A transitional period of Ca2+-dependent spike afterdepolarization and bursting in developing rat CA1 pyramidal cells.
During postnatal development neurones display discharge behaviours that are not present in the adult, yet they are essential for the normal maturation of the nervous system. Neonatal CA1 pyramidal cells, like their adult counterparts, fire regularly, but excitatory GABAergic transmission drives them to generate spontaneous high-frequency bursts until postnatal day (P) 15. Using intracellular recordings in hippocampal slices from rats at P8 to P25, we show herein that as the network-driven burst activity fades out, most CA1 pyramidal cells become intrinsically bursting neurones. The incidence of intrinsic bursters begins to rise at P11 and attains a peak of 74% by P18-P19, after which it decreases over the course of a week, disappearing almost entirely at P25. Analysis of the effects of different voltage-gated Ca2+ and Na+ channel antagonists, applied focally to proximal and distal parts of developing neurones, revealed a complex burst mechanism. Intrinsic bursting in developing neurones results from 'ping-pong' interplay between a back-propagating spike that activates T/R- and L-type voltage-gated Ca2+)channels in the distal apical dendrites and persistent voltage-gated Na+ channels in the somatic region. Thus, developing pyramidal neurones transitionally express not only distinctive synaptic properties, but also unique intrinsic firing patterns, that may contribute to the ongoing formation and refinement of synaptic connections.
Chen
Shmuel
S
Department of Physiology, Hebrew University School of Medicine, PO Box 12272, Jerusalem 91120, Israel.
Yue
Cuiyong
C
Yaari
Yoel
Y
D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000200:Action Potentials / Q000187:drug effects / Q000502:physiology*; D000779:Anesthetics, Local / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000502:physiology*; D002120:Calcium Channel Agonists / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D020746:Calcium Channels, L-Type / Q000502:physiology; D003712:Dendrites / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D008297:Male; D009924:Organ Culture Techniques; D010507:Periodicity; D017966:Pyramidal Cells / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D019782:Riluzole / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology
D000779:Anesthetics, Local; D002120:Calcium Channel Agonists; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D020746:Calcium Channels, L-Type; D018691:Excitatory Amino Acid Antagonists; D013779:Tetrodotoxin; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D019782:Riluzole; D002118:Calcium