期刊
JOURNAL OF NEUROSCIENCE
卷 24, 期 46, 页码 10353-10363出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3228-04.2004
关键词
glial cells; neuroglial plasticity; tanycytes; endothelial nitric oxide synthase; neurosecretion; hypothalamus
资金
- NCRR NIH HHS [K01 RR000163, RR00163, P51 RR000163] Funding Source: Medline
- NICHD NIH HHS [R01 HD025123, HD25123, U54 HD18185, U54 HD018185] Funding Source: Medline
Glial and endothelial cells interact throughout the brain to define specific functional domains. Whether endothelial cells convey signals to glia in the mature brain is unknown but is amenable to examination in circumventricular organs. Here we report that purified endothelial cells of one of these organs, the median eminence of the hypothalamus, induce acute actin cytoskeleton remodeling in isolated ependymoglial cells and show that this plasticity is mediated by nitric oxide (NO), a diffusible factor. We found that both soluble guanylyl cyclase and cyclooxygenase products are involved in this endothelial-mediated control of ependymoglia cytoarchitecture. We also demonstrate by electron microscopy that activation of endogenous NO release in the median eminence induces rapid structural changes, allowing a direct access of neurosecretory axons containing gonadotropin-releasing hormone (GnRH) (the neuropeptide controlling reproductive function) to the portal vasculature. Local in vivo inhibition of NO synthesis disrupts reproductive cyclicity, a process that requires a pulsatile, coordinated delivery of GnRH into the hypothalamic-adenohypophyseal portal system. Our results identify a previously unknown function for endothelial cells in inducing neuroglial plasticity and raise the intriguing possibility that endothelial cells throughout the brain may use a similar signaling mechanism to regulate glial-neuronal interactions.
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