Impact of progestins on estradiol potentiation of the glutamate calcium response

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97 Scopus citations


One mechanism by which estrogen may modulate cognitive function is through potentiation of glutamate-mediated rises in intracellular calcium ([Ca2+]i) with resultant effects on neuronal morphology and signaling. Since progesterone is a component of hormone replacement therapy (HRT), we sought to determine whether therapeutically relevant progestins attenuated or blocked estrogen potentiation of glutamate-induced [Ca2+]i rises. 17β-estradiol and progesterone, alone or in combination, significantly potentiated the rise in [Ca2+]i. When co-administered, progesterone attenuated the estrogen response to the level seen with progesterone alone. In contrast, medroxyprogesterone acetate (MPA) had no effect when administered alone and completely blocked the 17β-estradiol-induced potentiation when co-administered. These results may have important implications for effective use of HRT to maintain cognitive function during menopause and aging.

Original languageEnglish (US)
Pages (from-to)825-830
Number of pages6
Issue number6
StatePublished - May 7 2002
Externally publishedYes


  • Calcium
  • Cognitive function
  • Estrogen
  • Glutamate
  • Hormone replacement therapy
  • Neuron
  • Progesterone

ASJC Scopus subject areas

  • Neuroscience(all)


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