http://www.cnr.it/ontology/cnr/individuo/prodotto/ID59320

Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for ALS (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for ALS (Articolo in rivista) (literal)

Anno

2011-01-01T00:00:00+01:00 (literal)

Alternative label

Spalloni A.1,Origlia N.2, Sgobio C.1, Trabalza A.1,3, Nutini M.1,4, Berretta N.1, Bernardi G.4, Domenici L.2,5, Ammassari-Teule M.1,6, Longone P.1 (2011)
Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for ALS
in Cerebral cortex (N. Y. N. Y., 1991)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Spalloni A.1,Origlia N.2, Sgobio C.1, Trabalza A.1,3, Nutini M.1,4, Berretta N.1, Bernardi G.4, Domenici L.2,5, Ammassari-Teule M.1,6, Longone P.1 (literal)

Pagina inizio

796 (literal)

Pagina fine

805 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#altreInformazioni

DOI: http://dx.doi.org/10.1093/cercor/bhq152 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

21(4) (literal)

Rivista

Cerebral cortex (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note

(*) L'Unità Operativa di Servizio dell'Istituto di Neuroscienze di Roma è stata soppressa il 12/1/2011 con provvedimento prot. n. 0002130 ed è confluita nell'IBCN, costituito il 21/12/2010 con provvedimento prot. n. 0091899. (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

1 - Department of Experimental Neurology, Santa Lucia Foundation, 00143 Rome, Italy; 2 - CNR Institute for Neuroscience, 56124 Pisa, Italy; 3 - Department of Psychology, University \"La Sapienza,\" 00185 Rome, Italy; 4 - Department of Neuroscience, Tor Vergata University, 00133 Rome, Italy; 5- Department of Scienze e Tecnologie Biomediche, School of Medicine, University of L'Aquila, 67010, Italy; 6 - CNR Institute for Neuroscience, 00143 Rome, Italy(*). (literal)

Titolo

Postsynaptic alteration of NR2A subunit and defective autophosphorylation of alphaCaMKII at threonine-286 contribute to abnormal plasticity and morphology of upper motor neurons in presymptomatic SOD1G93A mice, a murine model for ALS (literal)

Abstract

Although amyotrophic lateral sclerosis (ALS) has long been considered as a lower motor neuron (MN) disease, degeneration of upper MNs arising from a combination of mechanisms including insufficient growth factor signaling and enhanced extracellular glutamate levels is now well documented. The observation that these mechanisms are altered in presymptomatic superoxide dismutase (SOD1) mice, an ALS mouse model, suggests that defective primary motor cortex (M1) synaptic activity might precede the onset of motor disturbances. To examine this point, we assessed the composition of AMPAR and NMDAR subunits and of the alphaCa(2+)/calmodulin-dependent kinase autophosphorylation at threonine-286 in the triton insoluble fraction from the M1 in postnatal P80-P85 SOD1(G93A) and wild-type mice. We show that presymptomatic SOD1(G93A) exhibit a selective decrease of NR2A subunit expression and of the alphaCa(2+)/calmodulin-dependent kinase autophosphorylation at threonine-286 in the triton insoluble fraction of upper MNs synapses. These molecular alterations are associated with synaptic plasticity defects, and a reduction in upper MN dendritic outgrowth revealing that abnormal neuronal connectivity in the M1 region precedes the onset of motor symptoms. We suggest that the progressive disruption of M1 corticocortical connections resulting from the SOD1(G93A) mutation might extend to adjacent regions and promote development of cognitive/dementia alterations frequently associated with ALS. (literal)

Prodotto di