Potassium current expression during prenatal corticogenesis in the rat.
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.
Mienville
J M
JM
Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892, USA.
Barker
J L
JL
D015761:4-Aminopyridine / Q000494:pharmacology; D000367:Age Factors; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002454:Cell Differentiation / Q000502:physiology; D002540:Cerebral Cortex / Q000737:chemistry / Q000166:cytology / Q000196:embryology*; D051668:Delayed Rectifier Potassium Channels; D005260:Female; D005333:Fetus / Q000737:chemistry / Q000166:cytology / Q000502:physiology; D005456:Fluorescent Dyes; D007546:Isoquinolines; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000737:chemistry / Q000166:cytology / Q000502:physiology; D009924:Organ Culture Techniques; D018408:Patch-Clamp Techniques; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D024642:Potassium Channels, Voltage-Gated; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D019789:Tetraethylammonium / Q000494:pharmacology
D051668:Delayed Rectifier Potassium Channels; D005456:Fluorescent Dyes; D007546:Isoquinolines; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D019789:Tetraethylammonium; C017475:lucifer yellow; D015761:4-Aminopyridine; D011188:Potassium; D002118:Calcium