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Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 09/2019
Journal Article
Science Signaling, ISSN 1945-0877, 02/2015, Volume 8, Issue 363, pp. fs3 - fs3
Piezo proteins-a family of mammalian cation-selective ion channels that respond to mechanical stretch-are molecular mediators of biological processes,... 
BIOCHEMISTRY & MOLECULAR BIOLOGY | PAIN | CELL BIOLOGY | TRPV Cation Channels - metabolism | Animals | Ion Channels - metabolism | Capsaicin - pharmacology | Humans | Phosphatidylinositols - metabolism | Ganglia, Spinal - cytology
Journal Article
Trends in Pharmacological Sciences, ISSN 0165-6147, 2004, Volume 25, Issue 9, pp. 465 - 470
The transmission of pain signals at the spinal level is crucially dependent on voltage-gated Ca channels in nociceptive neurons. Pharmacological and... 
Journal Article
Frontiers in Cellular Neuroscience, ISSN 1662-5102, 02/2014, Volume 8
Journal Article
Channels, ISSN 1933-6950, 01/2017, Volume 11, Issue 1, pp. 1 - 2
Journal Article
American Journal of Physiology - Gastrointestinal and Liver Physiology, ISSN 0193-1857, 07/2015, Volume 309, Issue 2, pp. G87 - G99
Quiescent phases of inflammatory bowel disease (IBD) are often accompanied by chronic abdominal pain. Although the transient receptor potential vanilloid 1... 
Inflammatory bowel disease | Transient receptor potential vanilloid 1 | Visceral pain | Substance P | Peripheral sensitization | PHYSIOLOGY | GENE-RELATED PEPTIDE | PRIMARY AFFERENT NEURONS | transient receptor potential vanilloid 1 | ULCERATIVE-COLITIS | inflammatory bowel disease | visceral pain | POTENTIAL VANILLOID 1 | INFLAMMATORY-BOWEL-DISEASE | IBS-LIKE SYMPTOMS | peripheral sensitization | CHRONIC-PANCREATITIS | PRIMARY SENSORY NEURONS | QUALITY-OF-LIFE | substance P | SUBSTANCE-P | GASTROENTEROLOGY & HEPATOLOGY | Hyperalgesia - chemically induced | Dextran Sulfate | Visceral Pain - chemically induced | Colitis - genetics | Humans | Colon - innervation | Ganglia, Spinal - physiopathology | TRPV Cation Channels - deficiency | Behavior, Animal | TRPV Cation Channels - metabolism | Transfection | Time Factors | Colitis - chemically induced | HEK293 Cells | Disease Models, Animal | Abdominal Pain - chemically induced | Acute Disease | Hyperalgesia - metabolism | Signal Transduction | Visceral Pain - physiopathology | Mice, Inbred C57BL | Abdominal Pain - physiopathology | Hyperalgesia - prevention & control | Abdominal Pain - metabolism | Visceral Pain - metabolism | TRPV Cation Channels - genetics | Hyperalgesia - physiopathology | Mice, Knockout | Visceral Pain - genetics | Animals | Colitis - physiopathology | Hyperalgesia - genetics | Abdominal Pain - genetics | Colitis - metabolism | Pain Threshold | Substance P - metabolism | Neurons, Afferent - metabolism | Pain Measurement | Ganglia, Spinal - metabolism | Abdominal pain | Care and treatment | Inflammation | Colitis | Dextran | Gastrointestinal diseases | Cell culture | Membranes | Pain | Sodium | Experiments
Journal Article
Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, 4/2013, Volume 110, Issue 18, pp. 7476 - 7481
Transient Receptor Potential Melastatin-8 (TRPM8), a recently identified member of the transient receptor potential (TRP) family of ion channels, is activated... 
Receptors | Nervous system diseases | Antiinflammatories | Cytokines | Neuropeptides | Inflammation | Mice | Colitis | Chemokines | Hypothermia | Crohn's disease | IBD | TRPV1 | CGRP | HYPOTHERMIA | ABDOMINAL-PAIN | CROHNS-DISEASE | MULTIDISCIPLINARY SCIENCES | ULCERATIVE-COLITIS | BOWEL-DISEASE | NEUROPATHIC PAIN | CHANNEL | LUNG EPITHELIAL-CELLS | PROSTATE-CANCER | COLD RECEPTOR | Dextran Sulfate | Inflammation - pathology | TRPM Cation Channels - deficiency | Humans | Colitis - complications | Colitis - pathology | Trinitrobenzenesulfonic Acid | Inflammation - complications | TRPV Cation Channels - metabolism | Inflammation Mediators - metabolism | Pyrimidinones - pharmacology | Colitis - drug therapy | Calcitonin Gene-Related Peptide - metabolism | Calcium Signaling | Disease Models, Animal | Colon - pathology | Pyrimidinones - therapeutic use | Colon - metabolism | Mice, Knockout | Animals | Colitis - physiopathology | TRPM Cation Channels - genetics | Chemokines - metabolism | TRPM Cation Channels - metabolism | Ion Channel Gating | Inflammation - physiopathology | Immunohistochemistry | Physiological aspects | Ion channels | Genetic aspects | Research | Gene expression | Health aspects | Inflammatory bowel disease | Proteins | Polymerase chain reaction | Membranes | Rodents | Chemical compounds | Biological Sciences
Journal Article
The Journal of Cell Biology, ISSN 0021-9525, 5/2008, Volume 181, Issue 3, pp. 551 - 565
Journal Article
Journal Article
SCIENTIFIC REPORTS, ISSN 2045-2322, 03/2019, Volume 9, Issue 1, pp. 3710 - 10
Immune activation may underlie the pathogenesis of irritable bowel syndrome (IBS), but the evidence is conflicting. We examined whether peripheral CD4+ T-cells... 
RESPONSES | CYTOKINE PROFILES | L-SELECTIN EXPRESSION | MULTIDISCIPLINARY SCIENCES | NEUROENDOCRINE | IMMUNE ACTIVATION | STRESS | IRRITABLE-BOWEL-SYNDROME | T-CELLS | SEVERITY | AXIS | Antiretroviral drugs | Immune response | Cytokines | Intestine | Secretion | Peripheral blood | Irritable bowel syndrome | CD62L protein | Lymphocytes T | Tumor necrosis factor-α | Cell migration | CD4 antigen
Journal Article