Cellular physiology of the neonatal rat cerebral cortex: intrinsic membrane properties, sodium and calcium currents.
The cellular physiology of the primary somatosensory cortex was studied in postnatal day (P) 0 to P5 rats using whole-cell patch-clamp recordings. Visually identified Cajal-Retzius, subplate, bifurcated pyramidal, and immature, putatively migrating neurons showed resting membrane potentials between -44 and -50 mV and TTX-sensitive action potentials. Immature pyramidal neurons with the smallest surface area ( approximately 1,600 microm(2)) revealed the largest input resistance ( approximately 1.8 GOmega), and subplate cells with the largest surface area ( approximately 6,200 microm(2)) showed an input resistance of approximately 1 GOmega. Ontogenetically older Cajal-Retzius and subplate cells revealed shorter and larger action potentials compared to bifurcated and immature pyramidal neurons. Whereas Cajal-Retzius and subplate cells responded to injection of depolarizing current pulses with a repetitive nonadapting and fast spiking firing pattern, immature pyramidal neurons showed strong adaptation. Subplate cells revealed the fastest action potentials, largest sodium current amplitude (-714 pA), and highest sodium current density (-38 microA/cm(2)), enabling these cells to transmit afferent activity faithfully to postsynaptic neurons. Whereas all cell types expressed a high-voltage-activated (HVA) calcium current, none of them showed a significant low-voltage-activated calcium current. The largest peak (-25.5 microA/cm(2)) and steady-state (-7.6 microA/cm(2)) HVA calcium current density could be observed in immature presumed migrating neurons. In contrast, Cajal-Retzius and subplate neurons showed a significantly lower peak (-4.9 microA/cm(2)) and steady-state (<-3.3 microA/cm(2)) HVA calcium current density. Whereas a large HVA calcium current may promote neuronal migration of immature neurons, low intracellular calcium levels may provoke apoptosis in Cajal-Retzius and subplate cells.
Luhmann
H J
HJ
Institute of Neurophysiology, University of Düsseldorf, Düsseldorf, Germany. luhmann@uni-duesseldorf.de
Reiprich
R A
RA
Hanganu
I
I
Kilb
W
W
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn / Q000033:anatomy & histology / Q000254:growth & development* / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism* / Q000648:ultrastructure; D003712:Dendrites / Q000187:drug effects / Q000378:metabolism / Q000648:ultrastructure; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D017966:Pyramidal Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism*; D013003:Somatosensory Cortex / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism
D015220:Calcium Channels; D015222:Sodium Channels