Neurogenesis in the amygdala: A new etiologic hypothesis of autism?

Abstract

Neurogenesis studies had an increased development after BrdU (5-bromo-3'-deoxyuridine), a marker of cell proliferation. Today, several studies have showed the relevance of neurogenesis in the hippocampal formation. Notwithstanding, other brains areas have been described presenting neurogenesis, including the amygdata. This key structure is a complex cerebral region which has been associated with social behaviors and the emotional significance of the daily experiences. Several studies have associated the amygdala to the autism, a severe neurodevetopmentat disorder. in this paper, we discuss the hypothesis of neurogenesis in the amygdata as a contributing cause of autism. the social skills require competent new neuronal connections, including efficient plasticity synaptic rearranging. Interestingly, emotional context cannot be imprinting in mature neurons in the presence of GABA, a neurotransmitter release during new environments experiences. However, it is known that new neurons are not welt responsive to GABA stimulation, allowing the tong-term potentiation necessary for the learning process. Based on these evidence it is tantalizing to hypothesize that the sociability impairment seen in some individuals with autism may partly be assigned to impaired regulation of the GABAergic system and to the impact of this impairment on the adequate functioning of the annygdala and on its capacity to store new experiences and to modulate the plasticity of the corticostriatal connections. (c) 2007 Elsevier B.V. All rights reserved.