Abstract
Background: Excitotoxicity is a common pathological process in neurodegenerative diseases associated with overactivity of N-methyl-D-aspartate (NMDA) and P/Q type voltage-gated calcium (Cav2.1) channels. Omega-lycotoxin-Gsp2671g is a therapeutic tool to modulate overactive Cav2.1 (P/Q type) channels. Omega-lycotoxin binds to Cav2.1 channels with high affinity and selectivity. This study aimed to investigate the effects of Omega-lycotoxin on the cognitive impairment induced by kainic acid in rats. Methods: The effect of pre-treatment and post-treatment trials of intra-hippocampal Cornu Ammonis-3 administration of omega-lycotoxin (0.5, 1 or 2µg) was studied on the cognitive impairment induced by kainic acid in rats. The rats’ learning and memory were assessed by the passive avoidance and a single-day testing version of the Morris water maze method. Results: Omega-lycotoxin caused a significant increase in the latency of the passive avoidance test and the duration of their presence in the target area of the Morris water maze test compared to the groups treated with kainic acid (P<0.0001). There were statistically significant differences for the effects of various doses of omega-lycotoxin. The post-treatment groups showed a greater improvement than those in the pretreatment groups. Conclusion: The findings demonstrated that a single dose of omega-lycotoxin can prevent or revert the memory impairment caused by kainic acid in rats.
Highlights
I n recent years, neurodegenerative conditions, such as Alzheimer’s, Parkinson’s and Huntington’s diseases have spread worldwide, and the prevalence is rapidly increasing [1]
The findings demonstrated that a single dose of omega-lycotoxin can prevent or revert the memory impairment caused by kainic acid in rats
The effect of pre-treatment groups of different doses of omega–lycotoxin on time spent in the target quadrant in the Morris water maze test
Summary
I n recent years, neurodegenerative conditions, such as Alzheimer’s, Parkinson’s and Huntington’s diseases have spread worldwide, and the prevalence is rapidly increasing [1] These diseases are progressive and disrupt the daily activities of many patients with such side effects as amnesia, paralysis, motor disorders, and eventually death [1, 2]. In the central nervous system of mammals, P/Q-type of voltage-gated calcium channels (Cav 2.1) control calciumdependent processes, such as synaptic plasticity and neurotransmitters release [5, 6]. These channels are located at the presynaptic terminals and initiate the fusion of presynaptic vesicles by the influx of calcium ions into nerve endings [4, 5]. This study aimed to investigate the effects of Omega-lycotoxin on the cognitive impairment induced by kainic acid in rats
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