Carina C. Elvira
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Carina C. Elvira has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Amanda M. Catalfio
Department of Pharmacology, University of Michigan, Ann Arbor, MI, 48109, USA
1 shared publication - Andrew D. Nelson
Weill Institute for Neurosciences, University of California
1 shared publication Atehsa Sahagun
Weill Institute for Neurosciences, University of California
1 shared publicationHenry Kyoung
Weill Institute for Neurosciences, University of California
1 shared publication- Julie M. Philippe
Department of Pharmacology, University of Michigan Medical School
1 shared publication - Kendall P. Dean
Cellular and Molecular Biology Graduate Program, University Of Michigan, Ann Arbor, MI
1 shared publication
Latest Publications
- Open Access
Physical and functional convergence of the autism risk genes Scn2a and Ank2 in neocortical pyramidal cell dendrites
Dysfunction in sodium channels and their ankyrin scaffolding partners have both been implicated in neurodevelopmental disorders, including autism spectrum disorder (ASD). In particular, the genes SCN2A, which encodes the sodium channel NaV1.2, and ANK2, which encodes ankyrin-B, have strong ASD association. Recent studies indicate that ASD-associated haploinsufficiency in Scn2a impairs dendritic excitability and synaptic function in neocortical pyramidal cells, but how NaV1.2 is anchored within dendritic regions is unknown. Here, we show that ankyrin-B is essential for scaffolding NaV1.2 to the dendritic membrane of mouse neocortical neurons, and that haploinsufficiency of Ank2 phenocopies intrinsic dendritic excitability and synaptic deficits observed in Scn2a+/- conditions. Thus, these results establish a direct, convergent link between two major ASD risk genes and reinforce an emerging framework suggesting that neocortical pyramidal cell dendritic dysfunction can be etiological to neurodevelopmental disorder pathophysiology.
Open AccessPhysical and functional convergence of the autism risk genes Scn2a and Ank2 in neocortical pyramidal cell dendrites
Dysfunction in sodium channels and their ankyrin scaffolding partners have both been implicated in neurodevelopmental disorders, including autism spectrum disorder (ASD). In particular, the genes SCN2A, which encodes the sodium channel NaV1.2, and ANK2, which encodes ankyrin-B, have strong ASD association. Recent studies indicate that ASD-associated haploinsufficiency in Scn2a impairs dendritic excitability and synaptic function in neocortical pyramidal cells, but how NaV1.2 is anchored within dendritic regions is unknown. Here, we show that ankyrin-B is essential for scaffolding NaV1.2 to the dendritic membrane of mouse neocortical neurons, and that haploinsufficiency of Ank2 phenocopies intrinsic dendritic excitability and synaptic deficits observed in Scn2a+/- conditions. Thus, these results establish a direct, convergent link between two major ASD risk genes and reinforce an emerging framework suggesting that neocortical pyramidal cell dendritic dysfunction can be etiological to neurodevelopmental disorder pathophysiology.