The ontogeny of repetitive firing and its modulation by norepinephrine in rat neocortical neurons.
The postnatal ontogeny of electrical properties was studied in rat sensorimotor cortical neurons (P6 to adult) using intracellular recording in an in vitro slice preparation. Many action potential properties and input resistance changed during the first 4 postnatal weeks. Repetitive firing behavior also changed during the first postnatal month. Spike-frequency adaptation was much stronger in immature neurons. At 1 week postnatal, the majority of cortical neurons would only fire for less than 200 ms regardless of the intensity of long depolarizing current injections. These cells were normal in other parameters and could fire throughout a depolarizing current injection in the presence of inorganic calcium channel blockers or norepinephrine (NE), suggesting that the inability to fire was not due to injury. The frequency with which we encountered cells with this extreme adaptation decreased with age. Spike-frequency adaptation in immature neurons appears to be primarily controlled by Ca-dependent K+ conductances as in mature neurons. In mature and immature neurons, three afterhyperpolarizations (AHPs) could be distinguished by their rate of decline. The fast AHP followed repolarization of a single spike and was only partially Ca- and K-dependent. The medium duration AHP was Ca-dependent and apamin-sensitive and the slow AHP was partially Ca-dependent and not blocked by apamin. NE decreased the slow Ca-dependent AHP via beta-adrenergic receptors. This effect of NE on AHPs appeared qualitatively similar throughout postnatal development. NE had a proportionately greater effect in younger neurons, however, due to their relatively larger slow AHP. The quantitative differences of NE's action on the slow AHP (sAHP) led to a qualitative difference in NE's effect on firing behavior. The effects of NE on firing behavior may therefore be greater during times critical for cortical maturation.
Department of Anatomy and Neurobiology, University of Tennessee, Memphis 38103-4901.
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Lorenzon
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Foehring
D000200:Action Potentials / Q000187:drug effects; D000375:Aging / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002540:Cerebral Cortex / Q000166:cytology / Q000187:drug effects / Q000254:growth & development*; D004594:Electrophysiology; D066298:In Vitro Techniques; D008839:Microelectrodes; D009474:Neurons / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D011712:Pyramidal Tracts / Q000166:cytology / Q000187:drug effects; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000187:drug effects / Q000502:physiology
D002121:Calcium Channel Blockers; D011943:Receptors, Adrenergic, beta; D002118:Calcium; D009638:Norepinephrine