FENS Forum 2006

FENS Forum 2006 - Vienna

For lectures, symposia and workshops, time indicates the beginning of the session.
For posters, authors are expected to be in attendance at their posters at the time indicated.

First author: Calvo, Soledad (poster)

Poster board 268 - Mon 10/07, 11:30 - Hall Y
Session 084 - Calcium channels
Abstract A084.7, published in FENS Forum Abstracts, vol. 3, 2006.
Ref.: FENS Abstr., vol.3, A084.7, 2006

Author(s) Calvo S., Benavides A., Pastor D. & Fradejas N.

Addresse(s) Fac. Medi. CRIB UCLM, Albacete, Spain

Title Long-term depolarization induces the downregulation of chromaffin cell calcium chanels.

Text Chromaffin cell calcium channels are inactivated by calcium and voltage in order to avoid excessive, detrimental intracellular calcium increases. This inactivation takes place in a short-term, membrane-delimited fashion and is relieved once voltage and calcium return to resting levels. We have investigated here if longer periods of depolarization and calcium rises regulate calcium channel activity in a more sustained way, affecting calcium channel subunit synthesis. We have used chronic depolarization with elevated extracellular KCl to study the effects of activity on the mRNAs coding for the different alpha1, pore-forming, calcium channel subunits, present in chromaffin cells. Real time PCR analysis with the specific oligonucleotides demonstrated that prolonged depolarization induced a significant decrease in the levels of the CaV1.1; CaV1.2, CaV1.3, CaV2.2 and CaV2.3 transcript levels while CaV 2.1 remained unchanged. This downregulation depended on the calcium entry though the L-type channels as pretreatment with nifedipine completely avoided the depolarization-induced mRNA downregulation. We conclude that a new feedback mechanism, involving the downregulation of calcium channel molecules, is activated in chromaffin cells under prolonged exposures to depolarizing conditions.
Supported by SAF2001-0760 from MCYT andPAI05-017 from JCCM to SC. DP is a predoctoral fellow from JCCM.

Theme Synaptic transmission and excitability
Voltage-dependent ion channels / Calcium channels

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Author(s)	Calvo S., Benavides A., Pastor D. & Fradejas N.
Addresse(s)	Fac. Medi. CRIB UCLM, Albacete, Spain
Title	Long-term depolarization induces the downregulation of chromaffin cell calcium chanels.
Text	Chromaffin cell calcium channels are inactivated by calcium and voltage in order to avoid excessive, detrimental intracellular calcium increases. This inactivation takes place in a short-term, membrane-delimited fashion and is relieved once voltage and calcium return to resting levels. We have investigated here if longer periods of depolarization and calcium rises regulate calcium channel activity in a more sustained way, affecting calcium channel subunit synthesis. We have used chronic depolarization with elevated extracellular KCl to study the effects of activity on the mRNAs coding for the different alpha1, pore-forming, calcium channel subunits, present in chromaffin cells. Real time PCR analysis with the specific oligonucleotides demonstrated that prolonged depolarization induced a significant decrease in the levels of the CaV1.1; CaV1.2, CaV1.3, CaV2.2 and CaV2.3 transcript levels while CaV 2.1 remained unchanged. This downregulation depended on the calcium entry though the L-type channels as pretreatment with nifedipine completely avoided the depolarization-induced mRNA downregulation. We conclude that a new feedback mechanism, involving the downregulation of calcium channel molecules, is activated in chromaffin cells under prolonged exposures to depolarizing conditions. Supported by SAF2001-0760 from MCYT andPAI05-017 from JCCM to SC. DP is a predoctoral fellow from JCCM.
Theme	Synaptic transmission and excitability Voltage-dependent ion channels / Calcium channels