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.

Centonze, D., Rossi, S., Gubellini, P., De Chiara, V., Tscherter, A., Prosperetti, C., et al. (2006). Deficits of glutamate transmission in the striatum of experimental hemiballism. NEUROSCIENCE, 143(1), 213-221 [10.1016/j.neuroscience.2006.07.024].

Deficits of glutamate transmission in the striatum of experimental hemiballism

CENTONZE, DIEGO;BERNARDI, GIORGIO;CALABRESI, PAOLO;
2006-11-17

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.
17-nov-2006
Pubblicato
Rilevanza internazionale
Articolo
Sì, ma tipo non specificato
Settore MED/26 - NEUROLOGIA
English
Con Impact Factor ISI
Dopamine Antagonists; Inhibitory Postsynaptic Potentials; Corpus Striatum; Dyskinesias; Rats; Animals; Triazines; Electric Stimulation; Patch-Clamp Techniques; Rats, Sprague-Dawley; Glutamic Acid; Disease Models, Animal; Tetrodotoxin; Excitatory Postsynaptic Potentials; Anesthetics, Local; Triazoles; Synaptic Transmission; Sulpiride
Centonze, D., Rossi, S., Gubellini, P., De Chiara, V., Tscherter, A., Prosperetti, C., et al. (2006). Deficits of glutamate transmission in the striatum of experimental hemiballism. NEUROSCIENCE, 143(1), 213-221 [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
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/28053
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