Painful nerve injury shortens the intracellular Ca2+ signal in axotomized sensory neurons of rats. Anesthesiology 2007 Jul;107(1):106-16
Date
06/23/2007Pubmed ID
17585222Pubmed Central ID
PMC3735132DOI
10.1097/01.anes.0000267538.72900.68Scopus ID
2-s2.0-34250852258 (requires institutional sign-in at Scopus site) 39 CitationsAbstract
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.
Author List
Fuchs A, Rigaud M, Hogan QHAuthor
Quinn H. Hogan MD Professor in the Anesthesiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsAxotomy
Calcium Signaling
Capsaicin
Cell Size
Cytophotometry
Electric Stimulation
Ganglia, Spinal
Hyperalgesia
Ligation
Male
Nerve Fibers
Neurons, Afferent
Nociceptors
Peripheral Nerve Injuries
Potassium
Rats
Rats, Sprague-Dawley
Spinal Nerves
Stimulation, Chemical
Wallerian Degeneration
