Spermine improves recognition memory deficit in a rodent model of Huntington’s disease

Huntington’s disease (HD) is a progressive neurodegenerative disorder associated with motor and cognitive impairment. Intrastriatal administration of quinolinic acid (QA) causes neurodegeneration, glial proliferation and cognitive impairment in animals, which are similar to these seen in human HD. S...

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Bibliographic Details
Published in:Neurobiology of learning and memory 2009-11, Vol.92 (4), p.574-580
Main Authors: Velloso, Nádia A., Dalmolin, Gerusa D., Gomes, Guilherme M., Rubin, Maribel A., Canas, Paula M., Cunha, Rodrigo A., Mello, Carlos F.
Format: Article
Language:English
Subjects:
Adult and adolescent clinical studies
Analysis of Variance
Animals
Astrocytes
Behavioral psychophysiology
Biological and medical sciences
Cognitive ability
Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
Disease Models, Animal
Dose-Response Relationship, Drug
Excitatory Amino Acid Agonists - therapeutic use
Fundamental and applied biological sciences. Psychology
Huntington Disease - chemically induced
Huntington Disease - complications
Huntington Disease - drug therapy
Huntingtons disease
Huntington’s disease
Male
Medical sciences
Memory
Memory Disorders - complications
Memory Disorders - drug therapy
Motor ability
Neostriatum - drug effects
Nervous system (semeiology, syndromes)
Nervous system as a whole
Neurology
Nootropic Agents - therapeutic use
Object discrimination
Organic mental disorders. Neuropsychology
Psychology. Psychoanalysis. Psychiatry
Psychology. Psychophysiology
Psychopathology. Psychiatry
Quinolinic Acid
Rats
Rats, Wistar
Receptors, N-Methyl-D-Aspartate - agonists
Recognition (Psychology) - drug effects
Rodents
Spermine
Spermine - therapeutic use
Statistics, Nonparametric
Striatum
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Summary:Huntington’s disease (HD) is a progressive neurodegenerative disorder associated with motor and cognitive impairment. Intrastriatal administration of quinolinic acid (QA) causes neurodegeneration, glial proliferation and cognitive impairment in animals, which are similar to these seen in human HD. Since polyamines improve memory in cognitive tasks, we now tested if the post-training intrastriatal administration of spermine, an agonist of the polyamine site at the NMDA receptor, reverses the deficits in the object recognition task induced by QA. Bilateral striatal injections of QA (180 or 360 nmol/site) caused object recognition impairment, neuronal death and reactive astrogliosis. A single injection of spermine (0.1 and 1 nmol/site), 5 days after QA injection, reversed QA-induced impairment of object recognition task. Spermine (0.1 nmol/site) also inhibited QA-induced reactive astrogliosis measured by a semi-quantitative determination of GFAP immunolabelling, but did not alter neuronal death, measured by a semi-quantitative determination of fluoro-Jade C staining. These results suggest that polyamine binding sites may be considered a novel therapeutic target to prevent reactive astrogliosis and mnemonic deficits in HD.
ISSN:1074-7427
1095-9564
DOI:10.1016/j.nlm.2009.07.006