3-Carene Modulates Baseline Brain Electrical Activity Without Suppressing 4-Aminopyridine-Induced Seizure Events: An In Vivo and In Vitro Electrophysiological Study
Creators
- 1. Karadeniz Tech Univ, Fac Med, Dept Physiol, TR-61080 Trabzon, Turkiye
- 2. Karadeniz Tech Univ, Fac Med, Dept Biophys, Trabzon, Turkiye
- 3. Karadeniz Tech Univ, Macka Vocat Sch, Lab & Vet Assistance Serv, Trabzon, Turkiye
- 4. Karadeniz Tech Univ, Fac Med, Dept Anat, Trabzon, Turkiye
- 5. Karadeniz Tech Univ, Grad Sch Hlth Sci, Dept Biophys, Trabzon, Turkiye
- 6. Sabanci Univ, Fac Engn & Nat Sci, Istanbul, Turkiye
Description
In the current study, we investigated the effects of 3-carene administration on basal brain activity and 4-aminopyridine (4-AP) induced epileptiform activity. Additionally, we examined the effects of asprosin on ECoG band powers. Thirty-five male Wistar rats were divided into five groups as follows: control (DMSO), 4-AP (2.5 mg/kg i.p.), 3-carene 10 mg/kg (i.p), 3-carene 50 mg/kg (i.p), 3-carene 50 mg/kg (i.p) post-treatment. Recordings lasting 60-70 min were conducted for all groups under ketamine/xylazine (90/10 mg/kg) anesthesia. Furthermore, we used thick acute horizontal hippocampal slices obtained from 30- to 35-day-old rats for in vitro experiments. Extracellular field potential recordings were evaluated in the CA1 region of the hippocampus. In vivo recordings revealed that intraperitoneal administration of 3-carene (10 mg/kg and 50 mg/kg) significantly suppressed basal brain activity across delta, theta, alpha, and beta bands. However, 3-carene failed to reduce epileptiform discharges induced by 4-AP. Complementary in vitro experiments using hippocampal and entorhinal cortex slices further confirmed the lack of anticonvulsant effect, as 3-carene did not alter the frequency or duration of 4-AP-induced ictal or interictal events. These findings suggest that while 3-carene modulates resting-state cortical oscillations, it lacks efficacy in suppressing seizure-like activity. The results highlight its potential as a neuromodulatory agent rather than a standalone anticonvulsant.
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