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Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
08:19

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

Nerve function and dysfunction in acute intermittent porphyria.

Cindy S-Y Lin1, Arun V Krishnan, Ming-Jen Lee

  • 1Prince of Wales Clinical School, Prince of Wales Medical Research Institute, School of Medical Sciences, University of New South Wales, Sydney, New South Wales, Australia.

Brain : a Journal of Neurology
|August 2, 2008
PubMed
Summary
This summary is machine-generated.

Acute intermittent porphyria (AIP) involves neurotoxic porphyrins. In patients without neuropathy, a reduced hyperpolarization-activated current (I(H)) was observed, suggesting subclinical axonal changes.

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Last Updated: Jul 3, 2026

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry
08:19

Assessing Mitochondrial Function in Sciatic Nerve by High-Resolution Respirometry

Published on: May 5, 2022

Area of Science:

  • Neuroscience
  • Metabolic Disorders
  • Genetics

Background:

  • Acute intermittent porphyria (AIP) is a rare genetic metabolic disorder.
  • Its clinical symptoms stem from the neurotoxic effects of elevated porphyrin precursors.
  • The precise mechanisms of porphyric neuropathy are not fully understood.

Purpose of the Study:

  • To investigate the neurotoxic impact of porphyrins on peripheral motor axons in AIP patients.
  • To correlate axonal excitability changes with genetic, biochemical, and clinical findings.
  • To elucidate the pathophysiology of porphyric neuropathy.

Main Methods:

  • Peripheral motor axon excitability studies (stimulus-response, threshold electrotonus, current-threshold relationship, recovery cycle) were performed on 20 AIP subjects.
  • Results were analyzed alongside genetic screening, biochemical assays, and conventional nerve conduction studies.
  • Mathematical modeling of human axons was used to simulate observed changes.

Main Results:

  • Five latent AIP patients showed normal axonal excitability.
  • Thirteen AIP patients experiencing acute porphyric episodes without clinical neuropathy (AIPWN) exhibited altered responses to hyperpolarizing currents, specifically a reduced hyperpolarizing I/V slope (P < 0.01).
  • Mathematical simulations suggested these changes in AIPWN patients are consistent with a reduction in the hyperpolarization-activated, cyclic nucleotide-dependent current (I(H)).
  • One patient during an acute neuropathic episode displayed high-threshold axons with reduced superexcitability, indicative of membrane depolarization.

Conclusions:

  • Porphyrin neurotoxicity in AIP may lead to subclinical reductions in axonal I(H) in patients without neuropathy (AIPWN).
  • Porphyric neuropathy might arise from reduced Na(+)/K(+) pump activity causing membrane depolarization.
  • Axonal excitability testing offers insights into the pathophysiology of AIP and its neurological complications.