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Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: a potential novel treatment in a rat model of Huntington's disease.
Mov Disord. 2003 Dec; 18(12):1499-507.MD

Abstract

Symptoms in the early stages of Huntington's disease (HD) are assumed to reflect basal ganglia circuit dysfunction secondary to degeneration of striatal projections to the external segment of the globus pallidus (GPe). The hypothesis that GPe lesion would ameliorate HD symptoms by "normalizing" the circuit's functioning was tested in a rat model of this disease. The performance of rats sustaining quinolinic acid lesion to the striatum (a rat model of HD) in a position discrimination and reversal task was compared with the performance of rats sustaining in addition a bilateral excitotoxic lesion to the globus pallidus (GP) carried out simultaneously with the striatal lesion (Experiment 1) or 1 month after the striatal lesion (Experiment 2), as well as a unilateral temporary lesion of the GP (Experiment 3). The striatal lesion-induced deficit in the task was effectively reversed by a bilateral excitotoxic GP lesion carried out simultaneously or 1 month after the striatal lesion, as well as by a temporary unilateral GP inactivation. Given that a similar dysfunction of basal ganglia circuitry is thought to subserve the behavioral alterations seen in quinolinic acid lesioned rats and some of the symptoms in HD, these results raise the possibility that lesion or inactivation of the GPe may alleviate some of HD symptoms.

Authors+Show Affiliations

Department of Psychology, Tel-Aviv University, Tel-Aviv, Israel. djoel@post.tau.ac.ilNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Evaluation Study
Journal Article

Language

eng

PubMed ID

14673887

Citation

Joel, Daphna, et al. "Deficits Induced By Quinolinic Acid Lesion to the Striatum in a Position Discrimination and Reversal Task Are Ameliorated By Permanent and Temporary Lesion to the Globus Pallidus: a Potential Novel Treatment in a Rat Model of Huntington's Disease." Movement Disorders : Official Journal of the Movement Disorder Society, vol. 18, no. 12, 2003, pp. 1499-507.
Joel D, Ayalon L, Tarrasch R, et al. Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: a potential novel treatment in a rat model of Huntington's disease. Mov Disord. 2003;18(12):1499-507.
Joel, D., Ayalon, L., Tarrasch, R., & Weiner, I. (2003). Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: a potential novel treatment in a rat model of Huntington's disease. Movement Disorders : Official Journal of the Movement Disorder Society, 18(12), 1499-507.
Joel D, et al. Deficits Induced By Quinolinic Acid Lesion to the Striatum in a Position Discrimination and Reversal Task Are Ameliorated By Permanent and Temporary Lesion to the Globus Pallidus: a Potential Novel Treatment in a Rat Model of Huntington's Disease. Mov Disord. 2003;18(12):1499-507. PubMed PMID: 14673887.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Deficits induced by quinolinic acid lesion to the striatum in a position discrimination and reversal task are ameliorated by permanent and temporary lesion to the globus pallidus: a potential novel treatment in a rat model of Huntington's disease. AU - Joel,Daphna, AU - Ayalon,Liat, AU - Tarrasch,Ricardo, AU - Weiner,Ina, PY - 2003/12/16/pubmed PY - 2004/4/29/medline PY - 2003/12/16/entrez SP - 1499 EP - 507 JF - Movement disorders : official journal of the Movement Disorder Society JO - Mov Disord VL - 18 IS - 12 N2 - Symptoms in the early stages of Huntington's disease (HD) are assumed to reflect basal ganglia circuit dysfunction secondary to degeneration of striatal projections to the external segment of the globus pallidus (GPe). The hypothesis that GPe lesion would ameliorate HD symptoms by "normalizing" the circuit's functioning was tested in a rat model of this disease. The performance of rats sustaining quinolinic acid lesion to the striatum (a rat model of HD) in a position discrimination and reversal task was compared with the performance of rats sustaining in addition a bilateral excitotoxic lesion to the globus pallidus (GP) carried out simultaneously with the striatal lesion (Experiment 1) or 1 month after the striatal lesion (Experiment 2), as well as a unilateral temporary lesion of the GP (Experiment 3). The striatal lesion-induced deficit in the task was effectively reversed by a bilateral excitotoxic GP lesion carried out simultaneously or 1 month after the striatal lesion, as well as by a temporary unilateral GP inactivation. Given that a similar dysfunction of basal ganglia circuitry is thought to subserve the behavioral alterations seen in quinolinic acid lesioned rats and some of the symptoms in HD, these results raise the possibility that lesion or inactivation of the GPe may alleviate some of HD symptoms. SN - 0885-3185 UR - https://www.unboundmedicine.com/medline/citation/14673887/Deficits_induced_by_quinolinic_acid_lesion_to_the_striatum_in_a_position_discrimination_and_reversal_task_are_ameliorated_by_permanent_and_temporary_lesion_to_the_globus_pallidus:_a_potential_novel_treatment_in_a_rat_model_of_Huntington's_disease_ L2 - https://doi.org/10.1002/mds.10622 DB - PRIME DP - Unbound Medicine ER -