Modulation of Pentylenetetrazol Induced Neuronal Circuit Epilepsy by p2y Purinoreceptor 3 (p2y3) in Sprague Dawley Rats
Modulation of Pentylenetetrazol Induced Neuronal Circuit Epilepsy by p2y Purinoreceptor 3 (p2y3) in Sprague Dawley Rats
Zhongjiang Niu1, Periyannan Velu2, Annamalai Vijayalakshmi2*
ABSTRACT
Epilepsy is a complex neurological disorder which causes abnormal electrical impulses in brain. The role of P2Y purinergic receptor in epilepsy is less known. NF45, a P2Y antagonist receptor, plays a crucial role in pentylenetetrazol (PTZ) kindled epilepsy. This study assessed the locomotion and hippocampal levels of mitochondrial complexes (IV, II, and I) in animal model. The experiment also assessed Thiobarbituric acid-reactive substance (TBARS), mean kindling score, hypertension, anxiety, discrimination ability (SNSE), learning, and memory in eight groups of rats. PTZ – kindling rats showed poor motor activity. PTZ-kindling rats showed increase in emotional tension, anxiety, learning and memory, pro-inflammatory mediators (IL-1β and TNF-α) in hippocampal tissue, neuronal damage (increased sNSE), mitochondrial dysfunction, and oxidative stress. PTZ-kindling augmented TBARS and reduced GSH and CAT. PTZ-kindling significantly decreased locomotion, memory and learning. Neuronal damage and hippocampus swelling were reversed with NF45 in a dose dependent manner. P2y agonist, methylene - ATP, significantly reduced the positive effect of NF45.P2y3 receptors had a significant role in epilepsy kindling. This mechanism has potential in epilepsy therapy and future research.
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