergic inhibition in medial geniculate body (MGB). Accumulating evidence suggests a role for inhibitory neurotransmitter dysfunction in the pathology of tinnitus. ![]()
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