Skip to main content

Neuroprotective Effects of Melatonin

  • Chapter
Recent Advances in Tryptophan Research

Abstract

The full range of physiological actions of melatonin is not completely known. In mammals, it modulates gonadal function and regulates biological rhythms. Furthermore, it has also been reported to have anxyolitic, sedative, and anticonvulsant properties, both in human and animals. Recently it has been shown that melatonin is a potent, endogenous hydroxyl radical scavenger suggesting that it might interfere with neurodegenerative processing involving free-radical formation and excitatory amino acid release. Using primary cultures of rat cerebellar neurons and in vivo models of brain injury in rats, we demonstrate that melatonin might be considered an endogenous neuroprotective factor useful for the pharmacological treatment of neurological disorders and neural degeneration produced by glutamate excitotoxicity and oxidative stress.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 84.99
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 109.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  • Brown, G.M., Pulido, O., and Niles, L.P., 1983, Differential localization of melatonin and N-acetyl serotonin in brain, in:“The pineal gland and its endocrine role”, J. Axelrod, F. Fraschini, and G.P. Velo, eds., Plenum Press, New York.

    Google Scholar 

  • Cagnoli, C.M., Atabay, C., Kharlamov, E., and Manev, H., 1995, Melatonin protecs neurons from singlet oxigen-induced apoptosis, J. Pineal Res., in press

    Google Scholar 

  • Champney, T. H., & Champney, J.-A. C., 1992, Novel anticonvulsant action of chronic melatonin in the gerbil, Neuro. Report, 3: 1152.

    CAS  Google Scholar 

  • Choi, D. W., 1988, Glutamate neurotoxicity and diseases of the nervous system. Neuron, 1: 623.

    Article  CAS  Google Scholar 

  • Chuang, J.I., & Lin M.T., 1994, Pharmacological effects of melatonin treatment on both locomotor activity and brain serotonin release in rats, J. Pineal Res, 17: 11.

    Article  CAS  Google Scholar 

  • Dykens, J.A., Stern, A., Trenker, E., 1987, Mechanism of kainate toxicity to cerebellar neurons in vitro is analogous to reperfusion tissue injury. J. Neurochem, 49: 1222.

    Article  CAS  Google Scholar 

  • Giusti, P., Gusella, M., Lipartiti, M., Milani, D., Zhu, W., Vicini, S., and Manev, H., 1995, Melatonin protects primary cultures of cerebellar granule neurons from kainate but not from N-methyl-d-aspartate excitotoxicity, Exp. Neurol., 131: 39.

    Article  CAS  Google Scholar 

  • Golombek, D.A., Martini M., and Cardinali, D.P., 1993, Melatonin as an anxiolytic in rats: time dependence and interaction with the central GABAergic system., Eur. J Pharmacol, 237: 231.

    Article  CAS  Google Scholar 

  • Gotz, M.E., Kunig G., Riederer, P., and Youdim, M.B.H., 1994, Oxidative stress: free radical production in neural degeneration, Pharmac. Ther, 63: 37.

    Article  CAS  Google Scholar 

  • Gusella, M., Lipartiti, M., Franceschini, D., Manev, H., and Giusti, P., 1995, Melatonin protects from kainate-induced neurotoxicity in cerebellar granule cells, Behav. Pharmacol, 6 (suppl.l): 98.

    Article  Google Scholar 

  • Lipton, S.A., and Rosemberg, P.A., 1994, Excitatory amino acids as a final common pathway for nerological disorders, New England J. Med, 330: 613.

    Article  CAS  Google Scholar 

  • Manev., H., Kharlamov, A., and Armstrong, D., 1994, Photochemical brain injury in rats triggers DNA fragmentation, p53 and HSP72, Neuro. Report, 5: 2661.

    CAS  Google Scholar 

  • Manev., H., Cagnoli, C.M., Atabay, C., Kharlamov, E., Ikomonovic, M.D., and Grayson, D.R., 1995, Neuronal apoptosis in an in vitro model of photochemically induced oxidative stress, Exp. Neurol., 133: in press.

    Google Scholar 

  • Mattson, M.P., & Scheff, S.W., 1994, Endogenous neuroprotection factors and traumatic brain injury. Mechanisms of action and implications for therapy, J. Neurotrauma, 11: 3.

    Article  CAS  Google Scholar 

  • Nakanishi, S., 1992, Molecular diversity of glutamate receptors and implications for brain function, Science, 258: 597.

    Article  CAS  Google Scholar 

  • Niles L., 1991, Melatonin interaction with the benzodiazepine-GABA receptor complex in the CNS, in:“Kynurenine and serotonin pathways”, R. Schwarcz, ed, Plenum Press, New York.

    Google Scholar 

  • Norlund, J.J., Lerner, A.B., 1977, The effects of oral melatonin on skin color and on the release of pituitary hormones, J. Clin. Endocrinol. Metab, 45: 768.

    Article  Google Scholar 

  • Pellegrini-Giampietro, D. E., Cherici, E. G., Alesiani, M., Carla, V., Moroni, F., 1990, Excitatory amino acid release and free radical formation may cooperate in the genesis of ischemia-induced neuronal damage, J. Neurosci, 10: 1035.

    CAS  Google Scholar 

  • Phillis, J.W., 1994,: A “radical” view of cerebral ischemic injury, Prog. Neurobiol. 42: 441

    Article  CAS  Google Scholar 

  • Puttfarcken, P. S., Getz, R. L., Coyle, J. T., 1993, Kainic acid-induced lipid peroxidation: Protection with butylate hydroxytoluene and U78517F in primary cultures of cerebellar granule cells. Brain Res., 624: 223.

    Article  CAS  Google Scholar 

  • Reiter, R. J., Poeggeler, B., Tan, D.-X., Chen, L. D., Manchester, L. C., and Guerrero, J. M., 1993, Antioxidant capacity of melatonin: A novel action not requiring receptors. Neuroendocrinol. Lett15: 103.

    CAS  Google Scholar 

  • Reiter, R. J., 1995, Oxidative processes and antioxidative defense mechanisms in the aging brain, FASEB J9: 526.

    CAS  Google Scholar 

  • Romijin, H. J., 1978, The pineal, a tranquilizing organ?, Life Science, 23: 2257.

    Article  Google Scholar 

  • Serafian, T.A., & Bredesen, D.E., 1994, Is apoptosis mediated by reactive oxygen species?, Free Rad. Res.. 21: 1.

    Article  Google Scholar 

  • Sperk, G., 1994, Kainic acid seizure in the rat, Progress in Neurobiology, 42: I.

    Article  CAS  Google Scholar 

  • Tamarkin, L., Baird, C.J., and Almeida, O.F.X., 1985, Melatonin: A coordinating signal for mammalian reproduction?, Science 227: 714.

    Article  CAS  Google Scholar 

  • Tan, D.-X., Chen, L.-D, Poeggeler, B., Manchester, L.C., and Russel, J. R., 1993. Melatonin: a potent, endogenous hydroxyl radical scavenger. Endocrine J., 1: 57.

    Google Scholar 

  • Wurtman, R. J., Axelrod, J., and Fisher, J. E., 1964, Melatonin synthesis in the pineal gland: Effect of the light mediated by the sympathetic nervous system, Science, 143: 1328.

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 1996 Plenum Press, New York

About this chapter

Cite this chapter

Lipartiti, M. et al. (1996). Neuroprotective Effects of Melatonin. In: Filippini, G.A., Costa, C.V.L., Bertazzo, A. (eds) Recent Advances in Tryptophan Research. Advances in Experimental Medicine and Biology, vol 398. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0381-7_49

Download citation

  • DOI: https://doi.org/10.1007/978-1-4613-0381-7_49

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-8026-9

  • Online ISBN: 978-1-4613-0381-7

  • eBook Packages: Springer Book Archive

Publish with us

Policies and ethics