AI Article Synopsis
- Autism spectrum disorder (ASD) is linked to genetic susceptibility and environmental factors, particularly maternal infections during pregnancy which increase autism risk in children.
- Research utilizing a maternal immune activation (MIA) model showed that MIA causes autistic behaviors due to specific changes in the brain, such as microglia activation and dendritic spine abnormalities in the prefrontal cortex (PFC).
- The overexpression of NKCC1, a key protein in these processes, was identified as a contributor to these changes, and the use of the NKCC1 inhibitor bumetanide successfully reduced autistic behaviors in affected offspring.
Article Abstract
Autism spectrum disorder (ASD) is thought to result from susceptibility genotypes and environmental risk factors. The offspring of women who experience pregnancy infection have an increased risk for autism. Maternal immune activation (MIA) in pregnant animals produces offspring with autistic behaviors, making MIA a useful model for autism. However, how MIA causes autistic behaviors in offspring is not fully understood. Here, we show that NKCC1 is critical for mediating autistic behaviors in MIA offspring. We confirmed that MIA induced by poly(I:C) infection during pregnancy leads to autistic behaviors in offspring. We further demonstrated that MIA offspring showed significant microglia activation, excessive dendritic spines, and narrow postsynaptic density (PSD) in their prefrontal cortex (PFC). Then, we discovered that these abnormalities may be caused by overexpression of NKCC1 in MIA offspring's PFCs. Finally, we ameliorated the autistic behaviors using PFC microinjection of NKCC1 inhibitor bumetanide (BTN) in MIA offspring. Our findings may shed new light on the pathological mechanisms for autism caused by pregnancy infection.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10968780 | PMC |
| http://dx.doi.org/10.3390/cimb46030121 | DOI Listing |
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