Deficits of glutamate transmission in the striatum of experimental hemiballism

D. Centonze, S. Rossi, P. Gubellini, V. De Chiara, A. Tscherter, C. Prosperetti, B. Picconi, G. Bernardi, P. Calabresi, C. Baunez

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Hemiballism (HB) is a quite rare disorder, generally secondary to stroke, neoplasms or demyelinating plaques, classically considered as almost pathognomonic of a lesion in the subthalamic nucleus (STN). This alteration causes involuntary movements in the chorea-ballism spectrum. One theory is that the output nuclei of the basal ganglia are overinhibited in HB, while little is known about the physiological state of the striatum, the major input structure of the basal ganglia. In the present study, we recorded spontaneous and miniature excitatory and inhibitory postsynaptic currents (sEPSCs, mEPSCs, sIPSCs, mIPSCs) from projection neurons of the striatum of experimental HB. We found a selective reduction of striatal sEPSC and mEPSC frequency following chemical lesion of the STN of the rat, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HB.

Original languageEnglish
Pages (from-to)213-221
Number of pages9
JournalNeuroscience
Volume143
Issue number1
DOIs
Publication statusPublished - Nov 17 2006

Fingerprint

Dyskinesias
Glutamic Acid
Basal Ganglia
Subthalamic Nucleus
Corpus Striatum
Chorea
Inhibitory Postsynaptic Potentials
Excitatory Postsynaptic Potentials
Stroke
Neurons
Neoplasms

Keywords

  • electrophysiology
  • hyperkinetic disorders
  • mEPSC
  • sEPSC
  • subthalamic nucleus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Centonze, D., Rossi, S., Gubellini, P., De Chiara, V., Tscherter, A., Prosperetti, C., ... Baunez, C. (2006). Deficits of glutamate transmission in the striatum of experimental hemiballism. Neuroscience, 143(1), 213-221. https://doi.org/10.1016/j.neuroscience.2006.07.024

Deficits of glutamate transmission in the striatum of experimental hemiballism. / Centonze, D.; Rossi, S.; Gubellini, P.; De Chiara, V.; Tscherter, A.; Prosperetti, C.; Picconi, B.; Bernardi, G.; Calabresi, P.; Baunez, C.

In: Neuroscience, Vol. 143, No. 1, 17.11.2006, p. 213-221.

Research output: Contribution to journalArticle

Centonze, D, Rossi, S, Gubellini, P, De Chiara, V, Tscherter, A, Prosperetti, C, Picconi, B, Bernardi, G, Calabresi, P & Baunez, C 2006, 'Deficits of glutamate transmission in the striatum of experimental hemiballism', Neuroscience, vol. 143, no. 1, pp. 213-221. https://doi.org/10.1016/j.neuroscience.2006.07.024
Centonze D, Rossi S, Gubellini P, De Chiara V, Tscherter A, Prosperetti C et al. Deficits of glutamate transmission in the striatum of experimental hemiballism. Neuroscience. 2006 Nov 17;143(1):213-221. https://doi.org/10.1016/j.neuroscience.2006.07.024
Centonze, D. ; Rossi, S. ; Gubellini, P. ; De Chiara, V. ; Tscherter, A. ; Prosperetti, C. ; Picconi, B. ; Bernardi, G. ; Calabresi, P. ; Baunez, C. / Deficits of glutamate transmission in the striatum of experimental hemiballism. In: Neuroscience. 2006 ; Vol. 143, No. 1. pp. 213-221.
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