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.
Rossi, S., Prosperetti, C., Picconi, B., De Chiara, V., Mataluni, G., Bernardi, G., et al. (2006). Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease. NEUROSCIENCE LETTERS, 410(1), 6-10 [10.1016/j.neulet.2006.09.056].
Deficits of glutamate transmission in the striatum of toxic and genetic models of Huntington's disease
BERNARDI, GIORGIO;CALABRESI, PAOLO;CENTONZE, DIEGO
2006-12-13
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.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
