Literature DB >> 9300409

Potassium current expression during prenatal corticogenesis in the rat.

J M Mienville1, J L Barker.   

Abstract

Using in situ patch-clamp techniques, we have studied K current expression in rat telencephalon from embryonic day 12 to 21. For cells recorded in the ventricular zone, the K current consisted of a delayed rectifier and a large-conductance calcium-activated component, and displayed little variation from embryonic day 12 to 21. Cells recorded in pial regions could be separated into two classes: radially oriented, putatively migrating cells, and cells tangentially oriented in layer I, which were assumed to be Cajal-Retzius cells. When using a voltage-clamp protocol that included a prepulse to -120 mV, Cajal-Retzius cells displayed a larger density of total K current than radial cells, and both types revealed an inactivating component (IA). The proportion of this component increased from embryonic day 18 to 21 in both cell types, although the amplitude of total K current, in the respective cell type, did not vary. This suggested a concomitant decrease in delayed rectifier current, which was verified directly with an appropriate protocol. The activation rate of the delayed rectifier current was slower for ventricular zone cells than for radial or Cajal-Retzius cells. IA was studied in Cajal-Retzius cells and displayed a strikingly negative (approximately -100 mV) voltage of half-maximal steady-state inactivation. Tetraethylammonium ions only blocked the non-inactivating component(s) of K current whereas 4-aminopyridine appeared to decrease both inactivating and non-inactivating components. The quantitative changes in K current expression are likely to underlie the overall increase in excitability of differentiating cells. On the other hand, the observation of qualitative differences among channel properties opens an interesting area of investigation into their physiological significance.

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Year:  1997        PMID: 9300409     DOI: 10.1016/s0306-4522(97)00171-1

Source DB:  PubMed          Journal:  Neuroscience        ISSN: 0306-4522            Impact factor:   3.590


  7 in total

1.  Low resting potential and postnatal upregulation of NMDA receptors may cause Cajal-Retzius cell death.

Authors:  J M Mienville; C Pesold
Journal:  J Neurosci       Date:  1999-03-01       Impact factor: 6.167

2.  Glutamate transporters and presynaptic metabotropic glutamate receptors protect neocortical Cajal-Retzius cells against over-excitation.

Authors:  Anton Dvorzhak; Petr Unichenko; Sergei Kirischuk
Journal:  Pflugers Arch       Date:  2012-06-05       Impact factor: 3.657

3.  Persistent depolarizing action of GABA in rat Cajal-Retzius cells.

Authors:  J M Mienville
Journal:  J Physiol       Date:  1998-11-01       Impact factor: 5.182

4.  Postnatal development of A-type and Kv1- and Kv2-mediated potassium channel currents in neocortical pyramidal neurons.

Authors:  Dongxu Guan; Leslie R Horton; William E Armstrong; Robert C Foehring
Journal:  J Neurophysiol       Date:  2011-03-30       Impact factor: 2.714

5.  Gene expression in cortical interneuron precursors is prescient of their mature function.

Authors:  Renata Batista-Brito; Robert Machold; Corinna Klein; Gord Fishell
Journal:  Cereb Cortex       Date:  2008-02-03       Impact factor: 5.357

6.  Integrative genomic analysis of early neurogenesis reveals a temporal genetic program for differentiation and specification of preplate and Cajal-Retzius neurons.

Authors:  Jia Li; Lei Sun; Xue-Liang Peng; Xiao-Ming Yu; Shao-Jun Qi; Zhi John Lu; Jing-Dong J Han; Qin Shen
Journal:  PLoS Genet       Date:  2021-03-24       Impact factor: 5.917

7.  Determining k channel activation curves from k channel currents often requires the goldman-hodgkin-katz equation.

Authors:  John R Clay
Journal:  Front Cell Neurosci       Date:  2009-12-23       Impact factor: 5.505

  7 in total

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