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Titolo:
HEREDITARY DEFICIENCIES IN COMPLEMENT C5 ARE ASSOCIATED WITH INTENSIFIED NEURODEGENERATIVE RESPONSES THAT IMPLICATE NEW ROLES FOR THE C-SYSTEM IN NEURONAL AND ASTROCYTIC FUNCTIONS
Autore:
PASINETTI GM; TOCCO G; SAKHI S; MUSLEH WD; DESIMONI MG; MASCARUCCI P; SCHREIBER S; BAUDRY M; FINCH CE;
Indirizzi:
MT SINAI MED CTR,DEPT PSYCHIAT NEW YORK NY 10029 BROOKDALE CTR MOL BIOL NEW YORK NY 10029 UNIV SO CALIF,DEPT NEUROBIOL LOS ANGELES CA 90089 UNIV SO CALIF,SCH MED,DEPT NEUROL LOS ANGELES CA 90089 MARIO NEGRI INST PHARMACOL RES I-20157 MILAN ITALY UNIV SO CALIF,ETHEL PERCY ANDRUS GERONTOL CTR,NEUROGERONTOL DIV LOS ANGELES CA 90089 UNIV SO CALIF,DEPT NEUROBIOL LOS ANGELES CA 90089
Titolo Testata:
Neurobiology of disease
fascicolo: 3, volume: 3, anno: 1996,
pagine: 197 - 204
SICI:
0969-9961(1996)3:3<197:HDICCA>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALZHEIMERS-DISEASE; RAT-BRAIN; APOLIPOPROTEIN-E; MESSENGER-RNAS; EXPRESSION; MICE; INTERLEUKIN-6; RECEPTOR; ACTIVATION; COMPONENTS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
G.M. Pasinetti et al., "HEREDITARY DEFICIENCIES IN COMPLEMENT C5 ARE ASSOCIATED WITH INTENSIFIED NEURODEGENERATIVE RESPONSES THAT IMPLICATE NEW ROLES FOR THE C-SYSTEM IN NEURONAL AND ASTROCYTIC FUNCTIONS", Neurobiology of disease, 3(3), 1996, pp. 197-204

Abstract

Possible roles of the complement (C) system in the normal and injuredbrain were explored with inbred mice that carried a frameshift mutation in the C5 gene. A congenic pair was used: the CS-sufficient (C5(+))B10.D2/nSnJ strain with the functional allele (Hc1) from the C57BL/10J donor strain was compared with the C5-deficient (C5(-)) B10.D2/oSnJ with the Hc0 allele from the C5-deficient DBA/2J donor strain. In response to the excitotoxin kainic acid (KA), C5(-) mice had more hippocampal pyramidal neuron death and greater induction of astrocyte mRNAs (GFAP, apoE, apoJ). In primary astrocyte cultures from unlesioned mice, an inflammatory stimulus (LPS) caused greater production of IL-6 and TNF production in C5(-) mice. These enhanced responses to KA and LPS suggest that hereditary C5 deficits modify responses to neurodegenerative stimuli of neurons and astrocytes. Moreover, unlesioned C5(-) mice had smaller input-output slopes for the NMDA component of the EPSP amplitude, but enhanced the Ca+2-dependent AMPA binding. Thus, C5 deficitsalso modify basal properties of glutamatergic neurotransmission that pertain to synaptic plasticity, These findings are also discussed in relation to roles of the C-system in Alzheimer disease (AD). C5 deficiencies may also be considered in the choice of strains as transgene hosts and for genetic analysis of normal and pathological brain functions. In recent transgenic studies for AD, C5(-) hosts showed greater neurodegeneration, consistent with the present data. These pleiotropic associations of C5 deficiency indicate roles for the C-system in neurodegeneration, but also in normal neural functions. (C) 1996 Academic Press, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 09:26:06