[Behavior characterization of a model of Huntington's disease in rats, induced by quinolinic acid].
BACKGROUND
Huntington's disease (HD) is a progressive neurodegenerative disorder, characterized by severe degeneration of basal ganglia neurons. Behavioral symptoms of HD include abnormal, uncontrollable and constant choreiform movements, impaired cognitive function and emotional disturbance.


OBJECTIVE
In order to explore the changes of cognitive and motor functions induced by quinolinate lesion we realized this experiment.


METHODS
We studied the behavior of rats with unilateral quinolinate induced lesions of the medial striatum. Intact 3 months old male rats (n = 23) were trained in the Morris Water Maze during three consecutive days, eight trials/day (acquisition), and before surgery they were randomly assigned either to intact or lesion groups. Fifteen days after the lesion the rats were tested using retention test (one day/four trials, with the escape platform in the same position as in acquisition test), on the next three days the rats were tested in the transfer test (three days/eight trials-day, with the platform in the new position). The Paw reaching test and the asymmetrical rotational behavior test in respond to amphetamine were also tested in these rats.


RESULTS
Lesioned animals exhibited deficient retrieval of stored memories of visuospatial skills and impaired transfer of learning. In relation with motor activity the lesioned rats showed a profound impairment in the skill of the left forelimb for reaching food compared with its right forelimb as well as with the forelimb abilities of intact rats. The lesioned animals showed significant rotational behavior induced by amphetamine agonist, ipsilateral to the lesioned striatum.


CONCLUSIONS
These results are consistent with the notion that the striatal degeneration could sufficiently account for the cognitive abnormalities associated with HD, and with the key role played by basal ganglia in enabling voluntary and postural adjustment of the movements.
Francis
L
L
Laboratorio de Biomodelos, Centro Internacional de Restauración Neurológica, La Habana, Cuba. pedago@teleda.get.cma.net
Cruz
R
R
Antúnez
I
I
Rosillo
J C
JC
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D003071:Cognition / Q000187:drug effects; D003342:Corpus Striatum / Q000378:metabolism; D004195:Disease Models, Animal; D018690:Excitatory Amino Acid Agonists / Q000009:adverse effects* / Q000493:pharmacokinetics; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006816:Huntington Disease / Q000139:chemically induced*; D007150:Immunohistochemistry; D008124:Locomotion / Q000187:drug effects; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D017378:Quinolinic Acid / Q000009:adverse effects* / Q000493:pharmacokinetics; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects; D012153:Retention, Psychology / Q000187:drug effects; D013037:Spatial Behavior / Q000187:drug effects; D014796:Visual Perception / Q000187:drug effects
D018690:Excitatory Amino Acid Agonists; D005904:Glial Fibrillary Acidic Protein; D016194:Receptors, N-Methyl-D-Aspartate; D017378:Quinolinic Acid