The L-type voltage-dependent calcium channel long-term potentiation is higher in the dorsal compared with the ventral associational/commissural CA3 hippocampal synapses

Shankar, Subbakrishna, Timothy J. Teyler, and Norman Robbins. Aging differentially alters forms of long-term potentiation in rat hippocampal area CA1. J. Neurophysiol. 79: 334–341, 1998. Long-term potentiation (LTP) of the Schaffer collateral/commissural inputs to CA1 in the hippocampus was shown to consist of N-methyl-d-aspartate receptor (NMDAR) and voltage-dependent calcium channel (VDCC) dependent forms. In this study, the relative contributions of these two forms of LTP in in vitro hippocampal slices from young (2 mo) and old (24 mo) Fischer 344 rats were examined. Excitatory postsynaptic potentials (EPSP) were recorded extracellularly from stratum radiatum before and after a tetanic stimulus consisting of four 200-Hz, 0.5-s trains given 5 s apart. Under control conditions, a compound LTP consisting of both forms was induced and was similar, in both time course and magnitude, in young and old animals. NMDAR-dependent LTP (nmdaLTP), isolated by the application of 10 μM nifedipine (a voltage-dependent calcium channel blocker), was significantly reduced in magnitude in aged animals. The VDCC dependent form (vdccLTP), isolated by the application of 50 μM d,l-2-amino-5-phosphonvalerate (APV), was significantly larger in aged animals. Although both LTP forms reached stable values 40–60 min posttetanus in young animals, in aged animals vdccLTP increased and nmdaLTP decreased during this time. In both young and old animals, the sum of the two isolated LTP forms approximated the magnitude of the compound LTP, and application of APV and nifedipine or genestein (a tyrosine kinase inhibitor) together blocked potentiation. These results suggest that aging causes a shift in synaptic plasticity from NMDAR-dependent mechanisms to VDCC-dependent mechanisms. The data are consistent with previous findings of increased L-type calcium current and decreased NMDAR number in aged CA1 cells and may help explain age-related deficits in learning and memory.

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Role of voltage-dependent calcium channel subtypes in spinal long-term potentiation of C-fiber-evoked field potentials

Pain ◽

10.1016/j.pain.2010.12.004 ◽

2011 ◽

Vol 152 (3) ◽

pp. 623-631 ◽

Cited By ~ 18

Author(s):

Soichiro Ohnami ◽

Mitsuo Tanabe ◽

Shunji Shinohara ◽

Keiko Takasu ◽

Akira Kato ◽

...

Keyword(s):

Calcium Channel ◽

Long Term Potentiation ◽

Field Potentials ◽

Voltage Dependent Calcium Channel ◽

Evoked Field Potentials ◽

Term Potentiation ◽

C Fiber ◽

Voltage Dependent

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Photolytic release of nitric oxide modulates NMDA receptor-mediated transmission but does not induce long-term potentiation at hippocampal synapses

Neuropharmacology ◽

10.1016/0028-3908(94)90039-6 ◽

1994 ◽

Vol 33 (11) ◽

pp. 1375-1385 ◽

Cited By ~ 57

Author(s):

K.P.S.J. Murphy ◽

J.H. Williams ◽

N. Bettache ◽

T.V.P. Bliss

Keyword(s):

Nitric Oxide ◽

Nmda Receptor ◽

Long Term Potentiation ◽

Term Potentiation ◽

Hippocampal Synapses

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Phosphorylation Changes of CaMKII, ERK1/2, PKB/Akt Kinases and CREB Activation During Early Long-Term Potentiation at Schaffer Collateral-CA1 Mouse Hippocampal Synapses

Neurochemical Research ◽

10.1007/s11064-009-0047-0 ◽

2009 ◽

Vol 35 (2) ◽

pp. 239-246 ◽

Cited By ~ 34

Author(s):

Mauro Racaniello ◽

Alessio Cardinale ◽

Cristiana Mollinari ◽

Margherita D’Antuono ◽

Giovanna De Chiara ◽

...

Keyword(s):

Long Term Potentiation ◽

Schaffer Collateral ◽

Creb Activation ◽

Term Potentiation ◽

Hippocampal Synapses

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Effect of tolbutamide on tetraethylammonium-induced postsynaptic zinc signals at hippocampal mossy fiber-CA3 synapses

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2016-0379 ◽

2017 ◽

Vol 95 (9) ◽

pp. 1058-1063 ◽

Cited By ~ 1

Author(s):

Fatima C. Bastos ◽

Vanessa N. Corceiro ◽

Sandra A. Lopes ◽

José G. de Almeida ◽

Carlos M. Matias ◽

...

Keyword(s):

Mossy Fiber ◽

Mossy Fibers ◽

Pyramidal Cells ◽

Long Term Potentiation ◽

Chemical Stimulation ◽

Term Potentiation ◽

Voltage Dependent ◽

Zinc Release ◽

Ca3 Pyramidal Cells

The application of tetraethylammonium (TEA), a blocker of voltage-dependent potassium channels, can induce long-term potentiation (LTP) in the synaptic systems CA3–CA1 and mossy fiber-CA3 pyramidal cells of the hippocampus. In the mossy fibers, the depolarization evoked by extracellular TEA induces a large amount of glutamate and also of zinc release. It is considered that zinc has a neuromodulatory role at the mossy fiber synapses, which can, at least in part, be due to the activation of presynaptic ATP-dependent potassium (KATP) channels. The aim of this work was to study properties of TEA-induced zinc signals, detected at the mossy fiber region, using the permeant form of the zinc indicator Newport Green. The application of TEA caused a depression of those signals that was partially blocked by the KATP channel inhibitor tolbutamide. After the removal of TEA, the signals usually increased to a level above baseline. These results are in agreement with the idea that intense zinc release during strong synaptic events triggers a negative feedback action. The zinc depression, caused by the LTP-evoking chemical stimulation, turns into potentiation after TEA washout, suggesting the existence of a correspondence between the observed zinc potentiation and TEA-evoked mossy fiber LTP.

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