Central administration of asprosin reduces baseline brain activity but does not attenuate 4-AP-induced epileptiform discharges: an in vivo electrophysiological study.

In the current study, we investigated the effects of central asprosin administration on baseline brain activity and 4-aminopyridine (4-AP) induced epileptiform activity. Additionally, we examined the effects of asprosin on electrocorticography (ECoG) band powers. Forty-two male Wistar rats were divided into six groups as follows: sham, 4-AP (2.5 mg/kg i.p.), asprosin 20 nmol (i.c.v.), asprosin 50 nmol (i.c.v.), asprosin 50 nmol (i.c.v.) posttreatment, and asprosin 50 nmol (i.c.v.) pre-treatment. Recordings lasting 60-70 min were conducted for all groups under ketamine/xylazine (90/10 mg/kg) anesthesia. In the posttreatment group, asprosin was injected 20 min after the induction of epileptiform activity. In the pre-treatment group, asprosin was injected after baseline recordings, and following a 20-min pre-treatment period, 4-AP was administered. 4-AP alone induced epileptiform activity in all animals, peaking at approximately the 30th minute. Asprosin significantly reduced ECoG power at doses of 20 nmol and 50 nmol. Furthermore, both doses of asprosin reduced alpha, beta, delta, theta, and gamma band activity in ECoG recordings at various time points. However, asprosin pre- and posttreatment had no significant effect on 4-AP-induced epileptiform activity. These findings suggest that asprosin modulates cortical excitability under physiological conditions but is ineffective in attenuating induced epileptiform activity.