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Related Experiment Videos

Cell-permeant calcium buffer induced neuroprotection after cortical devascularization.

Brenda L Bartnik1, Igor Spigelman, André Obenaus

  • 1Department of Radiation Medicine, Loma Linda University, Radiobiology Program CSP A1010, Loma Linda, CA 92354, USA. bbartnik@mednet.ucla.edu

Experimental Neurology
|March 10, 2005
PubMed
Summary

Cell-permeant calcium buffers, like APTRA-AM, show significant neuroprotection when administered after focal cerebral ischemia. This treatment effectively reduced infarct size and inflammation, offering a promising therapeutic strategy for stroke injury.

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Medical Imaging

Background:

  • Neuronal death after ischemia is linked to excitotoxicity and excessive intracellular calcium.
  • Cell-permeant calcium buffers are potential neuroprotective agents by managing calcium load and neurotransmitter release.

Purpose of the Study:

  • To evaluate the neuroprotective efficacy of 2-aminophenol-N, N, O-triacetic acid acetoxymethyl ester (APTRA-AM) when administered after focal cerebral ischemia.
  • To assess the impact of APTRA-AM on neuronal injury using diffusion-weighted magnetic resonance imaging (DWI) and histological methods.

Main Methods:

  • Focal cerebral ischemia was induced in animal models.
  • APTRA-AM was administered at 1 and 12 hours post-injury.
  • Diffusion-weighted magnetic resonance imaging (DWI), cresyl violet histology, and immunohistochemistry were employed for analysis.
Keywords:
NASA Discipline Radiation HealthNon-NASA Center

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Main Results:

  • Ischemia caused a decrease in apparent diffusion coefficient (ADC) within 12 hours, which normalized by 7 days.
  • APTRA-AM treated animals showed no significant ADC changes, indicating preserved tissue integrity.
  • APTRA-AM treatment resulted in an 85% reduction in infarct size and a 94% decrease in inflammatory cell infiltration.

Conclusions:

  • APTRA-AM demonstrates significant neuroprotection when administered therapeutically after focal cerebral ischemia.
  • APTRA-AM effectively mitigates neuronal damage and inflammatory responses post-injury.
  • These findings support APTRA-AM as a potential therapeutic agent for ischemic stroke.