Role of low-voltage-activated calcium current and extracellular calcium in controlling the firing pattern of developing CA1 pyramidal neurons
Autor: | Alberto Sanchez-Aguilera, A. Colino, José Luis Sánchez-Alonso, M.A. Vicente-Torres |
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Rok vydání: | 2016 |
Předmět: |
0301 basic medicine
chemistry.chemical_element Action Potentials Calcium Tissue Culture Techniques 03 medical and health sciences chemistry.chemical_compound Bursting 0302 clinical medicine BAPTA Nickel medicine Extracellular Animals Rats Wistar CA1 Region Hippocampal Cells Cultured Mibefradil Voltage-dependent calcium channel General Neuroscience Calcium channel Pyramidal Cells Calcium Channel Blockers EGTA 030104 developmental biology nervous system chemistry Biophysics Calcium Channels Extracellular Space Neuroscience 030217 neurology & neurosurgery medicine.drug |
Zdroj: | Neuroscience. 344 |
ISSN: | 1873-7544 |
Popis: | The firing pattern of individual neurons is an important element for information processing and storing. During the first weeks of development, there is a transitional period during which CA1 pyramidal neurons display burst-spiking behavior in contrast to the adult regular-firing pattern. Spike after-depolarizations (ADPs) constitute a major factor underlying burst-spiking behavior. Using current-clamp recordings, we studied ADP waveforms and firing patterns in CA1 pyramidal neurons of Wistar rats from 9 to 19 postnatal days (P9–19). The percentage of burst-spiking neurons increased up to P16, in correlation with the emergence of an active component in the ADP. The application of low-voltage-activated (LVA) calcium channel blockers such as nickel or mibefradil suppressed the generation of the active ADP component and burst-spiking behavior. In agreement with the development of the ADP waveform and burst-spiking behavior, voltage-clamp experiments in dissociated pyramidal neurons showed an increase in the LVA calcium current in P16–19 vs P9–12. Finally, we found that a reduction of extracellular calcium levels decreases the percentage of burst-spiking cells due to a reduction in the active component of the ADP. We conclude that a major contribution of LVA calcium channels to ADP determines the bursting capability of CA1 pyramidal neurons during a transitional postnatal period in contrast to adulthood. |
Databáze: | OpenAIRE |
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