Capsaicin presynaptically inhibits glutamate release through the activation of TRPV1 and calcineurin in the hippocampus of rats

Capsaicin is the major ingredient in hot peppers of the plantCapsicum genuswith neuroprotective effects in several preclinical models; its effect on glutamate release has been investigated in the rat hippocampus using isolated nerve terminals (synaptosomes) and brain slices.

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Enhancement of glutamate release from nerve terminals of rat hippocampus by pretreatment with tetanic stimulation: Indirect involvement of nitric oxide in long-term potentiation.

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)50564-9 ◽

1994 ◽

Vol 64 ◽

pp. 233

Author(s):

Yoshinori Kamisaki ◽

Yuhei Moriwaki ◽

Kazuhisa Maeda ◽

Masahiko Ishimura ◽

Hideshi Omura ◽

...

Keyword(s):

Nitric Oxide ◽

Glutamate Release ◽

Long Term Potentiation ◽

Rat Hippocampus ◽

Nerve Terminals ◽

Tetanic Stimulation ◽

Term Potentiation

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Hypothermia and Isoflurane Similarly Inhibit Glutamate Release Evoked by Chemical Anoxia in Rat Cortical Brain Slices

Anesthesiology ◽

10.1097/00000542-199609000-00020 ◽

1996 ◽

Vol 85 (3) ◽

pp. 600-607. ◽

Cited By ~ 35

Author(s):

Helge Eilers ◽

Philip E. Bickler

Keyword(s):

Minimum Alveolar Concentration ◽

Glutamate Release ◽

Brain Slices ◽

Neuronal Cell ◽

Release Rates ◽

Neuroprotective Effects ◽

In Vivo Models ◽

Chemical Anoxia

Background Accumulation of the excitatory neurotransmitter glutamate in ischemic brain tissue contributes to neuronal cell death. Volatile anesthetics at clinically relevant concentrations are neuroprotective in in vivo models of brain ischemia and reduce glutamate release in vivo and in vitro, but they appear to have weaker neuroprotective effects than hypothermia. The purpose of this study was to determine whether isoflurane reduces glutamate release in hypoxic brain slices, how large this effect is compared to that of hypothermia, and if it is diminished by hyperthermia. Methods Glutamate released from rat cortical brain slices during chemical anoxia (100 microM NaCN) was measured continuously with a fluorescence assay. The release rate was compared at three temperatures (28 degrees C, 37 degrees C, and 39 degrees C) with and without isoflurane at concentrations equipotent to 1 minimum alveolar concentration. At the same three temperatures, glutamate release rates before and after exposure to isoflurane were compared. Results Isoflurane reduced glutamate release from brain slices during chemical anoxia at 37 degrees C (19.6%, P < 0.01) and at 39 degrees C (25.4%, P < 0.01), but not at 28 degrees C. The reduction in glutamate release with hypothermia was similar to that with isoflurane. Hyperthermia (39 degrees C) caused greater glutamate release under basal and anoxic conditions than normo- and hypothermia. Isoflurane caused a slight increase in basal glutamate release rates, although this effect was smaller than the increase caused by hyperthermia. Conclusions In a brain slice model of cerebral anoxia, 1 minimum alveolar concentration isoflurane decreases glutamate release to a similar extent that hypothermia (28 degrees C) does. The increased glutamate release with hyperthermia (39 degrees C) is not prevented by isoflurane.

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