High-frequency stimulation of both zona incerta and subthalamic nucleus induces a similar normalization of basal ganglia metabolic activity in experimental parkinsonism.

ABDELHAMID BENAZZOUZ, CHUN HWEI TAI, WASSILIOS MEISSNER, BERNARD BIOULAC, ERWAN BEZARD, CHRISTIAN GROSS
The FASEB Journal. 2004-03-01; 18(3): 528-530
DOI: 10.1096/fj.03-0576fje

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1. FASEB J. 2004 Mar;18(3):528-30. Epub 2004 Jan 8.

High-frequency stimulation of both zona incerta and subthalamic nucleus induces a
similar normalization of basal ganglia metabolic activity in experimental
parkinsonism.

Benazzouz A(1), Tai CH, Meissner W, Bioulac B, Bezard E, Gross C.

Author information:
(1)Basal Gang, Laboratoire de physiologie et physiopathologie de la signalization
cellulaire, CNRS UMR 5543, Université Victor Segalen, Bordeaux, France.

High-frequency stimulation (HFS) of the subthalamic nucleus (STN) alleviates
dramatically motor symptoms in Parkinson’s disease, and recently it has been
suggested that zona incerta (ZI) stimulation might be as beneficial to patients.
We used in situ cytochrome oxidase (CoI) mRNA hybridization to investigate and
compare the effects of HFS of the STN and the ZI on metabolic activity of the
STN, globus pallidus (GP), and substantia nigra reticulata (SNr) in normal rats
as well as in rats with 6-hydroxydopamine (6-OHDA) lesion, an animal model of
Parkinson’s disease. In normal rats, HFS of the STN, as well as of the ZI,
induced a significant decrease in CoI mRNA expression within the STN and SNr but
an increase within the GP. In 6-OHDA rats, HFS of the STN reversed dopamine
denervation-induced changes in the expression of CoI mRNA in the STN, SNr, and
GP. Similar results were obtained with HFS of the ZI except for the STN, which
showed only a trend toward normalization. These data suggest that the ZI, as well
as the STN, are implicated in the functional mechanism of HFS supporting the
involvement of GABA transmission for the reduction of neuronal activity in the
basal ganglia output structures.

DOI: 10.1096/fj.03-0576fje
PMID: 14715698 [Indexed for MEDLINE]

Auteurs Bordeaux Neurocampus