PubMed · 4671164
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R E Hooper. 1972. Electrocochleography.. https://pubmed.ncbi.nlm.nih.gov/4671164/
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Nitric oxide (NO) is a short-lived radical species endowed with intercellular signalling functions in the mammalian brain. In the present study we have investigated the effects of focal injection into one inferior colliculus of N omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, on the acoustic middle latency responses (MLRs) evoked by click stimuli and recorded from the auditory cortex in anaesthetized rats. Microinfusion of L-NAME (1.0 mM) did not alter the latency of MLRs nor did it affect the evoked brain stem responses (ABRs). By contrast, L-NAME reduced P1a-N1 amplitude of MLRs by 51.7 +/- 6.6% (mean +/- SEM; n = 5) and almost complete recovery to background amplitude was obtained 15-25 min after treatment. The less active isomer, D-NAME (1.0 mM; n = 5), failed to produce consistent effects on the evoked MLRs. A higher concentration of L-NAME (5.0 mM; n = 5) yielded a 69.0 +/- 13.3% inhibition whereas maximum inhibition produced by 0.5 mM (n = 3) L-NAME was approximately equal to 10% of control value. The inhibitory effect typically evoked by 1.0 mM L-NAME was prevented by treating rats with L-arginine (5.0 mM; n = 5), the endogenous precursor of NO synthesis. Reduction of MLR amplitude was also obtained in rats receiving intracollicular injection of dizocilpine (MK801; 1.0 microM) and LY274614 (1.0 mM), two selective N-methyl-D-aspartate (NMDA) receptor antagonists. In conclusion, the present data support a role for intracollicular NO in the processing and transmission of the acoustic input to the auditory cortex in the rat.
We studied the effects of collision between a voluntary command and the startle response by interrupting a simple visual reaction time task with an acoustic startle. We observed two main effects. First, the reaction time was markedly shortened when the startle was delivered at intervals of 0-75 ms after the 'go' signal. Second, the startle response elicited when the subject's attention was focused onto reacting to the visual 'go' signal involved more muscles and induced larger EMG responses than when the startling stimulus was delivered unexpectedly. Startle response and voluntary commands may share a number of structures along the motor path. Reaction time can be shortened up to the latency of a startle response if the voluntary command is issued a short time after the startling stimulus. Facilitation of the startle responses during motor preparation may be due to the excitability enhancement that occurs in various neural structures along the motor path before the onset of EMG activity.
The aim of this study was to test whether the middle ear muscles (MEM) play a significant role in the phenomenon of sound conditioning in guinea pigs. After inducing a temporary threshold shift by noise exposure (2767 Hz tone, 103 dB SPL, 5 min), the magnitude and duration of loss, as well as the rate of recovery of the amplitude of the distortion product emission was determined at 1.75, 2.2, 2.8, and 3.5 kHz followed for 90 min post-exposure for (1) a sound conditioned group with intact MEM, and (2) a sound conditioned group with paralyzed MEM. Significant differences were not found for any of the distortion product parameters tested. The results suggest that the MEM do not significantly contribute to protection against noise trauma by sound conditioning.