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Perseverative behavior underlying attentional set-shifting deficits in rats chronically treated with the neurotoxin 3-nitropropionic acid.
Exp Neurol. 2001 Nov; 172(1):172-81.EN

Abstract

Huntington's disease (HD) is generally considered a prototypic motor disorder, but cognitive deficits are also prominent features of the disease. Systemic administration of the mitochondrial toxin 3-nitropropionic acid (3NP) has been proposed to be a phenotypic model of HD in rats and nonhuman primates. In this study, we investigated the effect of 5 days continuous subcutaneous infusion of 3NP on motor and cognitive abilities in Lewis rats. Intoxicated animals developed a motor syndrome consisting of bradykinesia as well as gait abnormalities and dystonic hindlimbs. Results from learning tasks showed that these rats: (1) did not exhibit learning deficits per se in our discrimination task but showed impairments in inhibiting behavioral responses when a transfer of learning (to new stimuli) or a transfer of response (new position of the lever) was required; (2) showed a marked tendency to persevere in choosing the compartment they previously visited in a T maze, thus leading to a clear retardation in learning a reinforced alternation task; and (3) did not show any memory deficit when a delay was introduced. Six months later, histological analyses showed severe neurodegeneration within the lateral striatum accompanied by apparent cell loss in the ventral pallidum and entopedoncular nucleus. We suggest that the 3NP rat model of basal ganglia neurodegeneration may provide a useful model for studying certain fundamental aspects of the physiopathology of HD and for evaluating the functional efficacy of new therapeutic strategies.

Authors+Show Affiliations

Laboratoire de Neurobiologie de l'Apprentissage, de la Mémoire, et de la Communication, Unité Mixte de Recherche 8620, Centre National de la Recherche Scientifique, Bt 446, Université Paris-Sud, 91405 Orsay Cedex, France.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11681849

Citation

El Massioui, N, et al. "Perseverative Behavior Underlying Attentional Set-shifting Deficits in Rats Chronically Treated With the Neurotoxin 3-nitropropionic Acid." Experimental Neurology, vol. 172, no. 1, 2001, pp. 172-81.
El Massioui N, Ouary S, Chéruel F, et al. Perseverative behavior underlying attentional set-shifting deficits in rats chronically treated with the neurotoxin 3-nitropropionic acid. Exp Neurol. 2001;172(1):172-81.
El Massioui, N., Ouary, S., Chéruel, F., Hantraye, P., & Brouillet, E. (2001). Perseverative behavior underlying attentional set-shifting deficits in rats chronically treated with the neurotoxin 3-nitropropionic acid. Experimental Neurology, 172(1), 172-81.
El Massioui N, et al. Perseverative Behavior Underlying Attentional Set-shifting Deficits in Rats Chronically Treated With the Neurotoxin 3-nitropropionic Acid. Exp Neurol. 2001;172(1):172-81. PubMed PMID: 11681849.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Perseverative behavior underlying attentional set-shifting deficits in rats chronically treated with the neurotoxin 3-nitropropionic acid. AU - El Massioui,N, AU - Ouary,S, AU - Chéruel,F, AU - Hantraye,P, AU - Brouillet,E, PY - 2001/10/30/pubmed PY - 2002/1/5/medline PY - 2001/10/30/entrez SP - 172 EP - 81 JF - Experimental neurology JO - Exp Neurol VL - 172 IS - 1 N2 - Huntington's disease (HD) is generally considered a prototypic motor disorder, but cognitive deficits are also prominent features of the disease. Systemic administration of the mitochondrial toxin 3-nitropropionic acid (3NP) has been proposed to be a phenotypic model of HD in rats and nonhuman primates. In this study, we investigated the effect of 5 days continuous subcutaneous infusion of 3NP on motor and cognitive abilities in Lewis rats. Intoxicated animals developed a motor syndrome consisting of bradykinesia as well as gait abnormalities and dystonic hindlimbs. Results from learning tasks showed that these rats: (1) did not exhibit learning deficits per se in our discrimination task but showed impairments in inhibiting behavioral responses when a transfer of learning (to new stimuli) or a transfer of response (new position of the lever) was required; (2) showed a marked tendency to persevere in choosing the compartment they previously visited in a T maze, thus leading to a clear retardation in learning a reinforced alternation task; and (3) did not show any memory deficit when a delay was introduced. Six months later, histological analyses showed severe neurodegeneration within the lateral striatum accompanied by apparent cell loss in the ventral pallidum and entopedoncular nucleus. We suggest that the 3NP rat model of basal ganglia neurodegeneration may provide a useful model for studying certain fundamental aspects of the physiopathology of HD and for evaluating the functional efficacy of new therapeutic strategies. SN - 0014-4886 UR - https://www.unboundmedicine.com/medline/citation/11681849/Perseverative_behavior_underlying_attentional_set_shifting_deficits_in_rats_chronically_treated_with_the_neurotoxin_3_nitropropionic_acid_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014488601977660 DB - PRIME DP - Unbound Medicine ER -