4 years ago

Corticotropin-releasing hormone suppresses synapse formation in hippocampus of male rats via inhibition of CXCL5 secretion by glia.

You Zheng, Xin Ni, Hui Sheng, Yanmin Zhang, Yongjun Xu
Corticotropin-releasing hormone (CRH) is implicated to play a critical role in stress-induced synaptic formation and modification. In the present study, we explored the mechanisms underlying CRH modulation of synaptic formation in hippocampus using various models in vitro. In cultured hippocampal slices, CRH treatment decreased synapsin I and PSD95 levels via CRH receptor type 1 (CRHR1). In isolated hippocampal neurons, however, it increased synapsin I-labeled presynaptic terminals and PSD95-labeled postsynaptic terminals via CRHR1. Interestingly, the inhibitory effect of CRH on synapsin I-labeled and PSD95-labeled terminals occurred in the model of neuron-glia co-cultures. These effects were prevented by CRHR1 antagonist. Moreover, treatment of the neurons with the media of CRH-treated glia led to a decrease in synaptic terminals formation. The media collected from CRH-treated glial cells with CRHR1 knockdown did not show an inhibitory effect on synaptic terminals in hippocampal neurons. Unbiased cytokine array coupled with confirmatory ELISA revealed that CRH suppressed C-X-C motif chemokine 5 (CXCL5) productions in glia via CRHR1. Administration of CXCL5 reversed the inhibitory effects of CRH-treated glia culture media on synaptic formation. Our data suggest that CRH suppresses synapse formation through inhibition of CXCL5 secretion from glia in hippocampus. Our study implicates that glia-neuron intercommunication is one of the mechanisms responsible for neuronal circuits remodeling during stress.

Publisher URL: http://doi.org/10.1210/en.2017-00336

DOI: 10.1210/en.2017-00336

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