Literature DB >> 8083757

Pharmacological identification of two types of presynaptic voltage-dependent calcium channels at CA3-CA1 synapses of the hippocampus.

L G Wu1, P Saggau.   

Abstract

The effects of voltage-dependent Ca channel (VDCC) antagonists on synaptic transmission were investigated at CA3-CA1 synapses of guinea pig hippocampal slices. After selectively loading presynaptic structures in area CA1 with the calcium indicator fura-2, we simultaneously recorded a presynaptic calcium transient ([Ca]t) and the corresponding field excitatory postsynaptic potential (fEPSP) evoked by a single stimulus given to the Schaffer collateral-commissural (SCC) pathway. Application of nifedipine did not reduce either the [Ca]t of the fEPSP, suggesting that nifedipine-sensitive Ca channels do not significantly contribute to evoked synaptic transmission at low stimulation frequency. Application of omega-conotoxin GVIA (omega-CgTX) or omega-agatoxin-IVA (omega-Aga-IVA) dose-dependently blocked both the [Ca]t and the fEPSP. The time course of the block of the [Ca]t was similar to that of the fEPSP. About 40% of the total [Ca]t was omega-CgTX sensitive, and more than 20% was omega-Aga-IVA sensitive. Combined application of these two blockers showed no overlap of the omega-CgTX-sensitive with the omega-Aga-IVA-sensitive [Ca]t. These results suggest that there are at least two types of presynaptic VDCCs at CA3-CA1 synapses of the hippocampus: omega-CgTX-sensitive and omega-Aga-IVA-sensitive Ca channels. Our results also suggest that these two types of Ca channels are colocalized at a single presynaptic terminal. During application of omega-CgTX or omega-Aga-IVA, the initial slope of the fEPSP varied approximately as the fourth power of the amplitude of the [Ca]t, suggesting that omega-CgTX-sensitive and omega-Aga-IVA-sensitive Ca channels have about equal efficacy in triggering transmitter release. These results in combination with similar findings at the squid giant synapse suggest that the nonlinear relationship between transmitter release and the Ca influx is well conserved from the molluscan to the mammalian nervous system.

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Year:  1994        PMID: 8083757      PMCID: PMC6577093     

Source DB:  PubMed          Journal:  J Neurosci        ISSN: 0270-6474            Impact factor:   6.167


  60 in total

1.  Decreased G-protein-mediated regulation and shift in calcium channel types with age in hippocampal cultures.

Authors:  E M Blalock; N M Porter; P W Landfield
Journal:  J Neurosci       Date:  1999-10-01       Impact factor: 6.167

2.  Implications of G-protein-mediated Ca2+ channel inhibition for neurotransmitter release and facilitation.

Authors:  R Bertram; M Behan
Journal:  J Comput Neurosci       Date:  1999 Nov-Dec       Impact factor: 1.621

3.  Contributions of residual calcium to fast synaptic transmission.

Authors:  C Chen; W G Regehr
Journal:  J Neurosci       Date:  1999-08-01       Impact factor: 6.167

4.  Calcium channels involved in the inhibition of acetylcholine release by presynaptic muscarinic receptors in rat striatum.

Authors:  V Dolezal; S Tucek
Journal:  Br J Pharmacol       Date:  1999-08       Impact factor: 8.739

5.  Effect of changes in action potential shape on calcium currents and transmitter release in a calyx-type synapse of the rat auditory brainstem.

Authors:  J G Borst; B Sakmann
Journal:  Philos Trans R Soc Lond B Biol Sci       Date:  1999-02-28       Impact factor: 6.237

6.  Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells.

Authors:  E V Kuzhikandathil; G S Oxford
Journal:  J Neurosci       Date:  1999-03-01       Impact factor: 6.167

7.  Upregulation of a T-type Ca2+ channel causes a long-lasting modification of neuronal firing mode after status epilepticus.

Authors:  Hailing Su; Dmitry Sochivko; Albert Becker; Jian Chen; Yanwen Jiang; Yoel Yaari; Heinz Beck
Journal:  J Neurosci       Date:  2002-05-01       Impact factor: 6.167

8.  Presynaptic Ca2+ channels and neurotransmitter release at the terminal of a mouse cortical neuron.

Authors:  J Qian; J L Noebels
Journal:  J Neurosci       Date:  2001-06-01       Impact factor: 6.167

9.  Calcium channel subtypes contributing to acetylcholine release from normal, 4-aminopyridine-treated and myasthenic syndrome auto-antibodies-affected neuromuscular junctions.

Authors:  F Giovannini; E Sher; R Webster; J Boot; B Lang
Journal:  Br J Pharmacol       Date:  2002-08       Impact factor: 8.739

10.  Prolonged attenuation of amygdala-kindled seizure measures in rats by convection-enhanced delivery of the N-type calcium channel antagonists omega-conotoxin GVIA and omega-conotoxin MVIIA.

Authors:  Maciej Gasior; Natalie A White; Michael A Rogawski
Journal:  J Pharmacol Exp Ther       Date:  2007-08-23       Impact factor: 4.030

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