Transcription factor regulation of prodynorphin gene expression following rat hindpaw inflammation

Messersmith, Donna J.; Kim, David J.; Iadarola, Michael J.

doi:10.1016/s0169-328x(97)00308-2

Cited by 82 publications

(58 citation statements)

References 41 publications

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“…This possibility has been suggested in studies addressing pCREB involvement with peripheral nerve injury (Gold et al, 1993), somatic (Ji and Rupp, 1997;Messersmith et al, 1998), and visceral inflammation and sympathetic neuron survival (Riccio et al, 1999). The influence of target organ-neuron interactions in the adult animal has been extensively demonstrated (Steers et al, 1991;Vizzard, 2000c;Qiao and Vizzard, 2002a;Murray et al, 2004;Steers and Tuttle, 2006).…”

Section: Vip Functions In the Lower Urinary Tractmentioning

confidence: 99%

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

et al. 2008

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The expression of phosphorylated cAMP response element binding protein (pCREB) in dorsal root ganglia (DRG) with and without CYP-induced cystitis (150 mg/kg, i.p; 48 hr) was determined in VIP −/− and wildtype (WT) mice. p-CREB-immunoreactivity (IR) was determined in bladder (Fastblue) afferent cells. Nerve growth factor (NGF) bladder content was determined by ELISAs. Basal expression of pCREB-IR in DRG of VIP −/− mice was (p ≤ 0.01) greater in L1, L2, L5-S1 DRG compared to WT mice. CYP treatment in WT mice increased (p ≤ 0.05) pCREB-IR in L1, L2, L5-S1 DRG. CYP treatment in VIP −/− mice (p ≤ 0.01) increased (p ≤ 0.01) p-CREB-IR in L6-S1 DRG compared to WT with CYP. In WT mice, bladder afferent cells (20-38%) in DRG expressed pCREB-IR under basal conditions. With CYP, pCREB-IR increased in bladder afferent cells (60-65%; L6-S1 DRG) in WT mice. In VIP −/− mice, bladder afferent cells (12-58%) expressed pCREB-IR under basal conditions and CYP increased pCREB expression (78-84%) in L6-S1 DRG. Urinary bladder NGF expression in VIP −/− mice under basal conditions or after cystitis was significantly greater than WT. Detrusor smooth muscle thickness was significantly increased in VIP −/− mice. Bladder NGF expression may contribute to differences in pCREB expression.

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Section: Vip Functions In the Lower Urinary Tractmentioning

confidence: 99%

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

et al. 2008

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“…ERK is required for c-Fos expression in the spinal cord in a rat model of radicular neuritis (Kominato et al, 2003). Noxious stimulation and peripheral inflammation evoke ipsilateral pERK induction and c-fos expression but a bilateral induction of pCREB in the dorsal horn (Ji and Rupp, 1997;Messersmith et al, 1998). pERK is predominantly induced in superficial dorsal horn neurons, whereas pCREB and c-fos are also induced in the deep dorsal horn.…”

Section: Erk Activation Creb Phosphorylation and Gene Transcriptionmentioning

confidence: 99%

“…Many inflammation-induced genes, such as c-fos, prodynorphin, Cox-2, NK-1, and TrkB, contain CRE sites in their promoter regions (Lonze and Ginty, 2002), and c-fos is regulated by the ERK/CREB pathway in pheochromocytoma 12 cells and cortical neurons (Ginty et al, 1994;Xia et al, 1996). Noxious stimulation and inflammation induce CREB phosphorylation in dorsal horn neurons (Ji and Rupp, 1997;Messersmith et al, 1998;Wu et al, 2002), but it is not known whether this is ERK dependent.…”

Section: Introductionmentioning

confidence: 99%

Ionotropic and Metabotropic Receptors, Protein Kinase A, Protein Kinase C, and Src Contribute to C-Fiber-Induced ERK Activation and cAMP Response Element-Binding Protein Phosphorylation in Dorsal Horn Neurons, Leading to Central Sensitization

Kawasaki¹,

Kohno²,

Zhuang³

et al. 2004

J. Neurosci.

339

284

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Molecular mechanisms underlying C-fiber stimulation-induced ERK (extracellular signal-regulated kinase) activation in dorsal hornneurons and its contribution to central sensitization have been investigated. In adult rat spinal slice preparations, activation of C-fiber primary afferents by a brief exposure of capsaicin produces an eightfold to 10-fold increase in ERK phosphorylation (pERK) in superficial dorsal horn neurons. The pERK induction is reduced by blockade of NMDA, AMPA/kainate, group I metabotropic glutamate receptor, neurokinin-1, and tyrosine receptor kinase receptors. The ERK activation produced by capsaicin is totally suppressed by inhibition of either protein kinase A (PKA) or PKC. PKA or PKC activators either alone or more effectively together induce pERK in superficial dorsal horn neurons. Inhibition of calcium calmodulin-dependent kinase (CaMK) has no effect, but pERK is reduced by inhibition of the tyrosine kinase Src. The induction of cAMP response element binding protein phosphorylation (pCREB) in spinal cord slices in response to C-fiber stimulation is suppressed by preventing ERK activation with the MAP kinase kinase inhibitor 2-(2-diamino-3-methoxyphenyl-4H-1-benzopyran-4-one (PD98059) and by PKA, PKC, and CaMK inhibitors. Similar signaling contributes to pERK induction after electrical stimulation of dorsal root C-fibers. Intraplantar injection of capsaicin in an intact animal increases expression of pCREB, c-Fos, and prodynorphin in the superficial dorsal horn, changes that are prevented by intrathecal injection of PD98059. Intrathecal PD98059 also attenuates capsaicin-induced secondary mechanical allodynia, a pain behavior reflecting hypersensitivity of dorsal horn neurons (central sensitization). We postulate that activation of ionotropic and metabotropic receptors by C-fiber nociceptor afferents activates ERK via both PKA and PKC, and that this contributes to central sensitization through post-translational and CREB-mediated transcriptional regulation in dorsal horn neurons.

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“…In addition to the classical cAMP-PKA pathway, there are several intracellular messengers, such as calmodulin-dependent protein kinase (CaMK), nerve growth factor (NGF)-mediated Ras/Raf mitogen-activated protein kinase kinase-1/2 (MEK-1/2) and extracellular regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 MAPK, and other kinases that are activated through different upstream transduction chains and may contribute to the regulation of CREB phosphorylation. 11,34 It has been shown that the ERK isoforms (ERK1/2) are phosphorylated in the spinal cord after peripheral inflammation and after PSNL. 35,36 Inhibitory effects on formalin-induced flinching, comparable with those observed in a study using p38 MAPK inhibitors, were seen when an ERK inhibitor was given intrathecally.…”

Section: Discussionmentioning

confidence: 99%

Adenylate cyclase inhibition attenuates neuropathic pain but lacks pre-emptive effects in rats

Liou

Liu

Mao

et al. 2009

Can J Anesth/J Can Anesth

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Purpose There is evidence that cyclic adenosine monophosphate (cAMP) transduction is involved in nociceptive processing. We previously showed that intrathecal injection of an adenylate cyclase inhibitor attenuated tactile allodynia caused by partial sciatic nerve ligation (PSNL) in rats. The present study investigates the pre-emptive effects of spinal cAMP transduction on nociceptive processing in a chronic neuropathic pain model. Methods Intrathecal catheterization and PSNL were performed in male Sprague-Dawley rats. Nociceptive responses to mechanical and thermal stimuli were evaluated at the hindpaw at 2 hr and at 3, 7, and 14 days after PSNL. The pre-emptive effects of the intrathecal adenylate cyclase inhibitor, SQ22536 (0.7 lmol Á L -1 , 30 min before or after nerve ligation) were assessed. Also, the spatial and temporal expression profiles and immunoreactivity in the spinal cord of the cAMP response element binding protein (CREB) and its phosphorylated proteins (CREB-IR and p-CREB-IR) were analyzed.Results Compared with the rats treated with the vehicle, allodynia and hyperalgesia were significantly attenuated at 1-3 days by the intrathecal injection of SQ22536 performed either before or after ligation. The expression of CREB was significantly higher after ligation (P \ 0.05), but differences were not observed between groups. Intrathecal injection of SQ22536, either before or after ligation, partially reduced p-CREB-IR protein expression in comparison with the vehicle control, especially after the first 3 days (P \ 0.05). Conclusion Our results show a possible association between the increase in p-CREB and PSNL-induced neuropathic pain. However, a pre-emptive effect of adenylate cyclase inhibitor administered before surgery was not observed. RésuméObjectif Des donne´es soutiennent que la transduction de l'ade´nosine monophosphate cyclique (AMPc) est implique´e dans le traitement des signaux nociceptifs. Nous avons pre´ce´demment montre´que l'injection intrathe´cale d'un inhibiteur de l'ade´nylcyclase atte´nuait l'allodynie tactile cause´e par une ligature partielle du nerf sciatique (PSNL) chez le rat. Cette e´tude explore les effets pre´ventifs de la transduction d'AMPc rachidienne sur le traitement des signaux nociceptifs dans un mode`le de douleur neuropathique chronique. Méthode Un cathe´te´risme intrathe´cal et une PSNL ont e´te´re´alise´s sur des rats maˆles Sprague-Dawley. Les re´actions nociceptives aux stimuli me´caniques et thermiques ont e´te´e´value´es a`la patte arrie`re a`2 heures et a`3, 7 et 14 jours post-PSNL. Les effets pre´ventifs de l'inhibiteur intrathe´cal de l'ade´nylcyclase, le SQ22536, (0.7 lmolÁL -1 , 30 min avant ou apre`s la ligature du nerf) ont e´te´e´value´s. De plus, les profils d'expression spatiale et temporelle et

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Transcription factor regulation of prodynorphin gene expression following rat hindpaw inflammation

Cited by 82 publications

References 41 publications

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

Expression of Phosphorylated cAMP Response Element Binding Protein (p-CREB) in Bladder Afferent Pathways in VIP−/− Mice with Cyclophosphamide (CYP)-Induced Cystitis

Ionotropic and Metabotropic Receptors, Protein Kinase A, Protein Kinase C, and Src Contribute to C-Fiber-Induced ERK Activation and cAMP Response Element-Binding Protein Phosphorylation in Dorsal Horn Neurons, Leading to Central Sensitization

Adenylate cyclase inhibition attenuates neuropathic pain but lacks pre-emptive effects in rats

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