One of the functions of glial receptors is to regulate synthesis and r
elease of a variety of neuropeptides and growth factor peptides, which
in turn act on neurons or other glia. Because of the potential import
ance of these interactions in injured brain, we have examined the role
of two different receptors in the regulation of astrocyte neuropeptid
e synthesis. Stimulation of beta-adrenergic receptors on type 1 astroc
ytes resulted in increased mRNA and protein for the proenkephalin (PE)
and somatostatin genes. This receptor also increased expression of ne
rve growth factor (NGF) and brain-derived neurotrophic factor (BDNF).
The potential role of opiate receptors was examined in several ways. T
reatment of newborn rats for 7 days with the opiate antagonist naltrex
one, prior to preparation of astrocytes, had no effect on PE mRNA or m
et-enkephalin content but resulted in a significant increase in NGF co
ntent. However, treatment of astrocytes in culture with met-enkephalin
, morphine, or naltrexone had no effect on any of these parameters. No
opiate binding could be detected, using either etorphine or bremazoci
ne, to membranes of astrocytes prepared from cortex, cerebellum, stria
tum, or hippocampus of 1-day, 7-day, or 14-day postnatal rats. Thus we
conclude that type I astrocytes do not express opiate receptors and t
hat the in vivo effects of naltrexone are mediated indirectly via some
other cell type/receptor. (C) 1994 Wiley-Liss, Inc.