Recommended Conferences

Human Genetics and Genetic Disorders

Miami, USA

Tissue Engineering and Regenerative Medicine

Chicago, USA
Related Subjects

A-type K+ channels encoded by Kv4

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


Rapidly activating and rapidly inactivating voltage-gated A-type K+ currents, IA, are key determinants of neuronal excitability and several studies suggest a critical role for the Kv4.2 pore-forming α subunit in the generation of IA channels in hippocampal and cortical pyramidal neurons. The experiments here demonstrate that Kv4.2, Kv4.3 and Kv1.4 all contribute to the generation of IA channels in mature cortical pyramidal (CP) neurons and that Kv4.2-, Kv4.3- and Kv1.4-encoded IA channels play distinct roles in regulating the intrinsic excitability and the firing properties of mature CP neurons. In vivo loss of Kv4.2, for example, alters the input resistances, current thresholds for action potential generation and action potential repolarization of mature CP neurons. Elimination of Kv4.3 also prolongs action potential duration, whereas the input resistances and the current thresholds for action potential generation in Kv4.3−/− and WT CP neurons are indistinguishable. In addition, although increased repetitive firing was observed in both Kv4.2−/− and Kv4.3−/− CP neurons, the increases in Kv4.2−/− CP neurons were observed in response to small, but not large, amplitude depolarizing current injections, whereas firing rates were higher in Kv4.3−/− CP neurons only with large amplitude current injections. In vivo loss of Kv1.4, in contrast, had minimal effects on the intrinsic excitability and the firing properties of mature CP neurons. Comparison of the effects of pharmacological blockade of Kv4-encoded currents in Kv1.4−/− and WT CP neurons, however, revealed that Kv1.4-encoded IA channels do contribute to controlling resting membrane potentials, the regulation of current thresholds for action potential generation and repetitive firing rates in mature CP neurons.

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

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.