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2016 ; 10
(ä): 72
Nephropedia Template TP
Front Neural Circuits
2016[]; 10
(ä): 72
PMID27630546
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Neurons at higher stages of sensory processing can partially compensate for a
sudden drop in peripheral input through a homeostatic plasticity process that
increases the gain on weak afferent inputs. Even after a profound unilateral
auditory neuropathy where >95% of afferent synapses between auditory nerve fibers
and inner hair cells have been eliminated with ouabain, central gain can restore
cortical processing and perceptual detection of basic sounds delivered to the
denervated ear. In this model of profound auditory neuropathy, auditory cortex
(ACtx) processing and perception recover despite the absence of an auditory
brainstem response (ABR) or brainstem acoustic reflexes, and only a partial
recovery of sound processing at the level of the inferior colliculus (IC), an
auditory midbrain nucleus. In this study, we induced a profound cochlear
neuropathy with ouabain and asked whether central gain enabled a compensatory
plasticity in the auditory thalamus comparable to the full recovery of function
previously observed in the ACtx, the partial recovery observed in the IC, or
something different entirely. Unilateral ouabain treatment in adult mice
effectively eliminated the ABR, yet robust sound-evoked activity persisted in a
minority of units recorded from the contralateral medial geniculate body (MGB) of
awake mice. Sound driven MGB units could decode moderate and high-intensity
sounds with accuracies comparable to sham-treated control mice, but low-intensity
classification was near chance. Pure tone receptive fields and synchronization to
broadband pulse trains also persisted, albeit with significantly reduced quality
and precision, respectively. MGB decoding of temporally modulated pulse trains
and speech tokens were both greatly impaired in ouabain-treated mice. Taken
together, the absence of an ABR belied a persistent auditory processing at the
level of the MGB that was likely enabled through increased central gain.
Compensatory plasticity at the level of the auditory thalamus was less robust
overall than previous observations in cortex or midbrain. Hierarchical
differences in compensatory plasticity following sensorineural hearing loss may
reflect differences in GABA circuit organization within the MGB, as compared to
the ACtx or IC.
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