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  • 1
    Online Resource
    Online Resource
    Frequency-Dependent ERK Phosphorylation in Spinal Neurons by Electric Stimulation of the Sciatic Nerve and the Role in Electrophysiological Activity
    SAGE Publications ; 2007
    In:  Molecular Pain Vol. 3 ( 2007-01-01), p. 1744-8069-3-18-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 3 ( 2007-01-01), p. 1744-8069-3-18-
    Abstract: The phosphorylation of extracellular signal-regulated kinase (pERK) in DRG and dorsal horn neurons is induced by the C-fiber electrical stimulation to the peripheral nerve. The present study was designed to investigate the expression and modulation of pERK in the rat dorsal horn neurons produced by repetitive electrical stimulation, and its involvement in the electrophysiological activity of dorsal horn neurons. Electrical stimulation of C-fiber intensity at different frequencies was applied to the sciatic nerve; the stimuli-induced pERK expression and the activity in dorsal horn neurons were studied by immunohistochemistry and extracellular recording, respectively. Electrical stimulation of C-fibers (3 mA) induced pERK expression in dorsal horn neurons in a frequency-dependent manner, indicating that the frequency of electrical stimulation is an important factor which activates the intracellular signal pathway in the spinal cord. To demonstrate the underlying mechanism of this frequency-dependent pERK expression, an NMDA receptor antagonist, MK-801, and a voltage sensitive calcium channel antagonist, nifedipine, were administrated intrathecally before the stimulation. We found that high frequency (0.5 Hz and 10 Hz) but not low frequent (0.05 Hz) stimulus-evoked pERK was partially inhibited by MK-801. Both high and low frequency stimulus-evoked pERK were inhibited by the nifedipine treatment. The extracellular single unit activities were recorded from the laminae I-II and V of the L4-5 dorsal horn, and we found that blockage of the intracellular ERK signal suppressed the wind-up responses in a dose-dependent manner. In contrast, any change in the mechanically evoked responses was not observed following the administration of ERK inhibitor. These observations indicate that ERK activation plays an important role in the induction of the wind-up responses in dorsal horn nociceptive neurons.
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/1744-8069-3-18
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2007
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  • 2
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    Inhibition of TRPA1 Channel Activity in Sensory Neurons by the Glial Cell Line-Derived Neurotrophic Factor Family Member, Artemin
    SAGE Publications ; 2011
    In:  Molecular Pain Vol. 7 ( 2011-01-01), p. 1744-8069-7-41-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 7 ( 2011-01-01), p. 1744-8069-7-41-
    Abstract: The transient receptor potential (TRP) channel subtype A1 (TRPA1) is known to be expressed on sensory neurons and respond to changes in temperature, pH and local application of certain noxious chemicals such as allyl isothiocyanate (AITC). Artemin is a neuronal survival and differentiation factor and belongs to the glial cell line-derived neurotrophic factor (GDNF) family. Both TRPA1 and artemin have been reported to be involved in pathological pain initiation and maintenance. In the present study, using whole-cell patch clamp recording technique, in situ hybridization and behavioral analyses, we examined the functional interaction between TRPA1 and artemin. Results: We found that 85.8 ± 1.9% of TRPA1-expressing neurons also expressed GDNF family receptor alpha 3 (GFR α3), and 87.5 ± 4.1% of GFRα3-expressing neurons were TRPA1-positive. In whole-cell patch clamp analysis, a short-term treatment of 100 ng/ml artemin significantly suppressed the AITC-induced TRPA1 currents. A concentration-response curve of AITC resulting from the effect of artemin showed that this inhibition did not change EC 50 but did lower the AITC-induced maximum response. In addition, pre-treatment of artemin significantly suppressed the number of paw lifts induced by intraplantar injection of AITC, as well as the formalin-induced pain behaviors. Conclusions: These findings that a short-term application of artemin inhibits the TRPA1 channel's activity and the sequential pain behaviors suggest a role of artemin in regulation of sensory neurons.
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/1744-8069-7-41
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2011
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  • 3
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    Online Resource
    Peripherally Increased Artemin is a Key Regulator of TRPA1/V1 Expression in Primary Afferent Neurons
    SAGE Publications ; 2015
    In:  Molecular Pain Vol. 11 ( 2015-08-28), p. s12990-015-0004-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 11 ( 2015-08-28), p. s12990-015-0004-
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/s12990-015-0004-7
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2015
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  • 4
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    Expression of Leukotriene Receptors in the Rat Dorsal Root Ganglion and the Effects on Pain Behaviors
    SAGE Publications ; 2010
    In:  Molecular Pain Vol. 6 ( 2010-01-01), p. 1744-8069-6-57-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 6 ( 2010-01-01), p. 1744-8069-6-57-
    Abstract: Leukotrienes (LTs) belong to the large family of lipid mediators implicated in various inflammatory conditions such as asthma and rheumatoid arthritis. Four distinct types (BLT1, BLT2, CysLT1 and CysLT2) of G-protein-coupled receptors for LTs have been identified. Several studies have reported that LTs are involved in inflammatory pain, but the mechanism and the expression of LT receptors in the nociceptive pathway are unknown. Results: We investigated the precise expression of these four types of LT receptors in the adult rat dorsal root ganglion (DRG) using reverse transcription-polymerase reaction (RT-PCR) and radioisotope-labeled in situ hybridization histochemistry (ISHH). We detected mRNAs for BLT1 and CysLT2 in the DRG, but not for BLT2 and CysLT1. CysLT2 mRNA was preferentially expressed by small sized DRG neurons (about 36% of total neurons), whereas BLT1 mRNA was expressed by non-neuronal cells. Double labeling analysis of CysLT2 with NF-200, calcitonin gene-related peptide (CGRP), isolectin B4 (IB4), transient receptor potential vanilloid subfamily 1 (TRPV1) and P2X3 receptor revealed that many CysLT2-labeled neurons were localized with unmyelinated and non-peptidergic neurons, and interestingly, CysLT2 mRNA heavily co-localized with TRPV1 and P2X3-positive neurons. Intraplantar injection of LTC4, a CysLT2 receptor agonist, itself did not induce the thermal hyperalgesia, spontaneous pain behaviors or swelling of hind paw. However, pretreatment of LTC4 remarkably enhanced the painful behaviors produced by alpha, beta-methylene adenosine 5′-triphosphate (αβ-me-ATP), a P2X3 receptor agonist. Conclusions: These data suggests that CysLT2 expressed in DRG neurons may play a role as a modulator of P2X3, and contribute to a potentiation of the neuronal activity following peripheral inflammation.
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/1744-8069-6-57
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
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  • 5
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    Online Resource
    Nursing Support for Caregiver Burden in Family Caregivers of Patients With Cancer: A Scoping Review
    SAGE Publications ; 2023
    In:  American Journal of Hospice and Palliative Medicine®
    Details
    In: American Journal of Hospice and Palliative Medicine®, SAGE Publications
    Abstract: Purpose: To identify nursing support for caregiver burden in family caregivers of patients with cancer. Methods: This scoping review was guided by Arksey and O’Malley’s six-stage scoping review framework. All available published articles from database inception to July 31, 2023 were systematically searched through PubMed, CINAHL, CENTRAL, and Ichushi-Web of the Japan Medical Abstract Society databases with additional relevant studies from the article list. Each key journal was manually searched. Results: Overall, 502 articles were screened, and 34 were finally included. The results of the qualitative thematic analysis were categorized into 7 components of nursing support: psychological and educational support, psychological and educational support using mainly non-face-to-face (Information and Communication Technology), psychological and educational support mainly using non-face-to-face (telephone) methods, mindfulness to support, support aimed at reducing caregiver stress, support for both patients and caregivers, and others. Of the 34 studies, 23 were randomized controlled trials (RCT), and the remaining 11 were non-RCTs. Conclusion: The results of the scoping review categorized nursing support for caregiver burden in the family caregivers of patients with cancer into 7 components. Future research should examine the feasibility of implementing these components.
    Type of Medium: Online Resource
    ISSN: 1049-9091 , 1938-2715
    URL: Article
    DOI: 10.1177/10499091231215808
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2023
    detail.hit.zdb_id: 2236674-X
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  • 6
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    Up-Regulation of Platelet-Activating Factor Synthases and its Receptor in Spinal Cord Contribute to Development of Neuropathic Pain following Peripheral Nerve Injury
    SAGE Publications ; 2012
    In:  Molecular Pain Vol. 8 ( 2012-01-01), p. 1744-8069-8-8-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 8 ( 2012-01-01), p. 1744-8069-8-8-
    Abstract: Platelet-activating factor (PAF; 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine) is a lipid mediator derived from cell membrane. It has been reported that PAF is involved in various pathological conditions, such as spinal cord injury, multiple sclerosis, neuropathic pain and intrathecal administration of PAF leads to tactile allodynia. However, the expression of PAF synthases and its receptor in the spinal cord following peripheral nerve injury is unknown. Methods: Using the rat spared nerve injury (SNI) model, we investigated the expression of PAF synthases (LPCAT1 and 2) and PAF receptor (PAFr) mRNAs in the spinal cord. Reverse transcription polymerase chain reaction (RT-PCR) and double-labeling analysis of in situ hybridization histochemistry (ISHH) with immunohistochemistry (IHC) were employed for the analyses. Pain behaviors were also examined with PAFr antagonist (WEB2086). Results: RT-PCR showed that LPCAT2 mRNA was increased in the ipsilateral spinal cord after injury, but not LPCAT1 mRNA. Double-labeling of ISHH with IHC revealed that LPCAT1 and 2 mRNAs were constitutively expressed by a subset of neurons, and LPCAT2 mRNA was increased in spinal microglia after nerve injury. RT-PCR showed that PAFr mRNA was dramatically increased in the ipsilateral spinal cord after nerve injury. Double-labeling analysis of ISHH with IHC revealed that after injury PAFr mRNA was predominantly colocalized with microglia in the spinal cord. Continuous intrathecal administration of the PAFr antagonist suppressed mechanical allodynia following peripheral nerve injury. Delayed administration of a PAFr antagonist did not reverse the mechanical allodynia. Conclusions: Our data show the histological localization of PAF synthases and its receptor in the spinal cord following peripheral nerve injury, and suggest that PAF/PAFr signaling in the spinal cord acts in an autocrine or paracrine manner among the activated microglia and neurons, thus contributing to development of neuropathic pain.
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/1744-8069-8-8
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2012
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  • 7
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    Analgesic effect of gastrin-releasing peptide in the dorsal horn
    SAGE Publications ; 2022
    In:  Molecular Pain Vol. 18 ( 2022-04), p. 174480692211089-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 18 ( 2022-04), p. 174480692211089-
    Abstract: Itch and pain are both unpleasant, but they are discrete sensations. Both of these sensations are transmitted by C-fibers and processed in laminae I-II of the dorsal horn. To examine whether pruriception modulates pain, we first confirmed the activation of cells in the itch-related circuits that were positive for gastrin-releasing peptide (GRP) and GRP receptor (GRPR) using a paw formalin injection model. This pain model with typical biphasic pain behavior increased c-Fos but did not affect the expressions of GRP and GRPR mRNAs in the dorsal horn. Using c-Fos expression as a marker for activated cells, we confirmed that formalin injection increased the number of cells double-labeled for c-Fos and GRP or GRPR in the dorsal horn. The emergence of these neurons indicates the activation of itch-related circuits by acute pain signals. The effect of an antagonist for a GRPR was examined in the paw formalin injection model. Intrathecal chronic antagonization of spinal GRPR enhanced the onset of phase II of paw formalin injection-induced pain behavior. Exogenous intrathecal GRP infusion to the paw-formalin injection model not only showed significant reduction of pain behavior but also increased c-Fos in the inhibitory neurons in the dorsal horn. The anti-nociceptive effect of spinal GRP infusion was observed in the peripheral inflammation model (complete Freund’s adjuvant injection model). In this study we suggest that painful stimuli activated itch-related neuronal circuits and uncovered the spinal activation of the itch-induced analgesic effect on acute and established inflammatory pain.
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1177/17448069221108965
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2022
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  • 8
    Online Resource
    Online Resource
    Leukotriene Enhances NMDA-Induced Inward Currents in Dorsal Horn Neurons of the Rat Spinal Cord after Peripheral Nerve Injury
    SAGE Publications ; 2015
    In:  Molecular Pain Vol. 11 ( 2015-08-28), p. s12990-015-0059-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 11 ( 2015-08-28), p. s12990-015-0059-
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/s12990-015-0059-5
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2015
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  • 9
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    Online Resource
    Differential expression of mGluRs in rat spinal dorsal horns and their modulatory effects on nocifensive behaviors
    SAGE Publications ; 2019
    In:  Molecular Pain Vol. 15 ( 2019-01), p. 174480691987502-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 15 ( 2019-01), p. 174480691987502-
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1177/1744806919875026
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2019
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  • 10
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    Differential Activation of p38 and Extracellular Signal-Regulated Kinase in Spinal Cord in a Model of Bee Venom-Induced Inflammation and Hyperalgesia
    SAGE Publications ; 2008
    In:  Molecular Pain Vol. 4 ( 2008-01-01), p. 1744-8069-4-17-
    Details
    In: Molecular Pain, SAGE Publications, Vol. 4 ( 2008-01-01), p. 1744-8069-4-17-
    Abstract: Honeybee's sting on human skin can induce ongoing pain, hyperalgesia and inflammation. Injection of bee venom (BV) into the intraplantar surface of the rat hindpaw induces an early onset of spontaneous pain followed by a lasting thermal and mechanical hypersensitivity in the affected paw. The underlying mechanisms of BV-induced thermal and mechanical hypersensitivity are, however, poorly understood. In the present study, we investigated the role of mitogen-activated protein kinase (MAPK) in the generation of BV-induced pain hypersensitivity. Results: We found that BV injection resulted in a quick activation of p38, predominantly in the L4/L5 spinal dorsal horn ipsilateral to the inflammation from 1 hr to 7 d post-injection. Phosphorylated p38 (p-p38) was expressed in both neurons and microglia, but not in astrocytes. Intrathecal administration of the p38 inhibitor, SB203580, prevented BV-induced thermal hypersensitivity from 1 hr to 3 d, but had no effect on mechanical hypersensitivity. Activated ERK1/2 was observed exclusively in neurons in the L4/L5 dorsal horn from 2 min to 1 d, peaking at 2 min after BV injection. Intrathecal administration of the MEK inhibitor, U0126, prevented both mechanical and thermal hypersensitivity from 1 hr to 2 d. p-ERK1/2 and p-p38 were expressed in neurons in distinct regions of the L4/L5 dorsal horn; p-ERK1/2 was mainly in lamina I, while p-p38 was mainly in lamina II of the dorsal horn. Conclusion: The results indicate that differential activation of p38 and ERK1/2 in the dorsal horn may contribute to the generation and development of BV-induced pain hypersensitivity by different mechanisms.
    Type of Medium: Online Resource
    ISSN: 1744-8069 , 1744-8069
    URL: Article
    DOI: 10.1186/1744-8069-4-17
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2008
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