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Chunk #1 — Introduction

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Chronic ethanol and withdrawal effects on kainate receptor-mediated excitatory neurotransmission in the rat basolateral amygdala.
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The basolateral amygdala (BLA) is a central component of the neural circuitry governing anxiety-related information and is also involved with alcohol withdrawal-related behaviors. The flow of information through the amygdala starts with cortical and thalamic input into the lateral and basolateral nuclei, then proceeds from there through efferent projections to the central nucleus of the amygdala, bed nucleus of the stria terminalis and the nucleus accumbens (De Olmos et al., 1985). Alcohol interacts with neurotransmitter systems mediating both fast excitatory and inhibitory synaptic transmission in the amygdala. Importantly, the balance of these neurotransmitter systems can be disrupted to alter anxiety-related behavior (Lack et al., 2007; Sanders and Shekhar, 1995). Recent work has shown that chronic intermittent ethanol and withdrawal produce a significant up-regulation of the glutamatergic system in the BLA that may ultimately influence anxiety-like behavior (Lack et al., 2007).