Electrophysiological and metabolic evidence that high-frequency stimulation of the subthalamic nucleus bridles neuronal activity in the subthalamic nucleus and the substantia nigra reticulata.

CHUN-HWEI TAI, THOMAS BORAUD, ERWAN BEZARD, BERNARD BIOULAC, CHRISTIAN GROSS, ABDELHAMID BENAZZOUZ
The FASEB Journal. 2003-10-01; 17(13): 1820-1830
DOI: 10.1096/fj.03-0163com

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1. FASEB J. 2003 Oct;17(13):1820-30.

Electrophysiological and metabolic evidence that high-frequency stimulation of
the subthalamic nucleus bridles neuronal activity in the subthalamic nucleus and
the substantia nigra reticulata.

Tai CH(1), Boraud T, Bezard E, Bioulac B, Gross C, Benazzouz A.

Author information:
(1)Laboratoire de Neurophysiologie, Basal Gang, CNRS UMR 5543, Université Victor
Segalen, 146, Rue Léo-Saignat, 33076 Bordeaux Cedex, France.

High-frequency stimulation (HFS) of the subthalamic nucleus (STN) has been shown
to produce a dramatic alleviation of motor symptoms in patients with advanced
Parkinson’s disease. Its functional mechanism, however, remains obscure. We used
extracellular recording and in situ cytochrome oxidase (CoI) mRNA hybridization
to investigate the effects of HFS of the STN on neuronal activity of the STN and
the substantia nigra reticulata (SNr) in normal rats and rats with
6-hydroxydopamine (6-OHDA) lesion of the substantia nigra compacta (SNc). To
allow detection of spikes and analysis of firing activity, artifacts recorded
during stimulation were scaled down using a template subtraction method. In both
normal and lesioned rats, the activity of a majority of STN neurons was inhibited
during stimulation. In the SNr, HFS also induced an inhibition of the activity of
a majority of neurons in normal and lesioned rats. In situ hybridization
histochemistry confirmed these results in that it showed a significant decrease
in levels of CoI mRNA expression in the STN and SNr in both normal and lesioned
rats during stimulation. These data afford an interesting insight into the
functional mechanism of deep brain stimulation and support the hypothesis that
HFS exerts an inhibitory influence on STN neuronal firing.

DOI: 10.1096/fj.03-0163com
PMID: 14519661 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus