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N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

Identifieur interne : 000551 ( Ncbi/Checkpoint ); précédent : 000550; suivant : 000552

N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

Auteurs : R A Lenz ; J J Wagner ; B E Alger

Source :

The Journal of Physiology [ 0022-3751 ] ; 1998.

RBID : PMC:2231194

Abstract

We investigated depolarization-induced suppression of inhibition (DSI) under whole-cell voltage clamp in CA1 pyramidal neurons of rat hippocampal slices. DSI, a transient reduction in monosynaptic evoked GABA_Aergic IPSCs lasting for ∼1 min, was induced by depolarizing the pyramidal cell to −10 or 0 mV for 1 or 2 s.

Raising extracellular Ca²⁺ concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca²⁺ channels.

The P- and Q-type Ca²⁺ channel blocker ω-agatoxin TK (200 nm and 1 μm) and the R- and T-type Ca²⁺ channel blocker Ni²⁺ (100 μm) reduced IPSCs without reducing DSI.

The specific N-type Ca²⁺ channel antagonist ω-conotoxin GVIA (250 nm) reduced IPSC amplitudes and almost completely abolished DSI.

Blocking L-type Ca²⁺ channels with nifedipine (10 μm) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na⁺- and Ca²⁺-dependent spikes that occurred when 2(triethylamino)-N-(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution.

Although intracellular Ca²⁺ stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20–40 μm), a blocker of Ca²⁺ uptake into intracellular stores.

We conclude that DSI is initiated by Ca²⁺ influx through N- and, under certain conditions, L-type Ca²⁺ channels.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2231194

DOI: 10.1111/j.1469-7793.1998.061bf.x
PubMed: 9729617
PubMed Central: 2231194

Affiliations:

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PMC:2231194

Le document en format XML

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<author><name sortKey="Wagner, J J" sort="Wagner, J J" uniqKey="Wagner J" first="J J" last="Wagner">J J Wagner</name>
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<author><name sortKey="Alger, B E" sort="Alger, B E" uniqKey="Alger B" first="B E" last="Alger">B E Alger</name>
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<series><title level="j">The Journal of Physiology</title>
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<front><div type="abstract" xml:lang="en"><p><list list-type="order"><list-item><p>We investigated depolarization-induced suppression of inhibition (DSI) under whole-cell voltage clamp in CA1 pyramidal neurons of rat hippocampal slices. DSI, a transient reduction in monosynaptic evoked GABA<sub>A</sub>
ergic IPSCs lasting for ∼1 min, was induced by depolarizing the pyramidal cell to −10 or 0 mV for 1 or 2 s.</p>
</list-item>
<list-item><p>Raising extracellular Ca<sup>2+</sup>
 concentration increased DSI, and varying the DSI-inducing voltage step showed that the voltage dependence of DSI was like that of high-voltage-activated Ca<sup>2+</sup>
 channels.</p>
</list-item>
<list-item><p>The P- and Q-type Ca<sup>2+</sup>
 channel blocker ω-agatoxin TK (200 n<sc>m</sc>
 and 1 μ<sc>m</sc>
) and the R- and T-type Ca<sup>2+</sup>
 channel blocker Ni<sup>2+</sup>
 (100 μ<sc>m</sc>
) reduced IPSCs without reducing DSI.</p>
</list-item>
<list-item><p>The specific N-type Ca<sup>2+</sup>
 channel antagonist ω-conotoxin GVIA (250 n<sc>m</sc>
) reduced IPSC amplitudes and almost completely abolished DSI.</p>
</list-item>
<list-item><p>Blocking L-type Ca<sup>2+</sup>
 channels with nifedipine (10 μ<sc>m</sc>
) had no effect on IPSCs or DSI induced by our standard protocol, but reduced DSI induced by the unclamped Na<sup>+</sup>
- and Ca<sup>2+</sup>
-dependent spikes that occurred when 2(triethylamino)-<italic>N-</italic>
(2,6-dimethylphenyl)acetamide (QX-314) was omitted from the recording pipette solution.</p>
</list-item>
<list-item><p>Although intracellular Ca<sup>2+</sup>
 stores were not measured, DSI was not affected by cyclopiazonic acid (CPA, 20–40 μ<sc>m</sc>
), a blocker of Ca<sup>2+</sup>
 uptake into intracellular stores.</p>
</list-item>
<list-item><p>We conclude that DSI is initiated by Ca<sup>2+</sup>
 influx through N- and, under certain conditions, L-type Ca<sup>2+</sup>
 channels.</p>
</list-item>
</list>
</p>
</div>
</front>
</TEI>
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<tree><noCountry><name sortKey="Alger, B E" sort="Alger, B E" uniqKey="Alger B" first="B E" last="Alger">B E Alger</name>
<name sortKey="Lenz, R A" sort="Lenz, R A" uniqKey="Lenz R" first="R A" last="Lenz">R A Lenz</name>
<name sortKey="Wagner, J J" sort="Wagner, J J" uniqKey="Wagner J" first="J J" last="Wagner">J J Wagner</name>
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N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

N- and L-type calcium channel involvement in depolarization-induced suppression of inhibition in rat hippocampal CA1 cells

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Abstract

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