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 233 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two auditory neurophonic responses - one recorded from the scalp (frequency following response or FFR) and one from the auditory nerve (auditory nerve neurophonic or ANN) - were obtained following stimulation of the cat cochlea with amplitude-modulated (AM) high-frequency tones. The carrier frequencies varied between 2 and 30 kHz. The modulation frequencies varied between 400 and 3000 Hz. The AM responses were compared with pure-tone neurophonic responses. The AM response waveforms were found to have a similar spectral composition, similar rates of adaptation, and similar rates of recovery from forward masking as the comparable pure-tone responses. As with the pure-tone neurophonics, an unmodulated masking stimulus can produce prolonged depression of the probe response. The amount and duration of this depression is dependent upon the level and frequency of the masker. The frequency dependence of the depression is demonstrated by forward masked tuning curves which indicate that the AM responses arise from fiber populations which have restricted characteristic frequency distributions centered on the carrier frequency. Response amplitude as a function of stimulus level (I/O) functions, response amplitude as a function of carrier frequency (carrier transfer functions or CTF) and response amplitude as a function of modulation frequency (modulation transfer functions or MTF) were also measured. It was found that the I/O functions were saturating monotonic functions of stimulus intensity, CTFs were flat for carrier frequencies from 6 to 30 kHz, and MTFs were flat for modulation frequencies from 100 to 1500 Hz. These results are compared with similar data for single units and compound action potentials.
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PMID:Auditory neurophonic responses to amplitude-modulated tones: transfer functions and forward masking. 342 51

The normally positive force- and Ca2+ -frequency responses (FFR and CaFR) are inverted in heart failure (HF); whether oxidative stress contributes to these abnormalities is unknown. We evaluated the impact of acute and prolonged oxidative stress on contraction and Ca2+ handling in adult rat cardiomyocytes. Acute (30 min) exposure to H2O2 (100 microM) induced a twofold increase (P<0.025) in intracellular oxyradicals together with contractile depression despite preservation of the Ca2+ transient and the FFR and CaFR to 3 Hz, indicating reduced myofilament Ca2+ responsiveness. In contrast, prolonged (24 h) exposure to the copper-zinc superoxide dismutase inhibitor diethyldithiocarbamic acid (DDC, 1 microM) similarly augmented oxyradicals but also increased cell size, and contraction and Ca2+ transient duration (P<0.025). DDC-treated myocytes displayed inverted FFRs and attenuated (though still positive) CaFRs as compared to control, indicating reduced myofilament Ca2+ responsiveness coupled with altered Ca2+ handling. Protein levels of the Na+ -Ca2+ exchanger (NCX), sarcoplasmic reticular (SR) Ca2+ ATPase (SERCA2), and serine-16 phosphorylated phospholamban (pSer16-PLB) were increased (P<0.025), whereas dihydropyridine receptor abundance was decreased. Total PLB and ryanodine receptor protein expression were unchanged. Caffeine-induced Ca2+ release showed increased NCX activity (P<0.025) without changes in total releasable SR Ca2+, suggesting compensatory changes in SERCA2 and pSer16-PLB to maintain SR Ca2+ load. The superoxide scavenger Tiron attenuated these effects. Thus, acute oxyradical exposure rapidly depresses myofibrillar Ca2+ responsiveness. Prolonged oxidative stress further induces alterations in Ca2+ handling that combined with extant reductions in myofibrillar responsiveness invert the FFR. With regard to Ca2+ handling, reduced transsarcolemmal Ca2+ flux rather than reduced SR Ca2+ uptake was the primary determinant of a negative FFR. Analogous changes may be operative in HF, a state characterized by both oxidative stress and Ca2+ dysregulation.
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PMID:Prolonged oxidative stress inverts the cardiac force-frequency relation: role of altered calcium handling and myofilament calcium responsiveness. 1628 76