Alcohol abrogates intracellular Ca2+ elevation by angiotensin II and ATP in cultured rat astrocytes

Astrocytes have a robust and dynamic intracellular Ca activity in response to stimulation by various neurotransmitters and neuromodulators such as angiotensin II, glutamate, and ATP [1-4]. ATP evokes Ca bursts in astrocytes by activation of purinergic receptors [4] and angiotensin II (AngII) by stimulation of AT1 receptors [2]. Intracellular Ca mobilization by the peptide and high energy purine signaling molecules enhances astrocyte cycling excitatory neurotransmitter glutamate, which governs the social behavior and cognitive ability [5-7]. Acute alcohol overdose alters users’ social behavior and affects abusers’ cognition [8,9]. We hypothesize that alcohol impairs the intracellular Ca handling in astrocytes particularly in response to neurotransmitter/neuromodulator stimulation, which may play an important role in understanding alcohol intoxication. The impairment may relate to the development of alcohol addiction, dependence and tolerance. In this work, we studied the alteration of intracellular Ca signaling by alcohol treatment in cultured rat hippocampal astrocytes. The findings of this study enrich our understanding of ethanol intoxication and may lead to a new treatment target for alcoholism.