Gpr37 modulates the severity of inflammation-induced GI dysmotility by regulating enteric reactive gliosis.

Although loss of Gpr37 resulted in little to no differences in gene expression, ENS structure or whole GI transit, there was a slight trend in increased SI and colonic transit, and we cannot exclude the possibility that Gpr37 has a functional role at steady state in addition to its role in reactive gliosis.

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