Mapping of globus pallidus and ventral pallidum lesions that produce hyperkinetic treading.
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., Behav. Neurosci., 104 (1990) 778-795). Bilateral excitotoxin lesions were made using quinolinic acid (10 micrograms in 1 microliter) in the caudate/putamen, nucleus accumbens, globus pallidus or ventral pallidum/substantia innominata. In order to identify the precise center, borders, severity and size of lesion sites that caused these hyperkinetic treading syndromes, neuron counts (modified fractionator technique) and glial fibrillary acidic protein immunoreactivity (GFAP-IR) densitometry were used in 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% neuron loss bilaterally within a 0.8 x 1.0 x 1.0 mm subregion of the ventromedial GP produced this syndrome. The site of lesions that produced the combined syndrome of hyperkinetic treading and aversive enhancement was ventral to the globus pallidus, within the ventral pallidum/substantia innominata (VP/SI). Damage exceeding 70% neuron loss bilaterally within a 1.0 x 0.5 x 1.0 mm diameter subregion of the ventromedial ventral pallidum/substantia innominata produced this syndrome. This subterritory was located immediately lateral to the border of the lateral hypothalamus. Bilateral lesions to the caudate/putamen or nucleus accumbens did not produce either hyperkinetic treading syndrome. These results are discussed in terms of the connectivity of the ventral pallidal/substantia innominata and globus pallidus regions and in terms of neuropathological models of hyperkinetic disorders.
Cromwell
H C
HC
Department of Psychology, University of Michigan, Ann Arbor 48104, USA.
Berridge
K C
KC
D000818:Animals; D001931:Brain Mapping; D002452:Cell Count; D005247:Feeding Behavior / Q000187:drug effects / Q000502:physiology*; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D005917:Globus Pallidus / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D006948:Hyperkinesis / Q000139:chemically induced / Q000503:physiopathology*; D007150:Immunohistochemistry; D008297:Male; D017072:Neostriatum / Q000502:physiology; D009714:Nucleus Accumbens / Q000502:physiology; D017378:Quinolinic Acid; D051381:Rats; D017207:Rats, Sprague-Dawley; D013377:Substantia Innominata / Q000502:physiology; D013649:Taste / Q000502:physiology
D005904:Glial Fibrillary Acidic Protein; D017378:Quinolinic Acid