1,113 results match your criteria Molecular Pain [Journal]


[Express]A Novel Neuromodulation Strategy to Enhance the Prefrontal Control to Treat Pain.

Mol Pain 2019 Apr 23:1744806919845739. Epub 2019 Apr 23.

New York University Langone Medical Center.

Effective pharmacological treatment options for chronic pain remain very limited, and continued reliance on opioid analgesics has contributed to an epidemic in the U.S. On the other hand, non-pharmacologic neuromodulatory interventions provide a promising avenue for relief of chronic pain without the complications of dependence and addiction. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919845739DOI Listing

[EXPRESS] X-ray induces mechanical and heat allodynia in mouse via TRPA1 and TRPV1 activation.

Mol Pain 2019 Apr 23:1744806919849201. Epub 2019 Apr 23.

Second Affiliated Hospital of Soochow University.

Radiotherapy-related pain is a common adverse reaction with a high incidence among cancer patients undergoing radiotherapy and remarkably reduces the quality of life. However, the mechanisms of ionizing radiation (IR)-induced pain are largely unknown. In present study, mice were treated with 20 Gy X-ray to establish IR-induced pain model. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919849201DOI Listing

[EXPRESS] Tachykinins modulate nociceptive responsiveness and sensitization: In vivo electrical characterization of primary sensory neurons in tachykinin knockout (Tac1 KO) mice.

Mol Pain 2019 Apr 23:1744806919845750. Epub 2019 Apr 23.

Wake Forest Baptist Medical Center.

Since the failure of specific substance P antagonists to induce analgesia, the role of tachykinins in the development of neuropathic pain states has been discounted. This conclusion was reached without studies on the role of tachykinins in normal patterns of primary afferents response and sensitization or the consequences of their absence on the modulation of primary mechano-nociceptive afferents after injury. Nociceptive afferents from animals lacking tachykinins (Tac1 knockout: KO) showed a disrupted pattern of activation to tonic suprathreshold mechanical stimulation. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919845750DOI Listing

[EXPRESS] MicroRNA-7a ameliorates neuropathic pain in a rat model of spinal nerve ligation via the NEFL-dependent STAT3 signaling pathway.

Mol Pain 2019 Apr 15:1744806919842464. Epub 2019 Apr 15.

Xiangya Hospital, Central South University.

Neuropathic pain is a type of chronic pain induced by either central or peripheral nerve injury. MicroRNAs (miRs) have been recently linked to many diseases, including neuropathic pain. However, the role of miR-7a in neuropathic pain still remains elusive. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919842464DOI Listing

[Express] Electroacupuncture downregulates P2X3 receptor expression in dorsal root ganglia of the spinal nerve-ligated rat.

Mol Pain 2019 Apr 15:1744806919847810. Epub 2019 Apr 15.

University of Texas Medical Branch at Galveston.

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919847810DOI Listing

The Etiological Contribution of GABAergic Plasticity to the Pathogenesis of Neuropathic Pain.

Mol Pain 2019 Apr 12:1744806919847366. Epub 2019 Apr 12.

The Bonoi Academy of Science Education.

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919847366DOI Listing
April 2019
3.654 Impact Factor

[Express] Astrocyte D-serine modulates the activation of neuronal NOS leading to the development of mechanical allodynia in peripheral neuropathy.

Mol Pain 2019 Mar 22:1744806919843046. Epub 2019 Mar 22.

Spinal D-serine plays an important role in nociception via an increase in phosphorylation of the NMDA receptor GluN1 subunit (pGluN1). However, the cellular mechanisms underlying this process have not been elucidated. Here we investigate the possible role of neuronal nitric oxide synthase (nNOS) in the D-serine-induced potentiation of NMDA receptor function and the induction of neuropathic pain in a chronic constriction injury (CCI) model. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919843046DOI Listing
March 2019
1 Read

Atypical functional connectivity between the anterior cingulate cortex and other brain regions in a Rat Model of Recurrent Headache.

Mol Pain 2019 Mar 22:1744806919842483. Epub 2019 Mar 22.

Chinese PLA General Hospital.

We explored the atypical functional connectivity (FC) between the anterior cingulate cortex (ACC) and other brain areas in rats subjected to repeated meningeal nociception. The rat model was established by infusing an inflammatory soup (IS) through supradural catheters in conscious rats. Rats were subdivided according to the frequency of the IS infusions. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919842483DOI Listing

Effects of matrix metalloproteinase inhibitors on N-methyl-D-aspartate receptor and contribute to long-term potentiation in the anterior cingulate cortex of adult mice.

Mol Pain 2019 Jan-Dec;15:1744806919842958

1 Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, China.

Matrix metalloproteinases (MMPs) have been suggested to contribute to long-term potentiation, behavioral learning, and memory. In the dorsal horn of spinal cord, MMPs were reported to contribute to injury-related changes, and inhibitors of MMPs have been proposed as potential analgesics. However, it is unclear whether MMP inhibitors produce these effects by inhibiting the function of N-methyl-D-aspartate receptor (NMDAR), a key receptor for the induction of long-term potentiation. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919842958DOI Listing

[Express] Resilience factors may buffer cellular aging in individuals with and without chronic knee pain.

Mol Pain 2019 Mar 22:1744806919842962. Epub 2019 Mar 22.

University of Florida.

Telomere length, a measure of cellular aging, is inversely associated with chronic pain severity. While psychological resilience factors (e.g. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919842962DOI Listing
March 2019
1 Read

Calcium-stimulated adenylyl cyclase subtype 1 is required for presynaptic long-term potentiation in the insular cortex of adult mice.

Mol Pain 2019 Jan-Dec;15:1744806919842961

2 Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, People's Republic of China.

Recent studies indicate that presynaptic long-term potentiation in the anterior cingulate cortex may contribute to chronic pain-related anxiety. In addition to the anterior cingulate cortex, the insular cortex has also been indicated in chronic pain and its related emotional disorders. In the present study, we used a 64-channel multielectrode dish (MED64) system to record pre-long-term potentiation in the insular cortex. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919842961DOI Listing
March 2019
1 Read

Spinal glial cell line-derived neurotrophic factor infusion reverses reduction of Kv4.1-mediated A-type potassium currents of injured myelinated primary afferent neurons in a neuropathic pain model.

Mol Pain 2019 Jan-Dec;15:1744806919841196

2 Department of Anatomy and Neuroscience, Hyogo College of Medicine, Mukogawa-cho, Nishinomiya, Hyogo, Japan.

High frequency spontaneous activity in injured primary afferents has been proposed as a pathological mechanism of neuropathic pain following nerve injury. Although spinal infusion of glial cell line-derived neurotrophic factor reduces the activity of injured myelinated A-fiber neurons after fifth lumbar (L5) spinal nerve ligation in rats, the implicated molecular mechanism remains undetermined. The fast-inactivating transient A-type potassium current (I) is an important determinant of neuronal excitability, and five voltage-gated potassium channel (Kv) alpha-subunits, Kv1. Read More

View Article

Download full-text PDF

Source
http://journals.sagepub.com/doi/10.1177/1744806919841196
Publisher Site
http://dx.doi.org/10.1177/1744806919841196DOI Listing
March 2019
2 Reads

[EXPRESS] Longitudinal FDG-PET scan study of brain changes in mice with cancer-induced bone pain and after morphine analgesia.

Mol Pain 2019 Mar 14:1744806919841194. Epub 2019 Mar 14.

National Taiwan University.

Morphine is the most commonly used drug for treating physical and psychological suffering caused by advanced cancer. Although morphine is known to elicit multiple supraspinal analgesic effects, its behavioral correlates with respect to the whole brain metabolic activity during cancer-induced bone pain have not been elucidated. We injected 4T1 mouse breast cancer cells into the left femur bone marrow cavity of BALB/c mice. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919841194DOI Listing
March 2019
8 Reads

[EXPRESS] Sex differences in the contributions of spinal atypical PKCs and downstream targets to the maintenance of nociceptive sensitization.

Mol Pain 2019 Mar 11:1744806919840582. Epub 2019 Mar 11.

McGill University.

Chronic pain has been shown to depend on nociceptive sensitization in the spinal cord, and while multiple mechanisms involved in the initiation of plastic changes have been established, the molecular targets which maintain spinal nociceptive sensitization are still largely unknown. Building upon the established neurobiology underlying the maintenance of LTP in the hippocampus, this present study investigated the contributions of spinal atypical PKC isoforms PKCι/λ and PKM and their downstream targets (p62/GluA1 and NSF/GluA2 interactions, respectively) to the maintenance of spinal nociceptive sensitization in male and female rats. Pharmacological inhibition of atypical PKCs by ZIP reversed established allodynia produced by repeated intramuscular (i. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919840582DOI Listing

Peripheral and central oxidative stress in chemotherapy-induced neuropathic pain.

Mol Pain 2019 Jan-Dec;15:1744806919840098

1 Department of Neuroscience, Cell Biology, and Anatomy, University of Texas Medical Branch, Galveston, TX, USA.

Chemotherapy-induced peripheral neuropathy (CIPN) is an adverse side effect of many anti-cancer chemotherapeutic treatments. CIPN often causes neuropathic pain in extremities, and oxidative stress has been shown to be a major contributing factor to this pain. In this study, we determined the site of oxidative stress associated with pain (specifically, mechanical hypersensitivity) in cisplatin- and paclitaxel-treated mouse models of CIPN and investigated the neurophysiological mechanisms accounting for the pain. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919840098DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458664PMC
March 2019
6 Reads

[express] Memantine selectively prevented the induction of dynamic allodynia by blocking Kir2.1 channel and inhibiting the activation of microglia in spinal dorsal horn of mice in SNI model.

Mol Pain 2019 Mar 8:1744806919838947. Epub 2019 Mar 8.

Fudan University.

Memantine (MEM) is one of the important clinical medications in treating moderate to severe Alzheimer disease. The effect of MEM on preventing or treating punctate allodynia has been thoroughly studied but not on the induction of dynamic allodynia. The aim of this study is to investigate whether MEM could prevent the induction of dynamic allodynia and its underlying spinal mechanisms. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919838947DOI Listing
March 2019
7 Reads

[Express] Ageing alters signalling properties in the mouse spinal dorsal horn.

Mol Pain 2019 Mar 8:1744806919839860. Epub 2019 Mar 8.

The University of Newcastle.

A well-recognized relationship exists between ageing and increased susceptibility to chronic pain conditions, underpinning the view that pain signaling pathways differ in aged individuals. Yet despite the higher prevalence of altered pain states among the elderly, the majority of preclinical work studying mechanisms of aberrant sensory processing are conducted in juvenile or young adult animals. This mismatch is especially true for electrophysiological studies where patch clamp recordings from aged tissue are generally viewed as particularly challenging. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919839860DOI Listing

[Express] Downregulation of Glucose-6-phosphate dehydrogenase contributes to diabetic neuropathic pain through up-regulation of toll-like receptor 4 in rats.

Mol Pain 2019 Mar 6:1744806919838659. Epub 2019 Mar 6.

Soochow University.

Diabetic neuropathic pain is a refractory and disabling complication of diabetes mellitus (DM). The pathogenesis of the diabetic neuropathic pain is still unclear and treatment is insufficiency. The aim of this study is to investigate the roles of glucose-6-phosphate dehydrogenase (G6PD) and toll-like receptor 4 (TLR4) in neuropathic pain of rats with diabetes. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919838659DOI Listing

Characterization of neuromas in peripheral nerves and their effects on heterotopic bone formation.

Mol Pain 2019 Jan-Dec;15:1744806919838191

1 Center for Cell and Gene Therapy, Baylor College of Medicine, Texas Children's Hospital and Houston Methodist Hospital, Houston, TX, USA.

The formation of neuromas involves expansion of the cellular components of peripheral nerves. The onset of these disorganized tumors involves activation of sensory nerves and neuroinflammation. Particularly problematic in neuroma is arborization of axons leading to extreme, neuropathic pain. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919838191DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6440042PMC
March 2019
2 Reads

Bortezomib-induced aerobic glycolysis contributes to chemotherapy-induced painful peripheral neuropathy.

Mol Pain 2019 Jan-Dec;15:1744806919837429

1 Department of Neural and Pain Sciences, School of Dentistry, University of Maryland Baltimore, Baltimore, MD, USA.

Chemotherapy-induced painful peripheral neuropathy (CIPN) is the most common toxicity associated with widely used chemotherapeutics. CIPN is the major cause of dose reduction or discontinuation of otherwise life-saving treatment. Unfortunately, CIPN can persist in cancer survivors, which adversely affects their quality of life. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919837429DOI Listing
February 2019
2 Reads

Extracellular signal-regulated kinases mediate the enhancing effects of inflammatory mediators on resurgent currents in dorsal root ganglion neurons.

Mol Pain 2019 Jan-Dec;15:1744806919837104

1 Department of Pharmacology and Toxicology, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.

Previously we reported that a group of inflammatory mediators significantly enhanced resurgent currents in dorsal root ganglion neurons. To understand the underlying intracellular signaling mechanism, we investigated the effects of inhibition of extracellular signal-regulated kinases and protein kinase C on the enhancing effects of inflammatory mediators on resurgent currents in rat dorsal root ganglion neurons. We found that the extracellular signal-regulated kinases inhibitor U0126 completely prevented the enhancing effects of the inflammatory mediators on both Tetrodotoxin-sensitive and Tetrodotoxin-resistant resurgent currents in both small and medium dorsal root ganglion neurons. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919837104DOI Listing
February 2019

Nerve injury elevates functional Cav3.2 channels in superficial spinal dorsal horn.

Mol Pain 2019 Jan-Dec;15:1744806919836569

1 Center for Experimental Medicine, the First Affiliated Hospital of Nanchang University, Nanchang, China.

Cav3 channels play an important role in modulating chronic pain. However, less is known about the functional changes of Cav3 channels in superficial spinal dorsal horn in neuropathic pain states. Here, we examined the effect of partial sciatic nerve ligation (PSNL) on either expression or electrophysiological properties of Cav3 channels in superficial spinal dorsal horn. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919836569DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6458665PMC
February 2019
1 Read
3.654 Impact Factor

Upregulation of bone morphogenetic protein 2 ( Bmp2) in dorsal root ganglion in a rat model of bone cancer pain.

Mol Pain 2019 Jan-Dec;15:1744806918824250

1 Department of Anesthesiology, Shanghai Chest Hospital, Shanghai Jiao Tong University, Shanghai, China.

Bone cancer pain is one of the most severe and intractable complications in patients suffering from primary or metastatic bone cancer and profoundly compromises the quality of life. Emerging evidence indicates that the dorsal root ganglion play an integral role in the modulation of pain hypersensitivity. However, the underlying molecular mechanisms during dorsal root ganglion-mediated bone cancer pain remain elusive. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918824250DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329035PMC
February 2019
3.654 Impact Factor

Inhibiting STAT3 in a murine model of human breast cancer-induced bone pain delays the onset of nociception.

Mol Pain 2019 Jan-Dec;15:1744806918823477

1 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, Ontario, Canada.

Aggressive breast cancer subtypes utilize system x, a membrane antiporter, to import cystine for glutathione synthesis and maintenance of redox homeostasis, in turn releasing glutamate as a metabolic pro-nociceptive by-product. Metastatic breast cancers establish themselves at distal sites including bone, where changes in extracellular glutamate levels contribute to cancer-induced bone pain. We previously established that stearically blocking system x activity with sulfasalazine delays the onset of nociceptive behaviours and that xCT, the functional antiporter subunit, is positively regulated by signal transducer and activator of transcription 3 (STAT3). Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918823477DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329039PMC
February 2019

Inhibition by O-desmethyltramadol of glutamatergic excitatory transmission in adult rat spinal substantia gelatinosa neurons.

Mol Pain 2019 Jan-Dec;15:1744806918824243

1 Department of Physiology, Saga Medical School, Saga, Japan.

To reveal cellular mechanisms for antinociception produced by clinically used tramadol, we investigated the effect of its metabolite O-desmethyltramadol (M1) on glutamatergic excitatory transmission in spinal dorsal horn lamina II (substantia gelatinosa; SG) neurons. The whole-cell patch-clamp technique was applied at a holding potential of -70 mV to SG neurons of an adult rat spinal cord slice with an attached dorsal root. Under the condition where a postsynaptic action of M1 was inhibited, M1 superfused for 2 min reduced the frequency of spontaneous excitatory postsynaptic current in a manner sensitive to a μ-opioid receptor antagonist CTAP; its amplitude and also a response of SG neurons to bath-applied AMPA were hardly affected. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918824243DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348506PMC
February 2019

xCT knockdown in human breast cancer cells delays onset of cancer-induced bone pain.

Mol Pain 2019 Jan-Dec;15:1744806918822185

1 Michael G. DeGroote Institute for Pain Research and Care, McMaster University, Hamilton, Ontario, Canada.

Cancers in the bone produce a number of severe symptoms including pain that compromises patient functional status, quality of life, and survival. The source of this pain is multifaceted and includes factors secreted from tumor cells. Malignant cells release the neurotransmitter and cell-signaling molecule glutamate via the oxidative stress-related cystine/glutamate antiporter, system x, which reciprocally imports cystine for synthesis of glutathione and the cystine/cysteine redox cycle. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918822185DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6329019PMC
February 2019

Altered glial glutamate transporter expression in descending circuitry and the emergence of pain chronicity.

Mol Pain 2019 Jan-Dec;15:1744806918825044

1 Department of Neural and Pain Sciences, School of Dentistry, University of Maryland, Baltimore, MD, USA.

Background: The glutamate type 1 transporter (GLT1) plays a major role in glutamate homeostasis in the brain. Although alterations of GLT1 activity have been linked to persistent pain, the significance of these changes is poorly understood. Focusing on the rostral ventromedial medulla, a key site in pain modulation, we examined the expression and function of GLT1 and related transcription factor kappa B-motif binding phosphoprotein (KBBP) in rats after adjuvant-induced hind paw inflammation. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918825044DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6348548PMC
February 2019
1 Read

Dynamic changes in CGRP, PACAP, and PACAP receptors in the trigeminovascular system of a novel repetitive electrical stimulation rat model: Relevant to migraine.

Mol Pain 2019 Jan-Dec;15:1744806918820452

1 Department of Neurology, Chinese PLA General Hospital, Beijing, China.

Migraine is the seventh most disabling disorder globally, with prevalence of 11.7% worldwide. One of the prevailing mechanisms is the activation of the trigeminovascular system, and calcitonin gene-related peptide (CGRP) is an important therapeutic target for migraine in this system. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918820452DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365643PMC
February 2019
1 Read

Role of intraganglionic transmission in the trigeminovascular pathway.

Mol Pain 2019 Jan-Dec;15:1744806919836570

4 Department of Medical and Molecular Genetics, Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.

Migraine is triggered by poor air quality and odors through unknown mechanisms. Activation of the trigeminovascular pathway by environmental irritants may occur via activation of transient receptor potential ankyrin 1 (TRPA1) receptors on nasal trigeminal neurons, but how that results in peripheral and central sensitization is unclear. The anatomy of the trigeminal ganglion suggests that noxious nasal stimuli are not being transduced to the meninges by axon reflex but likely through intraganglionic transmission. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919836570DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6440047PMC
February 2019

Calcitonin gene-related peptide potentiated the excitatory transmission and network propagation in the anterior cingulate cortex of adult mice.

Mol Pain 2019 Jan-Dec;15:1744806919832718

1 Center for Neuron and Disease, Frontier Institute of Science and Technology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.

The neuropeptide of calcitonin gene-related peptide (CGRP) plays critical roles in chronic pain, especially in migraine. Immunohistochemistry and in situ hybridization studies have shown that CGRP and its receptors are expressed in cortical areas including pain perception-related prefrontal anterior cingulate cortex. However, less information is available for the functional roles of CGRP in cortical regions such as the anterior cingulate cortex (ACC). Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919832718DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6396051PMC
February 2019

Neuroinflammation and central PI3K/Akt/mTOR signal pathway contribute to bone cancer pain.

Mol Pain 2019 Jan-Dec;15:1744806919830240

4 Department of Clinical Laboratory, The First Hospital of Jilin University, Changchun, China.

Background: Pain is one of the most common and distressing symptoms suffered by patients with progression of cancer; however, the mechanisms responsible for hyperalgesia are not well understood. Since the midbrain periaqueductal gray is an important component of the descending inhibitory pathway controlling on central pain transmission, in this study, we examined the role for pro-inflammatory cytokines of the periaqueductal gray in regulating mechanical and thermal hyperalgesia evoked by bone cancer via phosphatidylinositide 3-kinase (PI3K)-mammalian target of rapamycin (mTOR) signals.

Methods: Breast sarcocarcinoma Walker 256 cells were implanted into the tibia bone cavity of rats to induce mechanical and thermal hyperalgesia. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919830240DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6390230PMC
February 2019
28 Reads
3.654 Impact Factor

Astrocyte activation in the periaqueductal gray promotes descending facilitation to cancer-induced bone pain through the JNK MAPK signaling pathway.

Mol Pain 2019 Jan-Dec;15:1744806919831909

2 Department of Anesthesiology and Pain Research Center, The First Affiliated Hospital of Jiaxing University, Jiaxing, China.

Descending nociceptive modulation from the supraspinal structures has an important role in cancer-induced bone pain (CIBP). Midbrain ventrolateral periaqueductal gray (vlPAG) is a critical component of descending nociceptive circuits; nevertheless, its precise cellular and molecular mechanisms involved in descending facilitation remain elusive. Our previous study has shown that the activation of p38 MAPK in vlPAG microglia is essential for the neuropathic pain sensitization. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919831909DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6388461PMC
February 2019
1 Read

TLR4 mediates upregulation and sensitization of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate-induced colitis.

Mol Pain 2019 Jan-Dec;15:1744806919830018

1 Department of Anatomy and Physiology, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Elevated excitability of primary afferent neurons underlies chronic pain in patients with functional or inflammatory bowel diseases. Recent studies have established an essential role for an enhanced transient receptor potential vanilloid subtype 1 (TRPV1) signaling in mediating peripheral hyperalgesia in inflammatory conditions. Since colocalization of Toll-like receptor 4 (TLR4) and TRPV1 has been observed in primary afferents including the trigeminal sensory neurons and the dorsal root ganglion neurons, we test the hypothesis that TLR4 might regulate the expression and function of TRPV1 in primary afferent neurons in 2,4,6-trinitrobenzene sulfate (TNBS)-induced colitis using the TLR4-deficient and the wild-type C57 mice. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919830018DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378437PMC
January 2019
6 Reads

ERK and p38 contribute to the regulation of nociceptin and the nociceptin receptor in human peripheral blood leukocytes.

Mol Pain 2019 Jan-Dec;15:1744806919828921

1 Department of Anaesthesiology and Pain Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland.

Little is known about the mechanisms involved in the regulation of nociceptin and its receptor (nociceptin opioid peptide receptor, NOP) in response to inflammation and pain in humans. In this study, specific signaling pathways contributing to the regulation of nociceptin and NOP in human peripheral blood leukocytes were investigated. After approval by the ethics committee, peripheral blood obtained from healthy donors was cultured with or without phorbol-12-myristate-13-acetate (PMA). Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919828921DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378488PMC
January 2019
7 Reads

Epigenetic control of hypersensitivity in chronic inflammatory pain by the de novo DNA methyltransferase Dnmt3a2.

Mol Pain 2019 Jan-Dec;15:1744806919827469

1 Department of Neurobiology, Interdisciplinary Centre for Neurosciences, Heidelberg University, Heidelberg, Germany.

Chronic pain is a pathological manifestation of neuronal plasticity supported by altered gene transcription in spinal cord neurons that results in long-lasting hypersensitivity. Recently, the concept that epigenetic regulators might be important in pathological pain has emerged, but a clear understanding of the molecular players involved in the process is still lacking. In this study, we linked Dnmt3a2, a synaptic activity-regulated de novo DNA methyltransferase, to chronic inflammatory pain. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919827469DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6362517PMC
January 2019
2 Reads

Differential regulation of GSK-3β in spinal dorsal horn and in hippocampus mediated by interleukin-1beta contributes to pain hypersensitivity and memory deficits following peripheral nerve injury.

Mol Pain 2019 Jan-Dec;15:1744806919826789

1 Pain Research Center and Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.

Accumulating evidence shows that inhibition of glycogen synthase kinase-3beta (GSK-3β) ameliorates cognitive impairments caused by a diverse array of diseases. Our previous work showed that spared nerve injury (SNI) that induces neuropathic pain causes short-term memory deficits. Here, we reported that GSK-3β activity was enhanced in hippocampus and reduced in spinal dorsal horn following SNI, and the changes persisted for at least 45 days. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806919826789DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6378430PMC
January 2019
15 Reads

C57BL/6 substrain differences in inflammatory and neuropathic nociception and genetic mapping of a major quantitative trait locus underlying acute thermal nociception.

Mol Pain 2019 Jan-Dec;15:1744806918825046

3 Department of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA.

Sensitivity to different pain modalities has a genetic basis that remains largely unknown. Employing closely related inbred mouse substrains can facilitate gene mapping of nociceptive behaviors in preclinical pain models. We previously reported enhanced sensitivity to acute thermal nociception in C57BL/6J (B6J) versus C57BL/6N (B6N) substrains. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918825046DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365993PMC
January 2019
2 Reads

Fibromyalgia: Genetics and epigenetics insights may provide the basis for the development of diagnostic biomarkers.

Mol Pain 2019 Jan-Dec;15:1744806918819944. Epub 2018 Nov 29.

1 Anesthesiology, Critical Care and Pain Medicine Division, Department of Medicine and Surgery, University of Parma, Parma, Italy.

Fibromyalgia is a disease characterized by chronic widespread pain with additional symptoms, such as joint stiffness, fatigue, sleep disturbance, cognitive dysfunction, and depression. Currently, fibromyalgia diagnosis is based exclusively on a comprehensive clinical assessment, according to 2016 ACR criteria, but validated biological biomarkers associated with fibromyalgia have not yet been identified. Genome-wide association studies investigated genes potentially involved in fibromyalgia pathogenesis highlighting that genetic factors are possibly responsible for up to 50% of the disease susceptibility. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918819944DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6322092PMC
November 2018
3 Reads

Evoked hypoalgesia is accompanied by tonic pain and immune cell infiltration in the dorsal root ganglia at late stages of diabetic neuropathy in mice.

Mol Pain 2018 Jan-Dec;14:1744806918817975. Epub 2018 Nov 20.

Institute of Pharmacology, Heidelberg University, Germany.

Diabetic peripheral neuropathy is a major debilitating late complication of diabetes, which significantly reduces the quality of life in patients. Diabetic peripheral neuropathy is associated with a wide spectrum of sensory abnormalities, where in loss of sensation or hypoalgesia to applied external stimuli is paradoxically accompanied by debilitating tonic spontaneous pain. In numerous studies on animal models of diabetic peripheral neuropathy, behavioural measurements have been largely confined to analysis of evoked withdrawal to mechanical and thermal stimuli applied to dermatomes, whereas spontaneous, on-going pain has not been widely studied. Read More

View Article

Download full-text PDF

Source
http://journals.sagepub.com/doi/10.1177/1744806918817975
Publisher Site
http://dx.doi.org/10.1177/1744806918817975DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6311571PMC
April 2019
5 Reads

Ethanol-induced enhancement of inhibitory synaptic transmission in the rat spinal substantia gelatinosa.

Mol Pain 2018 Jan-Dec;14:1744806918817969. Epub 2018 Nov 19.

1 Department of Neurophysiology, Hyogo College of Medicine, Nishinomiya, Japan.

Recent studies have shown that ethanol produces a widespread modulation of neuronal activity in the central nervous system. It is not fully understood, however, how ethanol changes nociceptive transmission. We investigated acute effects of ethanol on synaptic transmission in the substantia gelatinosa (lamina II of the spinal dorsal horn) and mechanical responses in the spinal dorsal horn. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918817969DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6293375PMC
April 2019
10 Reads

RNA-seq of spinal cord from nerve-injured rats after spinal cord stimulation.

Mol Pain 2018 Jan-Dec;14:1744806918817429. Epub 2018 Nov 19.

3 Department of Anesthesia and Critical Care Medicine, School of Medicine, Johns Hopkins University, Baltimore, MA, USA.

Spinal cord stimulation has become an important modality in pain treatment especially for neuropathic pain conditions refractory to pharmacotherapy. However, the molecular control of inhibitory and excitatory mechanisms observed after spinal cord stimulation are poorly understood. Here, we used RNA-seq to identify differences in the expression of genes and gene networks in spinal cord tissue from nerve-injured rats with and without repetitive conventional spinal cord stimulation treatment. Read More

View Article

Download full-text PDF

Source
http://journals.sagepub.com/doi/10.1177/1744806918817429
Publisher Site
http://dx.doi.org/10.1177/1744806918817429DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6293371PMC
April 2019
19 Reads
3.654 Impact Factor

Involvement of mGluR5 and TRPV1 in visceral nociception in a rat model of uterine cervical distension.

Mol Pain 2018 Jan-Dec;14:1744806918816850. Epub 2018 Nov 16.

1 Department of Anesthesia, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

Metabotropic glutamate receptor 5 (mGluR5) and transient receptor potential vanilloid subtype 1 (TRPV1) have been shown to play critical roles in the transduction and modulation of cutaneous nociception in the central nervous system. However, little is known regarding the possible involvement of mGluR5 and TRPV1 in regulating visceral nociception from the uterine cervix. In this study, we used a rat model of uterine cervical distension to examine the effects of noxious stimuli to the uterine cervix on expression of spinal mGluR5 and TRPV1. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918816850DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6302284PMC
April 2019
18 Reads

Expression of mitochondrial dysfunction-related genes and pathways in paclitaxel-induced peripheral neuropathy in breast cancer survivors.

Mol Pain 2018 Jan-Dec;14:1744806918816462. Epub 2018 Nov 14.

1 School of Nursing, University of California, San Francisco, San Francisco, CA, USA.

Background: Paclitaxel is one of the most commonly used drugs to treat breast cancer. Its major dose-limiting toxicity is paclitaxel-induced peripheral neuropathy (PIPN). PIPN persists into survivorship and has a negative impact on patient's mood, functional status, and quality of life. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918816462DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6293373PMC
April 2019
31 Reads

Structural homology of myelin basic protein and muscarinic acetylcholine receptor: Significance in the pathogenesis of complex regional pain syndrome.

Mol Pain 2018 Jan-Dec;14:1744806918815005. Epub 2018 Nov 5.

1 Department of Anesthesiology, University of California, San Diego, La Jolla, CA, USA.

Complex regional pain syndrome is an extremely painful condition that develops after trauma to a limb. Complex regional pain syndrome exhibits autoimmune features in part mediated by autoantibodies against muscarinic-2 acetylcholine (M2) receptor. The mechanisms underlying the M2 receptor involvement in complex regional pain syndrome remain obscure. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918815005DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6287297PMC
April 2019
10 Reads

A novel gain-of-function Na1.7 mutation in a carbamazepine-responsive patient with adult-onset painful peripheral neuropathy.

Mol Pain 2018 Jan-Dec;14:1744806918815007. Epub 2018 Nov 5.

1 Department of Neurology, Yale University School of Medicine, New Haven, CT, USA.

Voltage-gated sodium channel Na1.7 is a threshold channel in peripheral dorsal root ganglion (DRG), trigeminal ganglion, and sympathetic ganglion neurons. Gain-of-function mutations in Na1. Read More

View Article

Download full-text PDF

Source
http://journals.sagepub.com/doi/10.1177/1744806918815007
Publisher Site
http://dx.doi.org/10.1177/1744806918815007DOI Listing
February 2019
14 Reads

Differential modulation of voltage-gated sodium channels by nerve growth factor in three major subsets of TrkA-expressing nociceptors.

Mol Pain 2018 Jan-Dec;14:1744806918814640. Epub 2018 Nov 2.

1 Institute of Pharmacology, Heidelberg University, Heidelberg, Germany.

Nerve growth factor is an inflammatory mediator that induces long-lasting hyperalgesia, which can partially be attributed to nerve growth factor-induced sensitization of primary afferent nociceptors. It was shown that nerve growth factor increases the excitability of polymodal C-fibre nociceptors by modulating tetrodotoxin-sensitive and tetrodotoxin-resistant voltage-gated sodium channels, but hitherto only little is known about the effects of nerve growth factor on sodium currents in other nociceptor subtypes that express the nerve growth factor receptor TrkA. We previously characterized two reporter mouse lines that allow the unequivocal identification of two important subclasses of TrkA-expressing nociceptors - i. Read More

View Article

Download full-text PDF

Source
http://journals.sagepub.com/doi/10.1177/1744806918814640
Publisher Site
http://dx.doi.org/10.1177/1744806918814640DOI Listing
February 2019
4 Reads

Effects of cooling temperatures and low pH on membrane properties and voltage-dependent currents of rat nociceptive-like trigeminal ganglion neurons.

Mol Pain 2018 Jan-Dec;14:1744806918814350. Epub 2018 Oct 31.

1 Department of Anesthesiology and Perioperative Medicine, College of Medicine, University of Alabama at Birmingham, Birmingham, AL, USA.

Cooling temperatures and low pH have profound effects on somatosensory functions including nociception. The effects not only can be mediated by cooling temperature transducers and proton transducers expressed in subpopulations of somatosensory neurons but may also be mediated by ion channels involving membrane excitability such as voltage-dependent K channels in somatosensory neurons. In the present study, we performed the in situ patch-clamp recordings from nociceptive-like trigeminal ganglion neurons in ex vivo trigeminal ganglion preparations of adult rats. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918814350DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6249654PMC
February 2019
1 Read

Tetrahydroxystilbene glucoside relieves the chronic inflammatory pain by inhibiting neuronal apoptosis, microglia activation, and GluN2B overexpression in anterior cingulate cortex.

Mol Pain 2018 Jan-Dec;14:1744806918814367. Epub 2018 Nov 1.

1 Department of Orthopedics, Jinling Hospital, Medical School of Nanjing University, Nanjing, China.

Tetrahydroxystilbene glucoside (THSG) is one of the active ingredients of Polygonum multiflorum. It has been shown to exert a variety of pharmacological effects, including antioxidant, anti-aging, and anti-atherosclerosis. Because of its prominent anti-inflammatory effect, we explored whether THSG had analgesic effect. Read More

View Article

Download full-text PDF

Source
http://dx.doi.org/10.1177/1744806918814367DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6259074PMC
April 2019
9 Reads
3.654 Impact Factor

Analgesic effects of FAAH inhibitor in the insular cortex of nerve-injured rats.

Mol Pain 2018 Jan-Dec;14:1744806918814345. Epub 2018 Oct 31.

1 Department of Physiology and Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul, Republic of Korea.

The insular cortex is an important region of brain involved in the processing of pain and emotion. Recent studies indicate that lesions in the insular cortex induce pain asymbolia and reverse neuropathic pain. Endogenous cannabinoids (endocannabinoids), which have been shown to attenuate pain, are simultaneously degraded by fatty acid amide hydrolase (FAAH) that halts the mechanisms of action. Read More

View Article

Download full-text PDF

Source
http://journals.sagepub.com/doi/10.1177/1744806918814345
Publisher Site
http://dx.doi.org/10.1177/1744806918814345DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6247483PMC
February 2019
14 Reads