Auditory Network Modulation of Rosmarinic Acid ina Rat Model of Ketamine-Induced Schizophrenia


Acun A. D., Kantar Gül D.

5th International 34th National Biophysics Congress, İzmir, Türkiye, 6 - 09 Eylül 2023, İzmir, Türkiye, 06 Eylül 2023, ss.88-89

  • Yayın Türü: Bildiri / Özet Bildiri
  • Basıldığı Şehir: İzmir
  • Basıldığı Ülke: Türkiye
  • Sayfa Sayıları: ss.88-89
  • Akdeniz Üniversitesi Adresli: Evet

Özet

Aim: Sensory response abnormalities related to clinical symptoms and cognitive impairment have been reported in schizophrenia [1]. Besides, noise power (NP) reflects back ground oscillatory activity, provides relevant information about neural circuits in schizophrenia [2]. First aim of the study is examining auditory evoked oscillations and NP changes in ketamine-induced schizophrenia rat model. Evidence suggests that central factor in various oscillatory abnormalities is related with different neurotransmitter systems [1]. Rosmarinic acid (RA) is known to modulate both GABAergic and dopaminergic systems [3]. Second aim was evaluating the modulatory potential of RA on neural responses in schizophrenia model.

Materials and Methods: Rats were divided into three groups (n=6); sham (SH), ketamine (Ket) and RA treated (Ket_RA). Ketamine (30 mg/kg, ip) and RA (50 mg/kg, gavage) were applied for five and fifteen days, respectively. Auditory evoked responses were recorded using tones of 2000 Hz at the 70 dB with 800 msintertrial stimulus. Auditory evoked oscillations and NP in theta (4-7 Hz), alpha (8-12 Hz), beta (13-35 Hz) and gamma (35-45 Hz) bands were analyzed with Brainvision Analyzer.

Results: Ketamine increased NP in gamma, beta bands (p<0.05) and slightly increased NP in alpha and theta bands. While evoked gamma, beta and theta power decreased in the Ket group, alpha power increased in the same group (p<0.05). RA reversed ketamine induced evoked power changes in all frequency domains. However, RA caused an increment in NP values in the Ket_RA group versus the Ket group.

Conclusion: These findings show that RA modulated evoked power in the auditory network. Conversely, RA didn’t change background oscillatory activity in the same circuit. Therefore, we suggest that RA-induced increment in the dopaminergic transmission caused the observed changes in the evoked oscillatory responses while slightly potentiating the back ground activity. GABAergic system might contribute the effects of RA on evoked power.