Advances in mechanisms of alcohol-induced damage in basolateral amygdala leading to anxiety
Alcohol abuse is a serious public health problem and biomedical safety problem that can lead to a variety of neuropsychiatric disorders.In recent years,numerous studies have shown that alcohol can induce structural and functional disregulation in the basolateral amygdala(BLA).Alcohol exposure and withdrawal can cause negative emotion such as anxiety and fear,primarily mediated by glutamatergic neurons and inhibitory γ-aminobutyric acid ergic(GABAergic)interneurons in the BLA.Glutamatergic neurons are responsible for excitatory neurotransmitter glutamate release,while γ-aminobutyric acid ergic(GABAergic)interneurons provide feedback inhibition to suppress BLA function and alleviate negative emotions.However,alcohol intake can disrupt the balance of glutamatergic-GABAergic neural network,altering neuron excitabili-ty and subsequently leading to the generation of anxiety and fear.Moreover,alcohol also interferes with the corticotropin-releasing factor(CRF)system within the BLA,increasing the release of CRF,further stimulating anxiety-related emotions.Additionally,alcohol affects BLA-related neural circuits,such as BLA →medial prefrontal cortex,BLA →nucleus accumbens,and BLA →bed nucleus of the stria terminali pathways,thereby impacting anxiety-like behaviors.This review discusses the progress of neural signaling and circuits within the BLA in mediating alcohol-induced negative emotions,aiming to further elucidate the neurobiological mecha-nisms underlying anxiety triggered by alcohol exposure and withdrawal,in order to provide theoretical basis for clinical treatment in the future.
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