Neurological Sciences

, Volume 22, Issue 1, pp 61–62

An abnormal striatal synaptic plasticity may account for the selective neuronal vulnerability in Huntington's disease

Authors

  • D. Centonze
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy
  • P. Gubellini
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy
  • B. Picconi
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy
  • E. Saulle
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy
  • M. Tolu
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy
  • P. Bonsi
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy
  • P. Giacomini
    • Neurology Clinic II, University of Rome La Sapienza, Rome, Italy
  • P. Calabresi
    • Neurology Clinic, Neurosciences Department, University of Rome Tor Vergata, Via di Tor Vergata 135, I-00133 Rome, Italy and Fondazione Santa Lucia, Rome, Italy

DOI: 10.1007/s100720170047

Cite this article as:
Centonze, D., Gubellini, P., Picconi, B. et al. Neurol Sci (2001) 22: 61. doi:10.1007/s100720170047

Abstract

A marked decrease in the activity of mitochondrial complex II (succinate dehydrogenase, SD) has been found in the brains of Huntington's disease (HD) patients. Here we have examined the possibility that SD inhibitors might produce their toxic action by increasing corticostriatal glutamatergic transmission. We report that SD inhibitors produce a durable augmentation of NMDA-mediated corticostriatal excitation (DANCE) in striatal spiny neurons, but not in striatal cholinergic interneurons. DANCE involves increased intracellular calcium, activation of MAP kinase ERK and is critically dependent upon endogenous dopamine (DA) acting via D2-like receptors. This pathological form of corticostriatal synaptic plasticity might play a key role in the regional and cell-type specific neuronal death observed in HD.

Copyright information

© Springer-Verlag Italia 2001