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
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.