Modulation of fast excitatory synaptic transmission by cyclothiazide and GYKI 52466 in the rat hippocampus

G. Rammes; C. Parsons; W. Müller; D. Swandulla

doi:10.1016/0304-3940(94)91068-5

Modulation of fast excitatory synaptic transmission by cyclothiazide and GYKI 52466 in the rat hippocampus

G. Rammes, C. Parsons, W. Müller, D. Swandulla

Research output: Contribution to journal › Article › peer-review

32 Scopus citations

Abstract

The effects of cyclothiazide, a drug which potentiates AMPA receptor-mediated responses and GYKI 52466, a non-competitive AMPA receptor antagonist, were studied on fast glutamatergic transmission in rat hippocampal slices. Cyclothiazide prolonged the decay of AMPA receptor-mediated EPSCs (AMPA-EPSCs) in a concentration-dependent manner. GYKI 52466 reduced the peak amplitude of AMPA-EPSCs and blocked the induction of LTP. When GYKI 52466 was applied in the presence of cyclothiazide it still reduced the peak amplitude of AMPA-EPSCs but was not able to reverse the cyclothiazide induced prolongation of AMPA-EPSC duration. These data suggest that GYKI 52466 and cyclothiazide probably mediate their effects on the AMPA receptor via different binding sites.

Original language	English
Pages (from-to)	21-24
Number of pages	4
Journal	Neuroscience Letters
Volume	175
Issue number	1-2
DOIs	https://doi.org/10.1016/0304-3940(94)91068-5
State	Published - 4 Jul 1994
Externally published	Yes

Keywords

Cyclothiazide
GYKI 52466
Hippocampus
Long-term potentiation
Rat
Synaptic transmission

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10.1016/0304-3940(94)91068-5

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title = "Modulation of fast excitatory synaptic transmission by cyclothiazide and GYKI 52466 in the rat hippocampus",

abstract = "The effects of cyclothiazide, a drug which potentiates AMPA receptor-mediated responses and GYKI 52466, a non-competitive AMPA receptor antagonist, were studied on fast glutamatergic transmission in rat hippocampal slices. Cyclothiazide prolonged the decay of AMPA receptor-mediated EPSCs (AMPA-EPSCs) in a concentration-dependent manner. GYKI 52466 reduced the peak amplitude of AMPA-EPSCs and blocked the induction of LTP. When GYKI 52466 was applied in the presence of cyclothiazide it still reduced the peak amplitude of AMPA-EPSCs but was not able to reverse the cyclothiazide induced prolongation of AMPA-EPSC duration. These data suggest that GYKI 52466 and cyclothiazide probably mediate their effects on the AMPA receptor via different binding sites.",

keywords = "Cyclothiazide, GYKI 52466, Hippocampus, Long-term potentiation, Rat, Synaptic transmission",

author = "G. Rammes and C. Parsons and W. M{\"u}ller and D. Swandulla",

note = "Funding Information: We thank G. L. Collingridge for critically reading the manuscript and K. Clark for advicing patiently on patch clamp recording in slices. This work was supported in part by a grant from the Deutsche Forschungsgemein-schaft (Graduiertenkolleg, SFB 353) and through a Helmholtz-stipend to W.M. from the Bundesminis-terium fiir Forschung und Technologie.",

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doi = "10.1016/0304-3940(94)91068-5",

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T1 - Modulation of fast excitatory synaptic transmission by cyclothiazide and GYKI 52466 in the rat hippocampus

AU - Rammes, G.

AU - Parsons, C.

AU - Müller, W.

AU - Swandulla, D.

N1 - Funding Information: We thank G. L. Collingridge for critically reading the manuscript and K. Clark for advicing patiently on patch clamp recording in slices. This work was supported in part by a grant from the Deutsche Forschungsgemein-schaft (Graduiertenkolleg, SFB 353) and through a Helmholtz-stipend to W.M. from the Bundesminis-terium fiir Forschung und Technologie.

PY - 1994/7/4

Y1 - 1994/7/4

N2 - The effects of cyclothiazide, a drug which potentiates AMPA receptor-mediated responses and GYKI 52466, a non-competitive AMPA receptor antagonist, were studied on fast glutamatergic transmission in rat hippocampal slices. Cyclothiazide prolonged the decay of AMPA receptor-mediated EPSCs (AMPA-EPSCs) in a concentration-dependent manner. GYKI 52466 reduced the peak amplitude of AMPA-EPSCs and blocked the induction of LTP. When GYKI 52466 was applied in the presence of cyclothiazide it still reduced the peak amplitude of AMPA-EPSCs but was not able to reverse the cyclothiazide induced prolongation of AMPA-EPSC duration. These data suggest that GYKI 52466 and cyclothiazide probably mediate their effects on the AMPA receptor via different binding sites.

AB - The effects of cyclothiazide, a drug which potentiates AMPA receptor-mediated responses and GYKI 52466, a non-competitive AMPA receptor antagonist, were studied on fast glutamatergic transmission in rat hippocampal slices. Cyclothiazide prolonged the decay of AMPA receptor-mediated EPSCs (AMPA-EPSCs) in a concentration-dependent manner. GYKI 52466 reduced the peak amplitude of AMPA-EPSCs and blocked the induction of LTP. When GYKI 52466 was applied in the presence of cyclothiazide it still reduced the peak amplitude of AMPA-EPSCs but was not able to reverse the cyclothiazide induced prolongation of AMPA-EPSC duration. These data suggest that GYKI 52466 and cyclothiazide probably mediate their effects on the AMPA receptor via different binding sites.

KW - Cyclothiazide

KW - GYKI 52466

KW - Hippocampus

KW - Long-term potentiation

KW - Rat

KW - Synaptic transmission

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JO - Neuroscience Letters

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ER -

Modulation of fast excitatory synaptic transmission by cyclothiazide and GYKI 52466 in the rat hippocampus

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