Spinal cord injury (SCI) is an incurable trauma that frequently results in partial or complete loss of motor and sensory function. Massive neurons are damaged after the initial mechanical insult. Secondary injuries, which are triggered by immunological and inflammatory responses, also result in neuronal loss and axon retraction. This results in defects in the neural circuit and a deficiency in the processing of information. Although inflammatory responses are necessary for spinal cord recovery, conflicting evidence of their contributions to specific biological processes have made it difficult to define the specific role of inflammation in SCI. This review summarizes our understanding of the complex role of inflammation in neural circuit events following SCI, such as cell death, axon regeneration and neural remodeling. We also review the drugs that regulate immune responses and inflammation in the treatment of SCI and discuss the roles of these drugs in the modulation of neural circuits. Finally, we provide evidence about the critical role of inflammation in facilitating spinal cord neural circuit regeneration in zebrafish, an animal model with robust regenerative capacity, to provide insights into the regeneration of the mammalian central nervous system.
Neural circuit defects are a prominent feature of autism spectrum disorder (ASD). However, the specific defects in neural circuits and the resulting pathogenesis are not well understood. We conducted a systematic analysis of two ASD datasets and found alterations in multiple neurodevelopmental pathways and in dopaminergic signaling pathways. Interestingly, the dopaminergic signaling pathways are associated with neurodevelopmental pathways in patients with ASD. We also discovered that disruption of the dopaminergic system leads to neural circuit formation defects. Our study suggests a new therapeutic target for ASD.
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