“The Effects of Acetyl-L-Carnitine Administration on Auditory Evoked Potentials in Rats Subjected to Chronic Ethanol Exposure”


Er H., Kantar Gül D., Kuzzu A. D., Derin N., Ercan Kelek S.

5th International 34th National Biophysics Congress, İzmir, Türkiye, 6 - 09 Eylül 2023, ss.90-91

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: İzmir
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.90-91
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Aim: The brain is one of the organs most affected by chronic alcohol consumption. Besides, it is known that chronic alcohol consumption also has impacts on brain potentials. Acetyl-L-carnitine (ALCAR) is a carnitine metabolite found in the plasma and tissues of mammals and is thought to have neuroprotective properties. Therefore, this research aimed to examine the effects of ALCAR administration on auditory evoked potentials (AEP) in rats chronically exposed to ethanol.

Materials and Methods: 3 months old, 40 male Wistar rats were separated equally into four groups: Sham (Sh), chronic ethanol (CE), ALCAR administered (ALCAR), and chronic ethanol+ALCAR (CE+ALCAR). Distilled water to the Sh group, 5g/kg ethanol (25% v/v) to the CE group, 50 mg/kg ALCAR to the ALCAR group, and the same doses of ethanol+ALCAR to the CE+ALCAR group were given by gavage for four weeks. After this period, AEP recordings were taken from the temporal region of the rat brain under urethane anesthesia (1.2 g/kg), and the latencies of P1, N1, and P2 peaks and peak-to-peak amplitudes of P1N1 and N1P2 were then analyzed.

Results: According to our AEP signal analysis results, P1 (p=0.001), N1 (p<0.001), and P2 (p<0.05) latencies were significantly prolonged in the CE group compared to the Sh group. However, P1N1 (p<0.05) and N1P2 (p<0.05) peak-to-peak amplitudes were significantly increased in the CE group compared to the Sh group. When the CE and CE+ALCAR groups were compared, there was no significant difference in peak latencies, but P1N1 (p<0.05) and N1P2 (p<0.05) peak-to-peak amplitudes were significantly decreased in the CE+ALCAR group.

Conclusion: In brief, the findings from our study suggest that chronic alcoholism has a decelerating effect on signal transmission in the auditory pathway, as indicated by the latency data for P1, N1, and P2. However, the analysis of peak-to-peak amplitudes for P1N1 and N1P2 suggests that chronic alcoholism leads to enhanced neuronal activity relative to normal levels. However, it was determined that ALCAR (at the dose and duration we used) normalized neuronal activity but had no effect on signal transmission velocity.