QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

HOME  |   SEARCH  |   ARCHIVE  |   SUBSCRIBE  |   CONTACT  |   HELP

The Journal of Neuroscience, November 17, 2004, 24(46):10402-10409; doi:10.1523/JNEUROSCI.1664-04.2004

This Article Full Text Full Text (PDF) Supplemental data Submit an eLetter Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Scheuber, A. Articles by Poncer, J. C. Search for Related Content PubMed PubMed Citation Articles by Scheuber, A. Articles by Poncer, J. C. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CALCIUM COMPOUNDS CALCIUM, ELEMENTAL

 Previous Article  |  Next Article 

Cellular/Molecular
Presynaptic Cav2.1 and Cav2.2 Differentially Influence Release Dynamics at Hippocampal Excitatory Synapses

Anita Scheuber, Richard Miles, and Jean Christophe Poncer

Institut National de la Santé et de la Recherche Médicale, Equipe Mixte 224 Cortex et Epilepsie, Centre Hospitalier Universitaire Pitié-Salpêtrière, 75013 Paris, France

Presynaptic calcium influx at most excitatory central synapses is carried by both Cav2.1 and Cav2.2 channels. The kinetics and modulation of Cav2.1 and Cav2.2 channels differ and may affect presynaptic calcium influx. We compared release dynamics at CA3/CA1 synapses in rat hippocampus after selective blockade of either channel subtype and subsequent quantal content restoration. Selective blockade of Cav2.1 channels enhanced paired-pulse facilitation, whereas blockade of Cav2.2 channels decreased it. This effect was observed at short (50 msec) but not longer (500 msec) intervals and was maintained during prolonged bursts of presynaptic activity. It did not reflect differences in the distance of the channels from the calcium sensor. The suppression of this effect by preincubation with the G_o/i-protein inhibitor pertussis toxin suggests instead that high-frequency stimulation relieves inhibition of Cav2.2 by G_o/i, thereby increasing the number of available channels.

Key words: synaptic; plasticity; hippocampus; channels; calcium; G-protein

---

Received May 3, 2004; revised October 6, 2004; accepted October 7, 2004.

This article has been cited by other articles:

				H. Salgado, F. Tecuapetla, T. Perez-Rosello, A. Perez-Burgos, E. Perez-Garci, E. Galarraga, and J. Bargas A Reconfiguration of CaV2 Ca2+ Channel Current and Its Dopaminergic D2 Modulation in Developing Neostriatal Neurons J Neurophysiol, December 1, 2005; 94(6): 3771 - 3787. [Abstract] [Full Text] [PDF]

				H. Y. Sun, S. A Lyons, and L. E Dobrunz Mechanisms of target-cell specific short-term plasticity at Schaffer collateral synapses onto interneurones versus pyramidal cells in juvenile rats J. Physiol., November 1, 2005; 568(3): 815 - 840. [Abstract] [Full Text] [PDF]

Home  |   Search  |   Archive  |   Subscribe  |   Contact  |   Help