Prenatal alcohol exposure (PAE) is an insidious yet preventable cause of developmental disability. The prenatal stage is a critical period for brain development with the concurrence of high vulnerability to the acute and prolonged effects of PAE. There is substantial evidence from both human observations and laboratory experiments that PAE is a common risk factor that predisposes to an array of postnatal mental disorders, including emotional, cognitive, and motor deficits. Although it is well accepted that PAE causes substantial morbidity, available treatments are limited. One reason is the lack of sufficient understanding about the neuroalterations induced by PAE, and how these changes contribute to PAE-induced mental disorders. Among a number of brain structures that have been explored extensively in PAE, the striatum has attracted great attention in the last 20 years in the field of PAE neurobiology. Interestingly, in animal models, the striatum has been considered as a pivotal switch of brain dysfunction induced by PAE, such as addiction, anxiety, depression, and neurodegeneration. In this review, we focus on recent advances in the understanding of morphological and functional changes in brain regions related to alterations after PAE, in particular the striatum. Because this region is central for behavior, emotion and cognition, there is an urgent need for more studies to uncover the PAE-induced alterations at the circuit, neuronal, synaptic and molecular levels, which will not only improve our understanding of the neuroplasticity induced by PAE, but also provide novel biological targets to treat PAE-related mental disorders with translational significance.
Keywords: Accumbens; Medium-sized spiny neurons; Neuroplasticity; Prenatal alcohol exposure; Striatum.
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