Recent results indicate that astrocytic jS-adrenergic receptors (jSAR) participate in noradrenergic modulation of synaptic activity. In this study, we sought to examine whether neural activity can, in turn, regulate astrocytic jSAR. To address this question, an antiserum that recognizes jS-adrenergic receptors (jSAR) specifically in astrocytes was used to assess the distribution of the receptors across ocular dominance columns in VI of two monocular and four visually intact adult monkeys. Cytochrome oxidase histochemistry (CO) was used to identify the position of the cortical laminae and of the ocular dominance columns receiving visual inputs from the intact and enucleated eyes. This stain revealed the expected pattern within VI of monocular monkeys #x2014;i.e. darker and lighter bands of equal widths (aa. 500 jun) spanning laminae 4-6, each associated with larger and smaller blobs, respectively, in lamina 2/3. Alignment of CO sections with adjacent sections stained for astrocytic jSAR by the immunoperoxidase method revealed intense jSAR-like immunoreactivity (jSAR-li) in the superficial laminae, a slightly weaker staining in the infragranular laminae and weakest staining in lamina 4C. Within lamina 4C, a prominent striped pattern was evident. The darker bands of the stripe closely matched widths and positions of the lighter CO columns associated with the enucleated eye. On the other hand, immunocytochemical staining for the astrocytic intermediate filament protein, GFAP, within VI of monocular monkeys revealed no inter-columnar difference in the density of astrocytic cell bodies or processes. Nissl stain also revealed no overt inter-columnar differences in cell density. VI of visually intact monkeys exhibited a similar laminar distribution pattern of jSAR-li and of CO. Within lamina 4C, jSAR-li was uniformly Faint and CO staining was uniformly intense. This suggests that the striped pattern of jSAR-li seen in lamina 4C of monocular monkeys results from elevation of the jSAR-antigen within the inactive columns. The results indicate that astrocytic jSAR density is regulated by local neural activity. The mechanisms regulating jSAR density are likely to be independent of those regulating glial cell proliferation or GFAP synthesis. In vitro experimental results of others suggest that elevation of astrocytic jSAR may be a mechanism compensating for chronic neural inactivity, since the coincident release of noradrenaLine with visual stimulation would elevate neuropil excitability via the astrocytic mechanism of (1) decreasing the uptake of neuronally released L-glutamate; (2) increasing Gabaa uptake; and (3) stimulating glycogenolysis. Alternatively, the changes in jSAR-li may reflect an up-regulation of the receptors within inactive columns due to reduced levels of noradrenaLine release.
- Activity-dependent regulation
- Catecholamine receptors
- Monocular deprivation VI
ASJC Scopus subject areas
- Sensory Systems