MAPPING OF GLOBUS-PALLIDUS AND VENTRAL PALLIDUM LESIONS THAT PRODUCE HYPERKINETIC TREADING

Citation
Hc. Cromwell et Kc. Berridge, MAPPING OF GLOBUS-PALLIDUS AND VENTRAL PALLIDUM LESIONS THAT PRODUCE HYPERKINETIC TREADING, Brain research, 668(1-2), 1994, pp. 16-29
Citations number
82
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
0006-8993
Volume
668
Issue
1-2
Year of publication
1994
Pages
16 - 29
Database
ISI
SICI code
0006-8993(1994)668:1-2<16:MOGAVP>2.0.ZU;2-R
Abstract
The purpose of this study was to identify sites where striatopallidal lesions produce two distinct sensory-triggered hyperkinetic syndromes: (1) exaggerated forelimb treading alone to oral taste infusions and ( 2) sensorimotor exaggerated treading plus enhanced aversive reactions to taste infusions. The behavioral characteristics of these syndromes have been described previously (Berridge, K.C. and Cromwell, H.C., Beh av. Neurosci., 104 (1990) 778-795). Bilateral excitotoxin lesions were made using quinolinic acid (10 mu g in 1 mu l) in the caudate/putamen , nucleus accumbens, globus pallidus or ventral pallidum/substantia in nominata. In order to identify the precise center, borders, severity a nd size of lesion sites that caused these hyperkinetic treading syndro mes, neuron counts (modified fractionator technique) and glial fibrill ary acidic protein immunoreactivity (GFAP-IR) densitometry were used i n a stereological mapping analysis. The site of lesions that produced the hyperkinetic treading syndrome without enhanced aversion was found to be restricted to the globus pallidus (GP). Damage exceeding 60% ne uron loss bilaterally within a 0.8 x 1.0 x 1.0 mm subregion of the ven tromedial GP produced this syndrome. The site of lesions that produced the combined syndrome of hyperkinetic treading and aversive enhanceme nt was ventral to the globus pallidus, within the ventral pallidum/sub stantia innominata (VP/SI). Damage exceeding 70% neuron loss bilateral ly within a 1.0 x 0.5 x 1.0 mm diameter subregion of the ventromedial ventral pallidum/substantia innominata produced this syndrome. This su bterritory was located immediately lateral to the border of the latera l hypothalamus. Bilateral lesions to the caudate/putamen or nucleus ac cumbens did not produce either hyperkinetic treading syndrome. These r esults are discussed in terms of the connectivity of the ventral palli dal/substantia innominata and globus pallidus regions and in terms of neuropathological models of hyperkinetic disorders.