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Synaptically released zinc: physiological functions and pathological effects.

C J Frederickson1, A I Bush

  • 1NeuroBioTex, Inc., Biomedical Engineering and Anatomy and Neuroscience, The University of Texas Medical Branch, Galveston, USA. cjfrederickson@hotmail.com

Biometals : an International Journal on the Role of Metal Ions in Biology, Biochemistry, and Medicine
|February 8, 2002
PubMed
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Zinc is released from specialized neurons to modulate brain excitability and amino acid receptors. This release also contributes to Alzheimer's disease pathology and neuron injury, acting as a neural signal.

Area of Science:

  • Neuroscience
  • Neurochemistry

Background:

  • Zinc is a component of metalloproteins and is sequestered in presynaptic vesicles of specific neurons.
  • These 'zinc-containing' neurons release zinc, influencing physiological and pathological processes.

Purpose of the Study:

  • To review the physiological and pathological effects of zinc release from synaptic terminals.
  • To compare zinc signaling with calcium signaling.
  • To explore the novel role of zinc as a transmembrane neural signal.

Main Methods:

  • Literature review of zinc's role in neuronal signaling.
  • Compilation of parameters for comparing zinc and calcium signals.
  • Hypothesizing zinc's function in protein modification ('zincylation').

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Main Results:

  • Synaptically released zinc modulates brain excitability via amino acid receptors.
  • Zinc release accelerates plaque deposition in Alzheimer's disease and exacerbates excitotoxic injury.
  • Zinc acts as a conventional neurotransmitter/neuromodulator and unconventionally as a transmembrane signal.

Conclusions:

  • Zinc has dual roles: conventional neurotransmission and unconventional transmembrane signaling.
  • Zinc signaling may involve lasting protein modification ('zincylation'), altering protein function.
  • Further research is needed to fully elucidate zinc's signaling mechanisms and implications.