Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease

Silvia Rossi, Chiara Prosperetti, Barbara Picconi, Valentina De Chiara, Giorgia Mataluni, Giorgio Bernardi, Paolo Calabresi, Diego Centonze

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Altered glutamate transmission in the striatum has been proposed to play a critical role in the pathophysiology of Huntington's disease (HD), a genetic disorder associated with impaired activity of the mitochondrial complex II (succinate dehydrogenase, SD). In the present study, we recorded spontaneous (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) from striatal neurons of both toxic (systemic administration of 3-nitropropionic acid in rats) and genetic models of HD (R6/2 transgenic mice). In both models, we found a significant down-regulation of glutamate transmission, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HD.

Original languageEnglish
Pages (from-to)6-10
Number of pages5
JournalNeuroscience Letters
Volume410
Issue number1
DOIs
Publication statusPublished - Dec 13 2006

Fingerprint

Poisons
Genetic Models
Huntington Disease
Glutamic Acid
Corpus Striatum
Inborn Genetic Diseases
Succinate Dehydrogenase
Excitatory Postsynaptic Potentials
Basal Ganglia
Transgenic Mice
Down-Regulation
Neurons

Keywords

  • Corticostriatal transmission
  • eEPSCs
  • Electrophysiology
  • HD
  • mEPSCs

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease. / Rossi, Silvia; Prosperetti, Chiara; Picconi, Barbara; De Chiara, Valentina; Mataluni, Giorgia; Bernardi, Giorgio; Calabresi, Paolo; Centonze, Diego.

In: Neuroscience Letters, Vol. 410, No. 1, 13.12.2006, p. 6-10.

Research output: Contribution to journalArticle

Rossi, Silvia ; Prosperetti, Chiara ; Picconi, Barbara ; De Chiara, Valentina ; Mataluni, Giorgia ; Bernardi, Giorgio ; Calabresi, Paolo ; Centonze, Diego. / Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease. In: Neuroscience Letters. 2006 ; Vol. 410, No. 1. pp. 6-10.
@article{1bcc68976fd448168ce411e9947d4352,
title = "Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease",
abstract = "Altered glutamate transmission in the striatum has been proposed to play a critical role in the pathophysiology of Huntington's disease (HD), a genetic disorder associated with impaired activity of the mitochondrial complex II (succinate dehydrogenase, SD). In the present study, we recorded spontaneous (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) from striatal neurons of both toxic (systemic administration of 3-nitropropionic acid in rats) and genetic models of HD (R6/2 transgenic mice). In both models, we found a significant down-regulation of glutamate transmission, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HD.",
keywords = "Corticostriatal transmission, eEPSCs, Electrophysiology, HD, mEPSCs",
author = "Silvia Rossi and Chiara Prosperetti and Barbara Picconi and {De Chiara}, Valentina and Giorgia Mataluni and Giorgio Bernardi and Paolo Calabresi and Diego Centonze",
year = "2006",
month = "12",
day = "13",
doi = "10.1016/j.neulet.2006.09.056",
language = "English",
volume = "410",
pages = "6--10",
journal = "Neuroscience Letters",
issn = "0304-3940",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease

AU - Rossi, Silvia

AU - Prosperetti, Chiara

AU - Picconi, Barbara

AU - De Chiara, Valentina

AU - Mataluni, Giorgia

AU - Bernardi, Giorgio

AU - Calabresi, Paolo

AU - Centonze, Diego

PY - 2006/12/13

Y1 - 2006/12/13

N2 - Altered glutamate transmission in the striatum has been proposed to play a critical role in the pathophysiology of Huntington's disease (HD), a genetic disorder associated with impaired activity of the mitochondrial complex II (succinate dehydrogenase, SD). In the present study, we recorded spontaneous (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) from striatal neurons of both toxic (systemic administration of 3-nitropropionic acid in rats) and genetic models of HD (R6/2 transgenic mice). In both models, we found a significant down-regulation of glutamate transmission, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HD.

AB - Altered glutamate transmission in the striatum has been proposed to play a critical role in the pathophysiology of Huntington's disease (HD), a genetic disorder associated with impaired activity of the mitochondrial complex II (succinate dehydrogenase, SD). In the present study, we recorded spontaneous (sEPSCs) and miniature excitatory postsynaptic currents (mEPSCs) from striatal neurons of both toxic (systemic administration of 3-nitropropionic acid in rats) and genetic models of HD (R6/2 transgenic mice). In both models, we found a significant down-regulation of glutamate transmission, suggesting that reduced synaptic excitation of the input structure of the basal ganglia represents a physiological correlate of HD.

KW - Corticostriatal transmission

KW - eEPSCs

KW - Electrophysiology

KW - HD

KW - mEPSCs

UR - http://www.scopus.com/inward/record.url?scp=33750500719&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33750500719&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2006.09.056

DO - 10.1016/j.neulet.2006.09.056

M3 - Article

C2 - 17070651

AN - SCOPUS:33750500719

VL - 410

SP - 6

EP - 10

JO - Neuroscience Letters

JF - Neuroscience Letters

SN - 0304-3940

IS - 1

ER -