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Titolo:
Fragile X mice develop sensory hyperreactivity to auditory stimuli
Autore:
Chen, L; Toth, M;
Indirizzi:
Cornell Univ, Weill Med Coll, Dept Pharmacol, New York, NY 10021 USA Cornell Univ New York NY USA 10021 Dept Pharmacol, New York, NY 10021 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 4, volume: 103, anno: 2001,
pagine: 1043 - 1050
SICI:
0306-4522(2001)103:4<1043:FXMDSH>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
MENTAL-RETARDATION PROTEIN; TISSUE-SPECIFIC EXPRESSION; INFERIOR COLLICULUS; AUDIOGENIC-SEIZURES; ACOUSTIC STARTLE; TRANSGENIC MICE; WISTAR RATS; EPILEPSY; GENE; FMR-1;
Keywords:
prepulse inhibition; audiogenic seizure; fragile X syndrome; FMRP; c-Fos;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Toth, M Cornell Univ, Weill Med Coll, Dept Pharmacol, 1300 York Ave,LC 522, New York, NY 10021 USA Cornell Univ 1300 York Ave,LC 522 New York NY USA 10021 10021 USA
Citazione:
L. Chen e M. Toth, "Fragile X mice develop sensory hyperreactivity to auditory stimuli", NEUROSCIENC, 103(4), 2001, pp. 1043-1050

Abstract

Fragile X syndrome is the most prevalent cause of mental retardation. It is usually caused by the transcriptional inactivation of the FMR-I gene. Although the cognitive defect is the most recognized symptom of fragile X syndrome, patients also show behavioral problems such as hyperarousal, hyperactivity, autism, aggression, anxiety and increased sensitivity to sensory stimuli. Here we investigated whether fragile X mice (fmr-1 gene knockout mice) exhibit abnormal sensitivity to sensory stimuli. First, hyperreactivity of fragile X mice to auditory stimulus was indicated in the prepulse inhibition paradigm. A moderately intense prepulse tone, that suppresses startle response to a strong auditory stimulus, elicited a significantly stronger effect in fragile X than in control mice. Second, sensory hyperreactivity of fragile X mice was demonstrated by a high seizure susceptibility to auditory stimulation. Selective induction of c-Fos, an early-immediate gene product, indicated that seizures involve auditory brainstem and thalamic nuclei. Audiogenic seizures were not due to a general increase in brain excitability because three different chemical convulsants (kainic acid, bicuculline and pentylenetetrazole) elicited similar effects in fragile X and wild-type mice. These data are consistent with the increased responsiveness of fragile X patients to auditory stimuli. The auditory hypersensitivity suggests an abnormal processing in the auditory system of fragile X mice, which could provide a useful model to study the molecular and cellular changes underlying fragile X syndrome. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 17/01/20 alle ore 20:19:18