Are glial cells targets of the central noradrenergic system?
It has been suggested by a number of investigators that glial cells as well as neurons are targets of the central noradrenergic system. This important hypothesis, however, has not been presented previously in a systematic and unified manner. The present review was therefore undertaken to accomplish this. The evidence supporting noradrenergic action on glia consists primarily of findings that beta-adrenoceptors, norepinephrine (NE)-stimulated cyclic AMP (cAMP) responses and glycogen are localized preferentially in glial cells and that beta-receptor density and glycogen hydrolysis are under the control of neuronally released NE. While there is some disagreement as to the extent to which beta-receptors are preferentially localized in glia, there is a consensus that most glycogen in the forebrain is localized in this cellular compartment. The presumed function of the noradrenergic action on glia appears to be the release of glucose for production of energy, the synthesis of neurotrophic fa
