Interleukin - 11 @ - Mediated Regulation of 1 u - Opioid Receptor mRNA in Primary Astrocyte - Enriched Cultures

Opiolds have been found to modulate the immune system by regulating the function of immunocompetent cells. Several studies suggest that the interaction between immune and opioid systems is not unidirectional, but rather reciprocal, in nature. In the CNS, one cellular target of immune system activation is the astrocytes. These glial cells have been shown to produce the oploid peptide, proenkephalin, to express the it-, 6-, and K-opioid receptors, and to respond to the immune factor interleukin-1/3 (IL1/3) with an increased proenkephalin synthesis. To characterize more completely the astrocytic opioid response to immune factor stimulation, we examined the effect of IL1/3 (1 ng/ml) on the is-receptor mRNA expression in primary astrocyteenriched cultures derived from rat (postnatal day 1—2) cortex, striatum, cerebellum, hippocampus, and hypothalamus. A 24-h treatment with IL1/3 produced a 70—80% increase in the ti-receptor mRNA expression in the striatal, cerebellar, and hippocampal cultures but had no effect on this expression in the cortical and hypothalamic cultures. This observation represents one of the few demonstrated increases in levels of the it-receptor mRNA in vitro or in vivo, since the cloning of the receptor. The enhanced he-receptor mRNA expression, together with the previous observation that ILl/I stimulates proenkephalin synthesis in astrocytes, supports the ILl /3-mediated regulation of an astroglial opioid peptide and receptor in vitro, a phenomenon that may be significant in the modulation of the gliotic response to neuronal damage. Therefore, the astroglial opioid “system” may be important in the ILl /3-initiated, coordinated response to CNS infection, trauma, or injury.