2007
DOI: 10.1097/01.anes.0000267538.72900.68
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Painful Nerve Injury Shortens the Intracellular Ca2+ Signal in Axotomized Sensory Neurons of Rats

Abstract: Background-Neuropathic pain is inadequately treated and poorly understood at the cellular level. Because intracellular Ca 2+ signaling critically regulates diverse neuronal functions, the authors examined effects of peripheral nerve injury on the Ca 2+ transient that follows neuronal activation.

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Cited by 43 publications
(56 citation statements)
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References 42 publications
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“…Interruption of sensory activity by axotomy leads to loss of normal afferent neuronal traffic, particularly the low-threshold input into large myelinated somata. The loss of depolarization events decreases Ca 2ϩ influx through VGCC and diminishes release from intracellular stores (3,4). This is confirmed by our present results that indicate depressed [Ca 2ϩ ] i levels in SNL-H neurons both at rest and after ionomycin administration (Fig.…”
Section: Single-channel Properties Are Not Altered By Painful Nerve Isupporting
confidence: 90%
See 1 more Smart Citation
“…Interruption of sensory activity by axotomy leads to loss of normal afferent neuronal traffic, particularly the low-threshold input into large myelinated somata. The loss of depolarization events decreases Ca 2ϩ influx through VGCC and diminishes release from intracellular stores (3,4). This is confirmed by our present results that indicate depressed [Ca 2ϩ ] i levels in SNL-H neurons both at rest and after ionomycin administration (Fig.…”
Section: Single-channel Properties Are Not Altered By Painful Nerve Isupporting
confidence: 90%
“…These alterations include decreased Ca 2ϩ influx via voltage-gated calcium channels (VGCC), reduced [Ca 2ϩ ] i , and diminished Ca 2ϩ -induced Ca 2ϩ release (3,4). Additionally, ATPsensitive potassium (K ATP ) channels in large axotomized DRG neurons from rats with hyperalgesia exhibit decreased opening (5,6).…”
mentioning
confidence: 99%
“…Indeed, the loss of I h might be considered a compensatory measure in the context of injury. While the present experiments do not indicate a mechanism by which I h in decreased after axotomy, it is possible that axotomy-induced depression of both resting levels of cytosolic Ca 2+ as well as the transient rises of Ca 2+ that accompany neuronal activation (Fuchs et al, 2005;Fuchs et al, 2007) may result in lowered activity of Ca 2+ /calmodulindependent protein kinase II, which is a regulator of I h activity (Fan et al, 2005;Rigg et al, 2003).…”
Section: Discussioncontrasting
confidence: 72%
“…The changes occurred in lesioned animals only. It is known that peripheral axonal lesion induces ectopic discharges in the primary neuron, which is related to changes of ionic channels [50,51]. In cat spinal cord, the high frequency stimulation of sciatic nerve evoked increase in monoamines concentrations [52].…”
Section: Discussionmentioning
confidence: 99%