Masters Theses

Date of Award

6-1985

Degree Type

Thesis

Degree Name

Master of Science

Major

Life Sciences

Major Professor

Michael H. Sims

Committee Members

Joel Lubar, Hugh Welch

Abstract

The pharmacological effects of nicotine on the nervous system have been extensively investigated. In particular its effect on various evoked potentials has been studied in regard to whether it acted directly on acetylcholine (ACh) receptors or caused the release of ACh or other neurotransmitters such as serotonin from nerve terminals. In this study the effect of nicotine on the auditory pathway was investigated using two electrodiagnostic procedures, the acoustic reflex (AR) and the auditory brainstem response (ABR).

The AR is the reflexive contortion of the middle ear muscles in response to loud sound stimuli. This contraction results in a change in compliance of the middle ear system. The ABR is the far field recording of neural (electrical) activity in the brainstem which occurs within the first 10 ms after sound stimulation. To determine if any changes occurred during different experimental manipulations, the AR latency, amplitude, and threshold and the ABR wave latencies and amplitudes were measured.

In particular several questions were asked. First were there any changes in the AR or ABR due to nicotine administration? Secondly, were the effects dose or time dependent? Thirdly, did nicotine cause the release of ACh from nerve terminal endings or act on ACh receptors? Fourthly, did nicotine cause the release of serotonin? Fifthly, were AR and ABR changes related?

Six cats were anesthetized by sequential i.m. injections of xylazine ( 1.0 mg/kg) and ketamine (10 mg/kg). Ipsilateral and contralateral AR as well as monaural ABR were recorded from the left ear during each of the following the experiments; (a) saline, (b) nicotine, (40 ug kg -1 min -1), (c) nicotine, (60 ug kg -1 min -1), (d) atropine (0.4 mg/kg) followed by nicotine, (60 ug kg -1 min -1) j and (e) 5_Methoxy-N-N-Dimethyltryptamine (a serotonin analogue) (10 ug kg -1). Recordings were made after xylazine and ketamine and at time points of 5, 10, 20 and 30 minutes during the infusions.

There was a significant decrease in the AR threshold due to nicotine administration, and an increase in the AR amplitude after both atropine and nicotine were given. These results indicated a direct action on ACh receptors by nicotine. The ABR latency after giving nicotine increased more with pip-evoked responses than with the click-evoked responses. The amplitude of all ABR waves except wave VI decreased significantly for the click-evoked ABR. The pip-evoked responses showed biphasic changes in the amplitude of some waves. Recordings made using the -10 dB ART intensity pip stimulus were only affected by the higher nicotine dosage. There were no apparent time dependent differences.

Atropine had only a minor blocking effect on the ABR response and this was more apparent in the pip-evoked response. The increase in latency and decrease in amplitude seen with some waves of the ABR due to the injection of 5-MeODMT were independent of those seen with nicotine administration and were thus of different origin.

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