Subthalamic nucleus lesions

Baunez C, Robbins TW (1999) Effects of dopamine depletion of the dorsal striatum and further interaction with subthalamic nucleus lesions in an attentional task in the rat. Neuroscience 92 1343-1356. 

Henderson JM, Annett LE, Ryan LJ, Chiang W, Hidaka S, Torres EM, Dunnett SB (1999) Subthalamic nucleus lesions induce deficits as well as benefits in the hemiparkinsonian rat. Eur J Neurosci 11 2149-2151. 

Bergman, H., Wichmann, T. and DeLong, M. R. Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. Science 249 1436-1438,1990. 

Baunez C, Robbins TW (1997) Bilateral lesions of the subthalamic nucleus induce multiple deficits in an attentional task in rats. Eur J Neurosci 9 2086-2099. 

Phillips JM, Brown VJ (1999) Reaction time performance following unilateral striatal dopamine depletion and lesions of the subthalamic nucleus in the rat. Eur J Neurosci 77 1003-1010. 

Phillips JM, Latimer MP, Gupta S, Winn P, Brown VJ (1998) Excitotoxic lesions of the subthalamic nucleus ameliorate asymmetry induced by striatal dopamine depletion in the rat. Behav Brain Res 90 73-77. 

Various other lacunar syndromes have been described with rather poor clinical-pathological-anatomical correlation for example, chorea or hemiballismus usually appears to he caused by a lesion in the contralateral subthalamic nucleus or elsewhere in the basal ganglia and tends to get better (Ghika and Bogousslavsky 2001). 

Lesions in different anatomical sites of the structures that make up the motor loop can be used to create models of movement disorders (Fig. 1). When the subthalamic nucleus is lesioned, a disruption of the indirect pathway results the decline of glutamatergic stimulation of internal globus pallidus/substantia nigra zona reticulata (SNR) neurons via subthalamico-pallidonigral pathways reveals diminished inhibition of the excitatory thalamocortical pathways. The clinical consequence of this lesion is a proximal ballistic movement of the limbs. 

In a second paper Baunez et al. (1995) produced dopamine depletion in rats by infusing the neurotoxin 6-hydroxydopamine (6-OHDA) bilaterally into the dorsal part of the striatum. They found an increase in the number of delayed responses and a lengthening of RTs. Lesions of the subthalamic nucleus with ibotenic acid induced the opposite increase in the number of premature responses and a decrease of RTs. 

Baunez C, Nieoullon A, Amalric M (1995) In a rat model of parkinsonism, lesions of the subthalamic nucleus reverse increases of reaction time but induce a dramatic prematur responding deficit. J Neurosci 15(10) 6531-41... 

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