Sensory Adaptation in Hair Cells of the Bullfrog's Sacculus

Hair cells in the bullfrog's sacculus, a vestibular organ sensitive to linear acceleration, show sensory adaptation: the response to a constant stimulus peaks near the stimulus onset, then decays. This has been studied in two different preparations. In an excised in vitro preparation of the saccular sensory epithelium, intracellular responses of hair cells to step deflections of their hair bundles were recorded. The second set of experiments was conducted in vivo using steps of vertical linear acceleration as stimuli. The hair cell response was recorded extracellularly in the form of the saccular microphonic potential. Both the intracellular response to direct hair bundle deflection and the extracellular response to acceleration adapted to a steady-state value within the first 100 ms following the step onset. In both cases, the response decline was largely due to a shift in the operating range of the cells in the direction of the constant stimulus. This shift occurred without significant change in dynamic range or in sensitivity within the operating range. Thus the hair cells appear to respond to static stimuli by resetting the bias point of the operating range in the direction of the stimulus. The response of primary saccular neurons to acceleration steps also showed pronounced sensory adaptation. Comparison of the afferent activity and saccular microphonic potential suggests that adaptation of afferent responses to acceleration steps may be due largely to the adaptive operating range shift in the hair cell responses. The adaptation of saccular neurons to acceleration steps may be explained by the following simple model. The acceleration step causes displacement of the saccular otolith and deflection of the underlying hair bundles. The hair cells respond initially to the displacement, then adapt (as observed in vitro), and this information is faithfully translated postsynaptically into afferent spike rate. However, the possibility exists that the in vitro and in vivo adaptive shifts in operating range are not the same process. In vivo, one cannot distinguish an operating range shift within the hair cells from one due to mechanical adaptation of the stimulus to the hair bundles.</p

Retinoic acid degradation shapes zonal development of vestibular organs and sensitivity to transient linear accelerations

Each vestibular sensory epithelium in the inner ear is divided morphologically and physio- logically into two zones, called the striola and extrastriola in otolith organ maculae, and the central and peripheral zones in semicircular canal cristae. We found that formation of striolar/central zones during embryogenesis requires Cytochrome P450 26b1 (Cyp26b1)- mediated degradation of retinoic acid (RA). In Cyp26b1 conditional knockout mice, formation of striolar/central zones is compromised, such that they resemble extrastriolar/peripheral zones in multiple features. Mutants have deficient vestibular evoked potential (VsEP) responses to jerk stimuli, head tremor and deficits in balance beam tests that are consistent with abnormal vestibular input, but normal vestibulo-ocular reflexes and apparently normal motor performance during swimming. Thus, degradation of RA during embryogenesis is required for formation of highly specialized regions of the vestibular sensory epithelia with specific functions in detecting head motions

Communications Biophysics

Contains reports on seven research projects split into three sections, with research objective for the final section.National Institutes of Health (Grant 2 PO1 NS 13126)National Institutes of Health (Grant 5 RO1 NS 18682)National Institutes of Health (Grant 1 RO1 NS 20322)National Institutes of Health (Grant 1 RO1 NS 20269)National Institutes of Health (Grant 5 T32 NS 07047)Symbion, Inc.National Institutes of Health (Grant 5 RO1 NS10916)National Institutes of Health (Grant 1 RO1 NS16917)National Science Foundation (Grant BNS83-19874)National Science Foundation (Grant BNS83-19887)National Institutes of Health (Grant 5 RO1 NS12846)National Institutes of Health (Grant 5 RO1 NS21322)National Institutes of Health (Grant 5 RO1 NS 11080

Communications Biophysics

Contains research objectives and reports on eight research projects split into three sections.National Institutes of Health (Grant 2 PO1 NS13126)National Institutes of Health (Grant 5 RO1 NS18682)National Institutes of Health (Grant 5 RO1 NS20322)National Institutes of Health (Grant 1 RO1 NS 20269)National Institutes of Health (Grant 5 T32 NS 07047)Symbion, Inc.National Institutes of Health (Grant 5 R01 NS10916)National Institutes of Health (Grant 1 RO NS 16917)National Science Foundation (Grant BNS83-19874)National Science Foundation (Grant BNS83-19887)National Institutes of Health (Grant 5 RO1 NS12846)National Institutes of Health (Grant 1 RO1 NS21322-01)National Institutes of Health (Grant 5 T32-NS07099-07)National Institutes of Health (Grant 1 RO1 NS14092-06)National Science Foundation (Grant BNS77-21751)National Institutes of Health (Grant 5 RO1 NS11080

Communication Biophysics

Contains reports on six research projects.National Institutes of Health (Grant 5 PO1 NS13126)National Institutes of Health (Grant 5 RO1 NS18682)National Institutes of Health (Grant 5 RO1 NS20322)National Institutes of Health (Grant 5 R01 NS20269)National Institutes of Health (Grant 5 T32NS 07047)Symbion, Inc.National Science Foundation (Grant BNS 83-19874)National Science Foundation (Grant BNS 83-19887)National Institutes of Health (Grant 6 RO1 NS 12846)National Institutes of Health (Grant 1 RO1 NS 21322

The Negatively Activating Potassium Conductance of Rat Cochlear Hair Cells

Potassium channels are substantial to regulate electrical signaling andthe ionic composition of biological fluids. It has also been suggested that mutations inthe KCNQ4 K+ channel gene are responsible for autosomal dominant nonsyndromichearing impairment (DFNA2). Negatively activating potassium (K+) conductance inrodent cochlear hair cells called gK,n, comprises KCNQ4 subunit, member of the KCNQfamily of K+ channels. This conductance is important in setting the hair cells\u27 restingpotentials and input conductances. Here we try to examine the biophysical l?ropertiesof the conductance base on the voltage dependence, stability during whole-cell recordingand permeability to Cs+. gK.n was proved to exist in rat outer hair cells that it wasblocked by KCNQ4 blocker, linopirdine and has a significantly negative (mean Vl/2 =- 91.2 ± 1.06 mV) and broad (mean S-value= -12 ± 0.46 mV) voltage range of activation(n =24). However, gK,n does not show any permeability to Cs+ but only leak residualconductance with mean of 1.6± 0.44 nS (n =6). gK,n is stable i.e., its properties do notchange ("wash out") despite of the replacement of internal solution with pipette solutionduring whole-cell recordings