Abstract
Neuropeptides may have functions in the central nervous system (CNS) other than altering neuronal excitability. For example, they may act as regulators of brain metabolism by affecting glycogenolysis1. Since it has been suggested that glial cells might provide metabolic support for neuronal activity2,3, they may well be one of the targets for neuropeptide regulation of metabolism. Consistent with this view are reports that peptidecontaining nerve terminals have been seen apposed to astrocytes4,5, but it is also quite possible that peptides could act at sites lacking morphological specialization6,7. Primary cultures containing CNS glial cells have been shown to respond to β-adrenergic agonists with an increase in cyclic AMP and, as a result, with an increase in glycogenolysis8,9 and have also been shown to respond to a variety of peptides with changes in cyclic AMP10–12. In the study reported here, we have examined the effects of several peptides on relatively pure cultures of rat astrocytes. We demonstrate that the increase in intracellular cyclic AMP induced by noradrenaline is markedly enhanced by somatostatin and substance P and is inhibited by enkephalin, even though these peptides on their own have little or no effect on the basal levels of cyclic AMP. Vasoactive intestinal peptide ( VIP) on the other hand increases cyclic AMP in the absence of noradrenaline. These results suggest that neuropeptides influence glial cells as well as neurones in the CNS and, in the case of somatostatin and substance P, provide further examples of neuropeptides modulating the response to another chemical signal without having a detectable action on their own.
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Magistretti, P. J., Morrison, J. H., Shoemaker, W. J., Sapin, V. & Bloom, F. E. Proc. natn. Acad. Sci. U.S.A. 78, 6535–6539 (1981).
Guth, L. & Watson, P. K. Expl Neurol. 22, 590–602 (1968).
Pentreath, V. W., Seal, L. H. & Kai-Kai, M. A. Neuroscience 7, 759–767 (1982).
Barber, R. P. et al. J. comp. Neurol. 184, 331–352 (1979).
Tweedle, C. D. & Hatton, G. I. Brain Res. Bull. 8, 205–209 (1982).
Descarries, L., Watkins, K. C. & Lapierre, Y. Brain Res. 133, 197–222 (1977).
Jan, L. Y. & Jan, Y. N. J. Physiol, Lond. 327, 219–246 (1982).
Narumi, S., Kimelberg, H. K. & Bourke, R. S. J. Neurochem. 31, 1479–1490 (1978).
Cummins, C. J., Lust, W. D. & Passonneau, J. V. J. Neurochem. 40, 128–136 (1983).
Van Calker, D., Müller, M. & Hamprecht, B. Proc. natn. Acad. Sci. U.S.A. 77, 6907–6911 (1980).
Löffler, F., Van Calker, D. & Hamprecht, B. Embo J. 1, 297–302 (1982).
Van Calker, D., Löffler, F. & Hamprecht, B. J. Neurochem. 40, 418–427 (1983).
McCarthy, K. D. & de Vellis, J. J. Cell Biol. 85, 890–902 (1980).
Raff, M. C. et al. Brain Res. 174, 283–308 (1979).
Bartlett, P. F. et al. Brain Res. 204, 339–351 (1981).
Wood, J. N. & Anderton, B. H. Biosci. Rep. 1, 263–268 (1981).
Ranscht, B., Clapshaw, P. A., Price, J., Noble, M. & Seifort, W. Proc. natn. Acad. Sci. U.S.A. 79, 2709–2713 (1982).
Cailla, H. L. Analyt. Biochem. 56, 394–399 (1973).
Quach, T. T., Rose, C. & Schwartz, J. C. J. Neurochem. 30, 1335–1341 (1978).
Passonneau, J. V. & Crites, S. K. J. biol. Chem. 251, 2015–2022 (1976).
Sutherland, E. W., Rall, T. W. & Menon, T. J. biol. Chem. 237, 1220–1227 (1962).
Ross, E. M. & Gilman, A. G. A. Rev. Biochem. 49, 533–564 (1980).
Mizobe, F., Kozousek, V., Dean, D. M. & Livett, B. G. Brain Res. 178, 555–556 (1979).
Role, L. W., Leeman, S. E. & Perlman, R. L. Neuroscience 6, 1813–1821 (1981).
Lundberg, J. M. Acta physiol. scand. Suppl., 112, 496, 1–57 (1981).
Haefely, W., Pieri, L., Polc, P. & Schaffner, R. in Handbook of Pharmacology (ed. Hoffmeister, F.) 1–483 (1980).
Stallcup, W. B. & Patrick, J. Proc. natn. Acad. Sci. U.S.A. 77, 634–638 (1980).
Lundberg, J. M., Hedland, B. & Bartfai, T. Nature 295, 147–149 (1982).
Olsen, R. W. J. Neurochem. 37, 1–13 (1981).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Rougon, G., Noble, M. & Mudge, A. Neuropeptides modulate the β-adrenergic response of purified astrocytes in vitro. Nature 305, 715–717 (1983). https://doi.org/10.1038/305715a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/305715a0
This article is cited by
-
Neurotrophic effects of conditioned media of astrocytes isolated from different brain regions on hippocampal and cortical neurons
Experientia (1995)
-
Chronic treatment of newborn rats with naltrexone alters astrocyte production of nerve growth factor
Journal of Molecular Neuroscience (1993)
-
? andk opiate receptors in primary astroglial cultures part II: Receptor sets in cultures from various brain regions and interactions with �-receptor activated cyclic AMP
Neurochemical Research (1992)
-
Immunohistochemical identification of substance P in cutaneous sensory organs (electroreceptors) of gymnotid teleost fish
Cell and Tissue Research (1991)
-
Somatostatin binding sites on rat diencephalic astrocytes
Cell and Tissue Research (1991)
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.