Recommended Conferences

Genetic Engineering and Gene Therapy

Paris, France

Human Genetics and Genetic Disorders

Miami, USA

Tissue Engineering and Regenerative Medicine

Chicago, USA
Related Subjects

Impaired firing and cell-specific compensation in neurons lacking nav1

Author(s): Van Wart A, Matthews G


The ability of neurons to fire precise patterns of action potentials is critical for encoding inputs and efficiently driving target neurons. At the axon initial segment and nodes of Ranvier, where nerve impulses are generated and propagated, a high density of Nav1.2 sodium channels is developmentally replaced by Nav1.6 channels. In retinal ganglion cells (GCs), this isoform switch coincides with the developmental transition from single spikes to repetitive firing. Also, Nav1.6 channels are required for repetitive spiking in cerebellar Purkinje neurons. These previous observations suggest that the developmental appearance of Nav1.6 underlies the transition to repetitive spiking in GCs. To test this possibility, we recorded from GCs of med (Nav1.6-null) and wild-type mice during postnatal development. By postnatal day 18, when the switch to Nav1.6 at GC initial segments is normally complete, the maximal sustained and instantaneous firing rates were lower in med than in wild-type GCs, demonstrating that Nav1.6 channels are necessary to attain physiologically relevant firing frequencies in GCs. However, the firing impairment was milder than that reported previously in med Purkinje neurons, which prompted us to look for differences in compensatory sodium channel expression. Both Nav1.2 and Nav1.1 channels accumulated at initial segments and nodes of med GCs, sites normally occupied by Nav1.6. In med Purkinje cells, only Nav1.1 channels were found at initial segments, whereas in other brain regions, only Nav1.2 was detected at med initial segments and nodes. Thus, compensatory mechanisms in channel isoform distribution are cell specific, which likely results in different firing properties.

Similar Articles

Rat hippocampal neurons in dispersed cell culture

Author(s): Banker GA, Cowan WM

C1q induction and global complement pathway activation do not contribute to ALS toxicity in mutant SOD1 mice

Author(s): Lobsiger CS, Boillee S, Pozniak C, Khan AM, McAlonis-Downes M, et al.

A dramatic increase of C1q protein in the CNS during normal aging

Author(s): Stephan AH, Madison DV, Mateos JM, Fraser DA, Lovelett EA, et al.

When, where, and how much? Expression of the Kv3

Author(s): Gan L, Kaczmarek LK


Author(s): Yasuda T, Cuny H, Adams DJ

A-type K+ channels encoded by Kv4

Author(s): Carrasquillo Y, Burkhalter A, Nerbonne JM

Functional specialization of the axon initial segment by isoform-specific sodium channel targeting

Author(s): Boiko T, van Wart A, Caldwell JH, Levinson SR, Trimmer JS, et al.

Role of axonal NaV1

Author(s): Royeck M, Horstmann MT, Remy S, Reitze M, Yaari Y, et al.

The role of the Rho GTPases in neuronal development

Author(s): GovekEE, Newey SE, van Aelst L

EphB-mediated degradation of the RhoA GEF Ephexin5 relieves a developmental brake on excitatory synapse formation

Author(s): Margolis SS, Salogiannis J, Lipton DM, Mandel-Brehm C, Wills ZP, et al.

Potential role of culture mediums for successful isolation and neuronal differentiation of amniotic fluid stem cells

Author(s): Orciani M, Emanuelli M, Martino C, Pugnaloni A, Tranquilli AL, et al.