Painful neuropathy decreases membrane calcium current in mammalian primary afferent neurons

Quinn H. Hogan, J. Bruce McCallum, Konstantinos D. Sarantopoulos, Mark Aason, Michelle Mynlieff, Wai Meng Kwok, Zeljko J. Bosnjak

Research output: Contribution to journalArticle

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Abstract

Hyperexcitability of the primary afferent neuron leads to neuropathic pain following injury to peripheral axons. Changes in calcium channel function of sensory neurons following injury have not been directly examined at the channel level, even though calcium is a primary second messenger-regulating neuronal function. We compared calcium currents (I(Ca)) in 101 acutely isolated dorsal root ganglion neurons from 31 rats with neuropathic pain following chronic constriction injury (CCI) of the sciatic nerve, to cells from 25 rats with normal sensory function following sham surgery. Cells projecting to the sciatic nerve were identified with a fluorescent label applied at the CCI site. Membrane function was determined using patch-clamp techniques in current clamp mode, and in voltage-clamp mode using solutions and conditions designed to isolate I(Ca). Somata of peripheral sensory neurons from hyperalgesic rats demonstrated decreased I(Ca). Peak calcium channel current density was diminished by injury from 3.06±0.30 pS/pF to 2.22±0.26 pS/pF in medium neurons, and from 3.93±0.38 pS/pF to 2.99±0.40 pS/pF in large neurons. Under these voltage and pharmacologic conditions, medium-sized neuropathic cells lacked obvious T-type calcium currents which were present in 25% of medium-sized cells from control animals. Altered Ca2+ signalling in injured sensory neurons may contribute to hyperexcitability leading to neuropathic pain. Copyright (C) 2000 International Association for the Study of Pain. Published by Elsevier Science B.V. All rights reserved.

Original languageEnglish
Pages (from-to)43-53
Number of pages11
JournalPain
Volume86
Issue number1-2
DOIs
StatePublished - May 1 2000
Externally publishedYes

Fingerprint

Afferent Neurons
Calcium
Neuralgia
Sensory Receptor Cells
Membranes
Wounds and Injuries
Neurons
Sciatic Nerve
Calcium Channels
Constriction
Spinal Ganglia
Carisoprodol
Second Messenger Systems
Patch-Clamp Techniques
Axons
Painful Neuropathy

Keywords

  • Calcium channel
  • Electrophysiology
  • Nerve injury
  • Neuropathic pain

ASJC Scopus subject areas

  • Clinical Neurology
  • Psychiatry and Mental health
  • Neurology
  • Neuroscience(all)
  • Pharmacology
  • Clinical Psychology

Cite this

Hogan, Q. H., McCallum, J. B., Sarantopoulos, K. D., Aason, M., Mynlieff, M., Kwok, W. M., & Bosnjak, Z. J. (2000). Painful neuropathy decreases membrane calcium current in mammalian primary afferent neurons. Pain, 86(1-2), 43-53. https://doi.org/10.1016/S0304-3959(99)00313-9

Painful neuropathy decreases membrane calcium current in mammalian primary afferent neurons. / Hogan, Quinn H.; McCallum, J. Bruce; Sarantopoulos, Konstantinos D.; Aason, Mark; Mynlieff, Michelle; Kwok, Wai Meng; Bosnjak, Zeljko J.

In: Pain, Vol. 86, No. 1-2, 01.05.2000, p. 43-53.

Research output: Contribution to journalArticle

Hogan, QH, McCallum, JB, Sarantopoulos, KD, Aason, M, Mynlieff, M, Kwok, WM & Bosnjak, ZJ 2000, 'Painful neuropathy decreases membrane calcium current in mammalian primary afferent neurons', Pain, vol. 86, no. 1-2, pp. 43-53. https://doi.org/10.1016/S0304-3959(99)00313-9
Hogan, Quinn H. ; McCallum, J. Bruce ; Sarantopoulos, Konstantinos D. ; Aason, Mark ; Mynlieff, Michelle ; Kwok, Wai Meng ; Bosnjak, Zeljko J. / Painful neuropathy decreases membrane calcium current in mammalian primary afferent neurons. In: Pain. 2000 ; Vol. 86, No. 1-2. pp. 43-53.
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