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Updated: Jun 2, 2026

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Cellular mechanisms of acute decrease of glutamate release induced by raloxifene in rat cerebral cortex.

K L Hung1, C C Wang, S J Wang

  • 1School of Medicine, Fu Jen Catholic University, 510, Chung-Cheng Rd., Hsin-Chuang, Taipei Hsien 24205, Taiwan.

Neuropharmacology
|May 4, 2011
PubMed
Summary

Raloxifene inhibits glutamate release from rat brain nerve terminals by reducing calcium influx and suppressing the ERK/synapsin I pathway. This neuroprotective effect occurs independently of estrogen receptors.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Molecular Biology

Background:

  • Excessive glutamate release is implicated in neurological disease neuropathology.
  • Raloxifene, a selective estrogen receptor modulator, shows neuroprotective effects in vitro.
  • Understanding raloxifene's impact on glutamate release is crucial for neurological disorder research.

Purpose of the Study:

  • To investigate if raloxifene affects endogenous glutamate release in rat cerebral cortex synaptosomes.
  • To explore the underlying mechanisms of raloxifene's action on glutamate release.

Main Methods:

  • Studied 4-aminopyridine (4-AP)-evoked glutamate release from rat synaptosomes.
  • Utilized estrogen receptor antagonists, calcium chelators, and specific channel/transporter inhibitors.

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Last Updated: Jun 2, 2026

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  • Assessed cytosolic free Ca(2+) concentration, membrane potential, and MAPK/ERK signaling pathway activation.

    • Main Results:

    • Raloxifene dose-dependently inhibited 4-AP-evoked glutamate release, independent of estrogen receptors.
    • Inhibition was dependent on extracellular Ca(2+) and blocked by MEK inhibitors, indicating a role for the ERK pathway.
    • Raloxifene reduced depolarization-induced Ca(2+) influx via Ca(v)2.2 and Ca(v)2.1 channels and decreased MAPK/ERK1/2 and synapsin I phosphorylation.

    Conclusions:

    • Raloxifene's inhibition of evoked glutamate release is mediated by reduced presynaptic Ca(2+) entry and suppressed ERK/synapsin I signaling.
    • The neuroprotective mechanism of raloxifene in this context is independent of estrogen receptor modulation.
    • Findings suggest raloxifene as a potential therapeutic agent for neurological conditions involving excitotoxicity.