Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats.

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Research Abstract Details 

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Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Abstract Text:

Andreas Fuchs,Marcel Rigaud,Quinn H Hogan,

BACKGROUND: Neuropathic pain is inadequately treated and poorly understood at the cellular level. Because intracellular Ca signaling critically regulates diverse neuronal functions, the authors examined effects of peripheral nerve injury on the Ca transient that follows neuronal activation. METHODS: Cytoplasmic Ca levels were recorded by digital microfluorometry from dissociated dorsal root ganglion neurons of hyperalgesic animals after ligation of the fifth lumbar spinal nerve and control animals. Neurons were activated by field stimulation or by K depolarization. RESULTS: Transients in presumptively nociceptive, small, capsaicin-sensitive neurons were diminished after axotomy, whereas transient amplitude increased in axotomized nonnociceptive neurons. Axotomy diminished the upward shift in resting calcium after transient recovery. In contrast, nociceptive neurons adjacent to axotomy acquired increased duration of the transient and greater baseline shift after K activation. Transients of nonnociceptive neurons adjacent to axotomy showed no changes after injury. In nociceptive neurons from injured rats that did not develop hyperalgesia, transient amplitude and baseline offset were large after axotomy, whereas transient duration in the adjacent neurons was shorter compared with neurons excised from hyperalgesic animals, which show normalization of these features. CONCLUSIONS: A diminished Ca signal in axotomized neurons may be in part due to loss of Ca influx through voltage-gated Ca channels. The upward shift in resting Ca level after activation, which is diminished after axotomy in presumed nociceptive neurons, is a previously unrecognized aspect of neuronal plasticity. These changes in the critical Ca signal may mediate various injury-related abnormalities in Ca-dependent neuronal.

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Publishing Authors By Initials

A Fuchs,M Rigaud,QH Hogan,

For similar pathological conditions, signs and symptoms: pathologic processes: nerve degeneration: wallerian degeneration research abstracts see: pathological conditions, signs and symptoms: pathologic processes: nerve degeneration: wallerian degeneration research

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MEDLINE DATE:

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Anesthesiology

VOLUME: 107

Page Numbers: 106-16

Journal Abbreviation: Anesthesiology

ISSN: 0003-3022

DAY: 3

MONTH: Jul

YEAR: 2007

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 1300217

Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Keywords Mesh Terms:

KEYWORDS: Wallerian Degeneration

MESH TERMS: physiopathology

Chemical & Substance for Abstract: Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Information

Substance Name: Potassium

Registry Number: 7440-09-7

Grant and Affiliation Information for Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats.

AFFILIATION: Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.

Country: United States

AGENCY: United States NINDS

GRANT: NS-42150

ACRONYM: NS

MEDLINETA: Anesthesiology

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