Parole chiave di "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"

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• Parole chiave di "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)
• Keywords of "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)

Insieme di parole chiave di

• 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) (Prodotto della ricerca)

Ha membro

• SOD1G93A mutation (Parola chiave)
• AMPA and NMDA receptors (Parola chiave)
• cortical synaptic plasticity (Parola chiave)
• dendrite outgrowth (Parola chiave)
• familial amyotrophic lateral sclerosis (fALS) (Parola chiave)

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Insieme di parole chiave

• 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) (Prodotto della ricerca)

Membro di

• dendrite outgrowth (Parola chiave)
• cortical synaptic plasticity (Parola chiave)
• familial amyotrophic lateral sclerosis (fALS) (Parola chiave)
• SOD1G93A mutation (Parola chiave)
• AMPA and NMDA receptors (Parola chiave)