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Titolo:
The flathead mutation causes CNS-Specific developmental abnormalities and apoptosis
Autore:
Roberts, MR; Bittman, K; Li, WW; French, R; Mitchell, B; LoTurco, JJ; DMello, SR;
Indirizzi:
Univ Texas, Dept Mol & Cell Biol, Richardson, TX 75083 USA Univ Texas Richardson TX USA 75083 & Cell Biol, Richardson, TX 75083 USA Univ Connecticut, Dept Physiol & Neurobiol, Storrs, CT 06269 USA Univ Connecticut Storrs CT USA 06269 ol & Neurobiol, Storrs, CT 06269 USA Univ Connecticut, Dept Pathobiol, Storrs, CT 06269 USA Univ Connecticut Storrs CT USA 06269 Dept Pathobiol, Storrs, CT 06269 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 6, volume: 20, anno: 2000,
pagine: 2295 - 2306
SICI:
0270-6474(20000315)20:6<2295:TFMCCD>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
PURKINJE-CELL DEGENERATION; EMBRYONIC-DEVELOPMENT; CEREBELLAR CORTEX; MOUSE CEREBELLUM; CEREBRAL-CORTEX; RAT CEREBELLUM; MICE LACKING; MUTANT MICE; DEATH; MIGRATION;
Keywords:
proliferation; seizures; neural development; neurological mutant; apoptosis; autosomal recessive;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
37
Recensione:
Indirizzi per estratti:
Indirizzo: D'Mello, SR Univ Texas, Dept Mol & Cell Biol, 2601 N Floyd Rd, Richardson,TX 75083 USA Univ Texas 2601 N Floyd Rd Richardson TX USA 75083 X 75083 USA
Citazione:
M.R. Roberts et al., "The flathead mutation causes CNS-Specific developmental abnormalities and apoptosis", J NEUROSC, 20(6), 2000, pp. 2295-2306

Abstract

We describe a new mutation, flathead ( fh), that arose spontaneously in aninbred colony of Wistar rats. The mutation is autosomal recessive, and thebehavioral phenotype of fh/fh rats includes spontaneous seizures, tremor, impaired coordination, and premature death. A striking feature of the fh mutation is a dramatic reduction in brain size (40% of normal at birth). In contrast, no abnormalities are evident in the peripheral nervous system or in other tissues outside of the CNS. Although bromodeoxyuridine incorporation assays indicate that the rate of cell proliferation in the fh/fh cortex is similar to that of unaffected animals, in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin end-labeling assays reveal a dramatic increase in apoptotic cell death beginning after embryonic day 16 (E16). At E18there is a 20-fold increase in cell death in the ventricular zone of fh/fhneocortex, and at postnatal day 1 (P1), the number of apoptotic cells is still two times that of normal. However, by P8 the extent of cell death in fh/fh is comparable to that of unaffected littermates, indicating that the reduction in brain growth is caused by abnormally high apoptosis during a discrete developmental period. Late-developing structures such as the cerebellum, neocortex, hippocampus, and retina are most severely affected by the fh mutation. Within these structures, later-generated neuronal populations are selectively depleted. Together, these results suggest that the flathead gene is essential for a developmental event required for the generation andmaturation of late-born cell populations in the brain.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:31:10