Cholinergic and Peptidergic Regulation of Ganglionic Tyrosine Hydroxylase Activity

  • R. E. Zigmond
  • N. Y. Ip
Part of the Advances in Behavioral Biology book series (ABBI, volume 30)

Abstract

Acetylcholine has traditionally been thought to be the sole preganglionic neurotransmitter in sympathetic ganglia. However, this view was challenged 15 years ago by Nishi and Koketsu in their studies on a frog sympathetic ganglion (10). These workers found that certain of the postsynaptic electrophysiological consequences of preganglionic nerve stimulation could not be abolished by cholinergic antagonists. More recently, Jan, Jan and Kuffler (8, 9) identified the neurotransmitter responsible for these non-cholinergic effects as being a peptide that resembles, but is not identical to, luteinizing hormone-releasing hormone. We have recently obtained evidence that a non-cholinergic transmitter is released also by preganglionic neurons in a mammalian sympathetic ganglion, the rat superior cervical ganglion, and that this neurotransmitter is different from the non-cholinergic transmitter found in frog sympathetic ganglia. Our conclusions come from studies on a postsynaptic biochemical consequence of preganglionic nerve stimulation rather than on an electrophysiological consequence. The biochemical parameter we have been investigating is the activity of the enzyme tyrosine 3-monooxygenase (tyrosine hydroxylase; TH; EC 1.14.16.2), the enzyme which catalyzes the rate-limiting step in catecholamine biosynthesis.

Keywords

Acetylcholine Atropine Bradykinin Dopa Secretin 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Chalazonitis, A. and Zigmond, R.E. (1980): J. Physiol. (Lond.) 300: 525–538.Google Scholar
  2. 2.
    Chalazonitis, A., Rice, P.J. and Zigmond, R.E. (1980): J. Pharmacol. Exp. Ther. 213: 139–143.Google Scholar
  3. 3.
    Erny, R.E., Berezo, M.W. and Perlman, R.L. (1981): J. Biol. Chem. 256: 1335–1339.Google Scholar
  4. 4.
    Ip, N.Y. and Zigmond, R.E. (1984): Peptides 5: 309–312.CrossRefGoogle Scholar
  5. 5.
    Ip, N.Y., Perlman, R.L. and Zigmond, R.E. (1982): J. Pharmacol. Exp. Ther. 223: 280–283.Google Scholar
  6. 6.
    Ip, N.Y., Ho, C.K. and Zigmond, R.E. (1982): Proc. Natl. Acad. Sci. USA 79: 7566–7569.CrossRefGoogle Scholar
  7. 7.
    Ip, N.Y., Perlman, R.L. and Zigmond, R.E. (1983): Proc. Natl. Acad. Sci. USA 80: 2081–2085.CrossRefGoogle Scholar
  8. 8.
    Jan, Y.N., Jan, L.Y. and Kuffler, S.W. (1979): Proc. Natl. Acad. Sci. USA 76: 1501–1505.CrossRefGoogle Scholar
  9. 9.
    Jan, Y.N., Jan, L.Y. and Kuffler, S.W. (1980): Proc. Natl. Acad. Sci. USA 77: 5008–5012.CrossRefGoogle Scholar
  10. 10.
    Nishi, S. and Koketsu, K. (1968): J. Neurophysiol. 31: 109–121.Google Scholar
  11. 11.
    Raisman, G., Field, P.M., Ostberg, A.J.C., Iversen, L.L. and Zigmond, R.E. (1974): Brain Res. 71: 1–16.CrossRefGoogle Scholar
  12. 12.
    Zigmond, R.E. and Ben-Ari, Y. (1977): Proc. Natl. Acad. Sci. USA 74: 3078–3080.CrossRefGoogle Scholar
  13. 13.
    Zigmond, R.E. and Chalazonitis, A. (1979): Brain Res. 164: 137–152.CrossRefGoogle Scholar
  14. 14.
    Zigmond, R.E., Chalazonitis, A. and Joh, T. (1980): Neurosci. Lett. 20: 61–65.CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1986

Authors and Affiliations

  • R. E. Zigmond
    • 1
  • N. Y. Ip
    • 1
  1. 1.Department of PharmacologyHarvard Medical SchoolBostonUSA

Personalised recommendations