Alpha2-adrenoreceptor (α₂-AR) is a noradrenergic receptor that is frequently studied for modulation of seizure activity. However, the precise role of this receptor agonists in regulating seizure activity is still unclear. Our aim in this study was to investigate the effects of α₂-AR agonist dexmedetomidine (DEX) and atipamezole (α₂-AR antagonist, ATI) on seziures in rats. In the study, 32 adult male Wistar Albino rats (weighing 220–260 g) were used. To induce seizures in rats, pentylenetetrazole (PTZ, 35 mg/kg) was injected intraperitoneally (i.p.) and seizure stages were determined according to the Racine scale. After induction of seizures, DEX (0.1 mg/kg, i.p.) and ATI (1 mg/kg, i.p.) were administered to rats and their effects determined on seizures. GABA levels of the brain hippocampal tissue sample were measured using an ELISA kit and c-Fos positive cells of the dentate gyrus and hippocampal regions were quantitatively analyzed with Image J software. The results showed that DEX decreased the seizure stages according to the Racine scale, significantly prolonged the onset time of first myoclonic jerk (FMJ) and reduced the number of spikes and percentage seizure duration (p < 0.05). In contrast, ATI increased the seizure stage, the number of spikes and percentage seizure duration. The hippocampal GABA level was significantly decreased in rats with only PTZ injection (p < 0.05). In addition, DEX reduced the number of c-Fos positive cells in dentate gyrus and the hippocampal CA1 and CA3 regions. In conclusion, our findings showed that α2-AR agonist DEX had a reducing activity on PTZ-induced seizure, while α2-AR antagonist ATI facilitated seizure formation.

α2-肾上腺素受体 (α ₂ -AR) 是一种去甲肾上腺素能受体，经常被研究用于调节癫痫发作活动。然而，这种受体激动剂在调节癫痫发作活动中的确切作用仍不清楚。我们在本研究中的目的是研究 α ₂ -AR 激动剂右美托咪定 (DEX) 和阿替美唑 (α ₂-AR 拮抗剂，ATI) 对大鼠癫痫发作。在这项研究中，使用了 32 只成年雄性 Wistar Albino 大鼠（体重 220-260 克）。为了诱导大鼠癫痫发作，腹膜内（ip）注射戊四唑（PTZ，35 mg/kg）并根据拉辛量表确定癫痫发作阶段。在诱发癫痫发作后，将 DEX (0.1 mg/kg, ip) 和 ATI (1 mg/kg, ip) 施用于大鼠并确定它们对癫痫发作的影响。使用ELISA试剂盒测量脑海马组织样品的GABA水平，并使用Image J软件定量分析齿状回和海马区域的c-Fos阳性细胞。结果表明，根据拉辛量表，DEX 降低了癫痫发作阶段，显着延长了第一次肌阵挛 (FMJ) 的发作时间并减少了尖峰的数量和癫痫发作持续时间的百分比 (p < 0.05)。相比之下，ATI 增加了癫痫发作阶段、尖峰次数和癫痫发作持续时间百分比。仅注射 PTZ 的大鼠海马 GABA 水平显着降低 (p < 0.05)。此外，DEX 减少了齿状回和海马 CA1 和 CA3 区域中 c-Fos 阳性细胞的数量。总之，我们的研究结果表明，α2-AR 激动剂 DEX 对 PTZ 诱导的癫痫发作具有降低活性，而 α2-AR 拮抗剂 ATI 促进癫痫发作的形成。此外，DEX 减少了齿状回和海马 CA1 和 CA3 区域中 c-Fos 阳性细胞的数量。总之，我们的研究结果表明，α2-AR 激动剂 DEX 对 PTZ 诱导的癫痫发作具有降低活性，而 α2-AR 拮抗剂 ATI 促进癫痫发作的形成。此外，DEX 减少了齿状回和海马 CA1 和 CA3 区域中 c-Fos 阳性细胞的数量。总之，我们的研究结果表明，α2-AR 激动剂 DEX 对 PTZ 诱导的癫痫发作具有降低活性，而 α2-AR 拮抗剂 ATI 促进癫痫发作的形成。