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BACKGROUND Dexmedetomidine (Precedex; Abbott Laboratories, Abbott Park, IL) is a selective alpha2-adrenergic agonist that also has affinity for imidazoline receptors. In clinical studies, dexmedetomidine has sedative effects and impairs memory, but the action of dexmedetomidine on synaptic plasticity in the brain has yet to be established. In the present study, the authors investigated the effects of dexmedetomidine on two forms of synaptic plasticity-long-term potentiation (LTP) and paired-pulse facilitation-in the CA1 region of mouse hippocampal slices. METHODS The authors recorded Schaffer collateral-evoked field excitatory postsynaptic potentials from mouse hippocampal slices in CA1 stratum radiatum. The slope of the rising phase of the field excitatory postsynaptic potential was used to estimate the strength of synaptic transmission. RESULTS Application of dexmedetomidine for 20 min before "theta burst" stimulation dose-dependently attenuated LTP, and half-inhibitory concentration of dexmedetomidine was 28.6 +/- 5.7 nm. The inhibitory effect of dexmedetomidine on LTP was not abolished by an alpha2-adrenoceptor antagonist (yohimbine), an imidazoline type 1 receptor and alpha2-adrenoceptor antagonist (efaroxan), an alpha1-adrenoceptor antagonist (prazosin), or a gamma-aminobutyric acid type A receptor antagonist (picrotoxin). However, an imidazoline type 2 receptor and alpha2-adrenoceptor antagonist (idazoxan) completely blocked the dexmedetomidine-induced attenuation. Furthermore, 2-benzofuranyl-2-imidaloline, a selective imidazoline type 2 receptor ligand, reduced LTP. 2-(4,5-dihydroimidaz-2-yl)-quinoline, another imidazoline type 2 receptor ligand, abolished the 2-benzofuranyl-2-imidaloline-induced attenuation, but the inhibitory effect of dexmedetomidine on LTP was not abolished by 2-(4,5-dihydroimidaz-2-yl)-quinoline. Dexmedetomidine did not affect paired-pulse facilitation. CONCLUSIONS Dexmedetomidine impairs LTP in area CA1 of the mouse hippocampus via imidazoline type 2 receptors and alpha2-adrenoceptors.
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
December 1987,
Brain research,
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
August 1995,
Brain research,
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
March 2016,
Hippocampus,
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
January 1995,
Life sciences,
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
December 2020,
Hippocampus,
Isao Takamatsu, and
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Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
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Isao Takamatsu, and
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Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
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Philosophical transactions of the Royal Society of London. Series B, Biological sciences,
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
May 1996,
Neuroscience letters,
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
March 1996,
Science (New York, N.Y.),
Isao Takamatsu, and
Ayano Iwase, and
Makoto Ozaki, and
Tomiei Kazama, and
Keiji Wada, and
Masayuki Sekiguchi
June 2007,
Environmental health perspectives,
