Journal of neurophysiology
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The medial-olivocochlear (MOC) acoustic reflex is thought to provide frequency-specific feedback that adjusts the gain of cochlear amplification, but little is known about how frequency specific the reflex actually is. We measured human MOC tuning through changes in stimulus frequency otoacoustic emissions (SFOAEs) from 40-dB-SPL tones at probe frequencies (f(p)s) near 0.5, 1.0, and 4.0 kHz. MOC activity was elicited by 60-dB-SPL ipsilateral, contralateral, or bilateral tones or half-octave noise bands, with elicitor frequency (f(e)) varied in half-octave steps. ⋯ Ipsilateral and contralateral MOC reflexes often showed dramatic differences in plots of MOC effect vs. elicitor frequency, indicating that the contralateral reflex does not give an accurate picture of ipsilateral-reflex properties. These differences in MOC effects appear to imply that ipsilateral and contralateral reflexes have different actions in the cochlea. The implication of these results for MOC function, cochlear mechanics, and the production of SFOAEs are discussed.
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Comparative Study
Kinetics of GABAB autoreceptor-mediated suppression of GABA release in rat insular cortex.
Release of GABA is controlled by presynaptic GABA receptor type B (GABA(B)) autoreceptors at GABAergic terminals. However, there is no direct evidence that GABA(B) autoreceptors are activated by GABA release from their own terminals, and precise profiles of GABA(B) autoreceptor-mediated suppression of GABA release remain unknown. To explore these issues, we performed multiple whole-cell, patch-clamp recordings from layer V rat insular cortex. ⋯ Paired-pulse stimulation (interstimulus interval = 150 ms) of presynaptic FS cells revealed that the second uIPSC was also facilitated by CGP 52432, which had little effect on the amplitude and interevent interval of miniature IPSCs. In contrast, uEPSCs, responding to all five stimulations of a presynaptic pyramidal cell, were less affected by CGP 52432. These results suggest that a single presynaptic action potential is sufficient to activate GABA(B) autoreceptors and to suppress GABA release in the cerebral cortex.