Abstract
We studied the dynamics of the intracellular concentration of calcium ions ([Ca2+]i) and the influence of the endogenous cannabinoid N-arachidonoyldopamine (N-ADA) on disturbances of calcium homeostasis in cultured hippocampal neurons in the model of postischemic epileptogenesis (PE) in vitro, in accordance with a previously published method. It was found that 24 h after treatment with 20 μM glutamate, its application at a concentration of 50 μM results in a persistent increase in [Ca2+]i whereas in neurons that were not previously subjected to glutamate treatment an increase in [Ca2+]i after the application of 50 μM glutamate was reversible. The presence of N-ADA (5 μM) in the incubation medium both simultaneously with 20 μM glutamate exposure and for 24 h after it promoted recovery of the [Ca2+]i level to the initial level. The results indicate that application of N-ADA promotes normalization of neuronal calcium homeostasis in a PE model in vitro.
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