The effect of endoneurial nerve growth factor on calcitonin gene-related peptide expression in primary sensory neurons

Barría, Guido Ruiz; Baños, Josep-Eladi

doi:10.1016/j.brainres.2005.02.009

Cited by 21 publications

(16 citation statements)

References 46 publications

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“…In a previous report, endoneurial injection of nerve growth factor (NGF) increased the percentage of large-sized CGRP-IR DRG neurons [18]. Therefore, NGF seems to be implicated in a switch to CGRP expression in larger DRG neurons.…”

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confidence: 86%

Changes in calcitonin gene-related peptide expression following joint immobilization in rats

Nishigami

Osako

Tanaka

et al. 2009

Neuroscience Letters

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confidence: 86%

Changes in calcitonin gene-related peptide expression following joint immobilization in rats

Nishigami

Osako

Tanaka

et al. 2009

Neuroscience Letters

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“…CGRP is normally released under painful stimulation potentiating nociceptive signaling [42] , and plays important roles in the maintenance of both neuropathic and inflammatory pain states [22,23,43,44] . In MA, no significant differences in CGRP expression were found.…”

Section: Discussionmentioning

confidence: 99%

“…This was performed with the help of the ImageJ version 1.37 (free access software) computer program. At least 350 total cells with visible nuclei per rat (corresponding more or less to a sample of 1,500 cells per experimental group) were randomly chosen from 8 to 9 (every fifth) sections of the same DRG and were counted, as similarly described before [23,29] . pAkt immunoreactivity was expressed as the percentage of pAkt-IR cells in the total number of counted neurons.…”

Section: Discussionmentioning

confidence: 99%

“…It has been recognized as a nerve regeneration-promoting peptide, after neuronal damage [21] . More recently, its expression was shown to be either increased or decreased depending on the sciatic nerve injury, indicating that the nature of the peripheral injury has an impact on CGRP expression [22] even affecting different neuronal populations [23] . Thus, possible changes in CGRP expression during MA were also evaluated.…”

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confidence: 99%

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Neuronal Injury Marker ATF-3 Is Induced in Primary Afferent Neurons of Monoarthritic Rats

et al. 2011

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Activating transcription factor 3 (ATF-3) expression has been associated with several signaling pathways implicated in cellular stress response in many cell types and is usually regarded as a neuronal damage marker in dorsal root ganglia (DRG). We investigated ATF-3 expression in primary afferents in the monoarthritic (MA) model of chronic inflammatory joint pain. Immunohistochemistry revealed that ATF-3 is highly induced mainly in small and medium neurons, especially at 2 and 4 days of MA in L₅ DRGs. Colocalization with calcitonin gene-related peptide (CGRP) and isolectin B4 (IB4) demonstrated that ATF-3-immunoreactive cells are mainly peptidergic. The lack of significant differences in ATF-3 and pAkt colocalization indicated that ATF-3 is probably not involved in a pAkt-mediated survival pathway. Anti-inflammatory (ketoprofen) administration failed to reverse ATF-3 induction in MA rats, but significantly increased CGRP expression. These data suggest that ATF-3 expression is definitely involved in MA, actually marking injured neurons. Some degree of neuronal damage seems to occur right from the first days of disease, mainly affecting small-to-medium peptidergic neurons. The intra-articular injection of complete Freund’s adjuvant and the generation of a neuroinflammatory environment seem to be the plausible explanation for the local nerve damage.

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“…Measures were developed considering a correction method to establish an immunoreactivity threshold for each analyzed image, as was previously described (Ruiz & Baños, 2005). Viewing images of DRG sections from naïve rats, the substance P-immunoreactivity (SP-IR) was accurately discriminated, and standard values for background (from clearly unstained cells) and the IR-threshold were set.…”

Section: Image Analysismentioning

confidence: 99%

Heat Hyperalgesia Induced by Endoneurial Nerve Growth Factor and the Expression of Substance P in Primary Sensory Neurons

Barría

Baños

2009

International Journal of Neuroscience

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Endoneurial nerve growth factor (30 ng) produced significant heat hyperalgesia in rats on postinjection days 3 and 5. The percentage of neuron profiles expressing the sensory neuropeptide substance P in the dorsal root ganglion (DRG), and the density and distribution of substance P immunoreactivity at the DRG and the dorsal horn remained essentially unchanged throughout the 10 days of study. NGF increased pain scores in the second phase of the formalin test on postinjection day 3, but not on days 5 and 10. Our results indicate that the observed heat hyperalgesia is not dependent on NGF-induced changes in SP content and release from primary sensory neurons.

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The effect of endoneurial nerve growth factor on calcitonin gene-related peptide expression in primary sensory neurons

Cited by 21 publications

References 46 publications

Changes in calcitonin gene-related peptide expression following joint immobilization in rats

Changes in calcitonin gene-related peptide expression following joint immobilization in rats

Neuronal Injury Marker ATF-3 Is Induced in Primary Afferent Neurons of Monoarthritic Rats

Heat Hyperalgesia Induced by Endoneurial Nerve Growth Factor and the Expression of Substance P in Primary Sensory Neurons

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