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Article ; Online: Author Correction: Africa-specific human genetic variation near CHD1L associates with HIV-1 load.

McLaren, Paul J / Porreca, Immacolata / Iaconis, Gennaro / Mok, Hoi Ping / Mukhopadhyay, Subhankar / Karakoc, Emre / Cristinelli, Sara / Pomilla, Cristina / Bartha, István / Thorball, Christian W / Tough, Riley H / Angelino, Paolo / Kiar, Cher S / Carstensen, Tommy / Fatumo, Segun / Porter, Tarryn / Jarvis, Isobel / Skarnes, William C / Bassett, Andrew /

DeGorter, Marianne K / Sathya Moorthy, Mohana Prasad / Tuff, Jeffrey F / Kim, Eun-Young / Walter, Miriam / Simons, Lacy M / Bashirova, Arman / Buchbinder, Susan / Carrington, Mary / Cossarizza, Andrea / De Luca, Andrea / Goedert, James J / Goldstein, David B / Haas, David W / Herbeck, Joshua T / Johnson, Eric O / Kaleebu, Pontiano / Kilembe, William / Kirk, Gregory D / Kootstra, Neeltje A / Kral, Alex H / Lambotte, Olivier / Luo, Ma / Mallal, Simon / Martinez-Picado, Javier / Meyer, Laurence / Miro, José M / Moodley, Pravi / Motala, Ayesha A / Mullins, James I / Nam, Kireem / Obel, Niels / Pirie, Fraser / Plummer, Francis A / Poli, Guido / Price, Matthew A / Rauch, Andri / Theodorou, Ioannis / Trkola, Alexandra / Walker, Bruce D / Winkler, Cheryl A / Zagury, Jean-François / Montgomery, Stephen B / Ciuffi, Angela / Hultquist, Judd F / Wolinsky, Steven M / Dougan, Gordon / Lever, Andrew M L / Gurdasani, Deepti / Groom, Harriet / Sandhu, Manjinder S / Fellay, Jacques

Nature

2023 Volume 621, Issue 7979, Page(s) E42

Language	English
Publishing date	2023-09-01
Publishing country	England
Document type	Published Erratum
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06591-7
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Article ; Online: Africa-specific human genetic variation near CHD1L associates with HIV-1 load.

Nature

2023 Volume 620, Issue 7976, Page(s) 1025–1030

Abstract: HIV-1 remains a global health ... ...

Abstract	HIV-1 remains a global health crisis
MeSH term(s)	Humans ; Cell Line ; DNA Helicases/genetics ; DNA Helicases/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Genetic Variation ; HIV Infections/genetics ; HIV-1/growth & development ; HIV-1/physiology ; Viral Load/genetics ; Africa ; Chromosomes, Human, Pair 1/genetics ; Alleles ; RNA, Long Noncoding/genetics ; Virus Replication
Chemical Substances	CHD1L protein, human (EC 3.6.4.12) ; DNA Helicases (EC 3.6.4.-) ; DNA-Binding Proteins ; RNA, Long Noncoding
Language	English
Publishing date	2023-08-02
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06370-4
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Article: The signaling components of sensory fiber transmission involved in the activation of ERK MAP kinase in the mouse dorsal horn.

Lever, Isobel J / Pezet, Sophie / McMahon, Stephen B / Malcangio, Marzia

Molecular and cellular neurosciences

2003 Volume 24, Issue 2, Page(s) 259–270

Abstract: The stimulation of C-fiber sensory neurons is known to induce activation of the ERK MAP kinase signaling pathway in the spinal cord dorsal horn. In this study we have elucidated some of the signaling components of C-fiber transmission responsible for ERK ...

Abstract	The stimulation of C-fiber sensory neurons is known to induce activation of the ERK MAP kinase signaling pathway in the spinal cord dorsal horn. In this study we have elucidated some of the signaling components of C-fiber transmission responsible for ERK activation. Using an in vitro slice preparation of the mouse spinal cord dorsal horn, we compared the release of substance P (SP) and BDNF with the activation of ERK in postsynaptic neurons. We observed that primary afferent stimulation recruiting C-fibers was required for both SP and BDNF release and ERK activation in post-synaptic dorsal horn neurons. Glutamate transmission via NMDA and mGluR1 but not AMPA receptors was critical to this ERK activation. BDNF signaling via TrkB receptors but not SP signaling via NK(1) were also involved in ERK recruitment. In conclusion, glutamate and BDNF are the important C-fiber signaling components for ERK activation in dorsal horn neurons.
MeSH term(s)	Animals ; Electric Stimulation ; Enzyme Activation/drug effects ; Enzyme Activation/physiology ; Excitatory Amino Acid Antagonists/pharmacology ; Female ; In Vitro Techniques ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/physiology ; Male ; Mice ; Nerve Fibers/enzymology ; Nerve Fibers/physiology ; Neurons, Afferent/drug effects ; Neurons, Afferent/enzymology ; Neurons, Afferent/physiology ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/enzymology ; Posterior Horn Cells/physiology ; Synaptic Transmission/physiology
Chemical Substances	Excitatory Amino Acid Antagonists
Language	English
Publishing date	2003-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/s1044-7431(03)00200-8
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Article: Basal and activity-induced release of substance P from primary afferent fibres in NK1 receptor knockout mice: evidence for negative feedback.

Lever, Isobel J / Grant, Andrew D / Pezet, Sophie / Gerard, Norma P / Brain, Susan D / Malcangio, Marzia

Neuropharmacology

2003 Volume 45, Issue 8, Page(s) 1101–1110

Abstract: The concept that NK1 receptors are located pre-junctionally on substance P (SP)-containing nerves, acting as autoreceptors to inhibit SP release, has been suggested, but remains a controversial issue. To further investigate the existence of this receptor ...

Abstract	The concept that NK1 receptors are located pre-junctionally on substance P (SP)-containing nerves, acting as autoreceptors to inhibit SP release, has been suggested, but remains a controversial issue. To further investigate the existence of this receptor on central and peripheral terminals of primary afferent fibres, NK1 receptor knockout mice and an NK1 receptor antagonist were used in nerve-attached tissue preparations. These were the isolated dorsal horn of the spinal cord with dorsal roots attached, and the hairy skin of the hind paw with attached saphenous nerve. The results reveal that in the dorsal horn preparation, basal release of SP is significantly higher in NK1(-/-) mice than NK1(+/+) mice (P<0.05, n=7 mice/strain). However, a difference in SP release evoked in the dorsal horn by electrical stimulation of the dorsal roots or capsaicin application was not observed. In contrast, antidromic electrical stimulation of the saphenous nerve caused a substantially greater release of SP in the skin of NK1(-/-) mice than in NK1(+/+) mice (P<0.05, n=5 to 6 mice/strain). These results provide evidence for the existence of NK1 autoreceptors on sensory nerves in skin, which may be relevant to the modulation of their peripheral pathophysiological effector functions.
MeSH term(s)	Afferent Pathways/drug effects ; Afferent Pathways/metabolism ; Animals ; Capsaicin/pharmacology ; Electric Stimulation/methods ; Feedback, Physiological/drug effects ; Feedback, Physiological/physiology ; In Vitro Techniques ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurokinin-1 Receptor Antagonists ; Receptors, Neurokinin-1/deficiency ; Receptors, Neurokinin-1/genetics ; Substance P/genetics ; Substance P/metabolism
Chemical Substances	Neurokinin-1 Receptor Antagonists ; Receptors, Neurokinin-1 ; Substance P (33507-63-0) ; Capsaicin (S07O44R1ZM)
Language	English
Publishing date	2003-03-17
Publishing country	England
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	218272-5
ISSN	1873-7064 ; 0028-3908
ISSN (online)	1873-7064
ISSN	0028-3908
DOI	10.1016/s0028-3908(03)00298-3
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Article: Glial cell line-derived neurotrophic factor increases calcitonin gene-related peptide immunoreactivity in sensory and motoneurons in vivo.

Ramer, Matt S / Bradbury, Elizabeth J / Michael, Gregory J / Lever, Isobel J / McMahon, Stephen B

The European journal of neuroscience

2003 Volume 18, Issue 10, Page(s) 2713–2721

Abstract: Calcitonin gene-related peptide (CGRP) is expressed at high levels in roughly 50% of spinal sensory neurons and plays a role in peripheral vasodilation as well as nociceptive signalling in the spinal cord. Spinal motoneurons express low levels of CGRP; ... ...

Abstract	Calcitonin gene-related peptide (CGRP) is expressed at high levels in roughly 50% of spinal sensory neurons and plays a role in peripheral vasodilation as well as nociceptive signalling in the spinal cord. Spinal motoneurons express low levels of CGRP; motoneuronal CGRP is thought to be involved in end-plate plasticity and to have trophic effects on target muscle cells. As both sensory and motoneurons express receptors for glial cell line-derived neurotrophic factor (GDNF) we sought to determine whether CGRP was regulated by GDNF. Rats were treated intrathecally for 1-3 weeks with recombinant human GDNF or nerve growth factor (NGF) (12 microg/day) and dorsal root ganglia and spinal cords were stained for CGRP. The GDNF treatment not only increased CGRP immunoreactivity in both sensory and motoneurons but also resulted in hypertrophy of both populations. By combined in situ hybridization and immunohistochemistry we found that, in the dorsal root ganglia, CGRP was up-regulated specifically in neurons expressing GDNF but not NGF receptors following GDNF treatment. Despite the increase in CGRP in GDNF-treated rats, there was no increase in thermal or mechanical pain sensitivity, while NGF-treated animals showed significant decreases in pain thresholds. In motoneurons, GDNF increased the overall intensity of CGRP immunoreactivity but did not increase the number of immunopositive cells. As GDNF has been shown to promote the regeneration of both sensory and motor axons, and as CGRP appears to be involved in motoneuronal plasticity, we reason that at least some of the regenerative effects of GDNF are mediated through CGRP up-regulation.
MeSH term(s)	Animals ; Anterior Horn Cells/drug effects ; Anterior Horn Cells/metabolism ; Calcitonin Gene-Related Peptide/metabolism ; Carrier Proteins/metabolism ; Cell Count ; Gene Expression Regulation/drug effects ; Glial Cell Line-Derived Neurotrophic Factor ; Hyperalgesia ; Immunohistochemistry ; In Situ Hybridization ; Male ; Membrane Proteins/metabolism ; Nerve Growth Factor/metabolism ; Nerve Growth Factors/genetics ; Nerve Growth Factors/metabolism ; Nerve Growth Factors/pharmacology ; Pain Measurement ; Pain Threshold/drug effects ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/metabolism ; Rats ; Rats, Wistar ; Reaction Time ; Receptor, trkA ; Spinal Cord/cytology
Chemical Substances	Carrier Proteins ; Gdnf protein, rat ; Glial Cell Line-Derived Neurotrophic Factor ; Membrane Proteins ; Nerve Growth Factors ; Nerve Growth Factor (9061-61-4) ; Receptor, trkA (EC 2.7.10.1) ; Calcitonin Gene-Related Peptide (JHB2QIZ69Z)
Language	English
Publishing date	2003-10-28
Publishing country	France
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645180-9
ISSN	1460-9568 ; 0953-816X
ISSN (online)	1460-9568
ISSN	0953-816X
DOI	10.1111/j.1460-9568.2003.03012.x
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Article ; Online: Role of interleukin-1beta in postoperative cognitive dysfunction.

Cibelli, Mario / Fidalgo, Antonio Rei / Terrando, Niccolò / Ma, Daqing / Monaco, Claudia / Feldmann, Marc / Takata, Masao / Lever, Isobel J / Nanchahal, Jagdeep / Fanselow, Michael S / Maze, Mervyn

Annals of neurology

2010 Volume 68, Issue 3, Page(s) 360–368

Abstract: Objective: Although postoperative cognitive dysfunction (POCD) often complicates recovery from major surgery, the pathogenic mechanisms remain unknown. We explored whether systemic inflammation, in response to surgical trauma, triggers hippocampal ... ...

Abstract	Objective: Although postoperative cognitive dysfunction (POCD) often complicates recovery from major surgery, the pathogenic mechanisms remain unknown. We explored whether systemic inflammation, in response to surgical trauma, triggers hippocampal inflammation and subsequent memory impairment, in a mouse model of orthopedic surgery. Methods: C57BL/6J, knock out (lacking interleukin [IL]-1 receptor, IL-1R(-/-)) and wild type mice underwent surgery of the tibia under general anesthesia. Separate cohorts of animals were tested for memory function with fear conditioning tests, or euthanized at different times to assess levels of systemic and hippocampal cytokines and microglial activation; the effects of interventions, designed to interrupt inflammation (specifically and nonspecifically), were also assessed. Results: Surgery caused hippocampal-dependent memory impairment that was associated with increased plasma cytokines, as well as reactive microgliosis and IL-1beta transcription and expression in the hippocampus. Nonspecific attenuation of innate immunity with minocycline prevented surgery-induced changes. Functional inhibition of IL-1beta, both in mice pretreated with IL-1 receptor antagonist and in IL-1R(-/-) mice, mitigated the neuroinflammatory effects of surgery and memory dysfunction. Interpretation: A peripheral surgery-induced innate immune response triggers an IL-1beta-mediated inflammatory process in the hippocampus that underlies memory impairment. This may represent a viable target to interrupt the pathogenesis of postoperative cognitive dysfunction.
MeSH term(s)	Analysis of Variance ; Animals ; CD11b Antigen/metabolism ; Cognition Disorders/drug therapy ; Cognition Disorders/etiology ; Cognition Disorders/genetics ; Cognition Disorders/metabolism ; Conditioning, Psychological/physiology ; Discrimination, Psychological/physiology ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay/methods ; Fear ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/genetics ; Hippocampus/metabolism ; Inflammation/chemically induced ; Inflammation/prevention & control ; Interleukin 1 Receptor Antagonist Protein/pharmacology ; Interleukin 1 Receptor Antagonist Protein/therapeutic use ; Interleukin-1beta/metabolism ; Interleukin-6/metabolism ; Lipopolysaccharides ; Male ; Mental Recall/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Olfactory Bulb/drug effects ; Olfactory Bulb/pathology ; Olfactory Bulb/physiopathology ; Postoperative Complications/pathology ; Postoperative Complications/physiopathology ; Receptors, Interleukin-1/antagonists & inhibitors ; Receptors, Interleukin-1/deficiency ; Social Behavior ; Tongue/physiopathology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	CD11b Antigen ; Interleukin 1 Receptor Antagonist Protein ; Interleukin-1beta ; Interleukin-6 ; Lipopolysaccharides ; Receptors, Interleukin-1 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2010-09-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.22082
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Article ; Online: Duplex formation between the template and the nascent strand in the transcription-regulating sequences determines the site of template switching in SARS – CoV-2

D'souza, Aaron R / Buckingham, Amanda B / Salasc, Fanny / Ingemarsdotter, Carin / Iaconis, Gennaro / Jarvis, Isobel / Groom, Harriet C T / Kenyon, Julia / Lever, Andrew M L

bioRxiv

Abstract: Recently published transcriptomic data of the SARS-CoV-2 coronavirus show that there is a large variation in the frequency and steady state levels of subgenomic mRNA sequences. This variation is derived from discontinuous subgenomic RNA synthesis where ... ...

Abstract	Recently published transcriptomic data of the SARS-CoV-2 coronavirus show that there is a large variation in the frequency and steady state levels of subgenomic mRNA sequences. This variation is derived from discontinuous subgenomic RNA synthesis where the polymerase switches template from a 39 proximal genome body sequence to a 59 untranslated leader sequence. This leads to a fusion between the common 59 leader sequence and a 39 proximal body sequence in the RNA product. This process revolves around a common core sequence (CS) that is present at both the template sites that make up the fusion junction. Base-pairing between the leader CS and the nascent complementary minus strand body CS, and flanking regions (together called the transcription regulating sequence, TRS) is vital for this template switching event. However, various factors can influence the site of template switching within the same TRS duplex. Here, we model the duplexes formed between the leader and complementary body TRS regions, hypothesising the role of the stability of the TRS duplex in determining the major sites of template switching for the most abundant mRNAs. We indicate that the stability of secondary structures and the speed of transcription play key roles in determining the probability of template switching in the production of subgenomic RNAs.
Keywords	covid19
Language	English
Publishing date	2020-12-11
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2020.12.11.416818
Database	COVID19

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Article ; Online: Localization of the endocannabinoid-degrading enzyme fatty acid amide hydrolase in rat dorsal root ganglion cells and its regulation after peripheral nerve injury.

Lever, Isobel J / Robinson, Michelle / Cibelli, Mario / Paule, Cleoper / Santha, Peter / Yee, Louis / Hunt, Stephen P / Cravatt, Benjamin F / Elphick, Maurice R / Nagy, Istvan / Rice, Andrew S C

The Journal of neuroscience : the official journal of the Society for Neuroscience

2009 Volume 29, Issue 12, Page(s) 3766–3780

Abstract: Fatty acid amide hydrolase (FAAH) is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide (AEA). AEA acts as an endocannabinoid and an endovanilloid by activating cannabinoid and vanilloid type 1 transient receptor ... ...

Abstract	Fatty acid amide hydrolase (FAAH) is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide (AEA). AEA acts as an endocannabinoid and an endovanilloid by activating cannabinoid and vanilloid type 1 transient receptor potential (TRPV1) receptors, respectively, on dorsal root ganglion (DRG) sensory neurons. Inhibition of FAAH activity increases AEA concentrations in nervous tissue and reduces sensory hypersensitivity in animal pain models. Using immunohistochemistry, Western blotting, and reverse transcription-PCR, we demonstrate the location of the FAAH in adult rat DRG, sciatic nerve, and spinal cord. In naive rats, FAAH immunoreactivity localized to the soma of 32.7 +/- 0.8% of neurons in L4 and L5 DRG. These were small-sized (mean soma area, 395.96 +/- 5.6 mum(2)) and predominantly colabeled with peripherin and isolectin B4 markers of unmyelinated C-fiber neurons; 68% colabeled with antibodies to TRPV1 (marker of nociceptive DRG neurons), and <2% colabeled with NF200 (marker of large myelinated neurons). FAAH-IR was also present in small, NF200-negative cultured rat DRG neurons. Incubation of these cultures with the FAAH inhibitor URB597 increased AEA-evoked cobalt uptake in a capsazepine-sensitive manner. After sciatic nerve axotomy, there was a rightward shift in the cell-size distribution of FAAH-immunoreactive (IR) DRG neurons ipsilateral to injury: FAAH immunoreactivity was detected in larger-sized cells that colabeled with NF200. An ipsilateral versus contralateral increase in both the size and proportion of FAAH-IR DRG occurred after spinal nerve transection injury but not after chronic inflammation of the rat hindpaw 2 d after injection of complete Freund's adjuvant. This study reveals the location of FAAH in neural tissue involved in peripheral nociceptive transmission.
MeSH term(s)	Amidohydrolases/genetics ; Amidohydrolases/metabolism ; Animals ; Cannabinoid Receptor Modulators/metabolism ; Endocannabinoids ; Freund's Adjuvant ; Ganglia, Spinal/cytology ; Ganglia, Spinal/enzymology ; Immunohistochemistry ; Inflammation/chemically induced ; Inflammation/enzymology ; Male ; Pain/enzymology ; RNA, Messenger/metabolism ; Rats ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Sciatic Nerve/enzymology ; Sciatic Nerve/injuries ; Sensory Receptor Cells/enzymology ; Spinal Nerves/enzymology ; Spinal Nerves/injuries
Chemical Substances	Cannabinoid Receptor Modulators ; Endocannabinoids ; RNA, Messenger ; Freund's Adjuvant (9007-81-2) ; Amidohydrolases (EC 3.5.-) ; fatty-acid amide hydrolase (EC 3.5.1.-)
Language	English
Publishing date	2009-03-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	604637-x
ISSN	1529-2401 ; 0270-6474
ISSN (online)	1529-2401
ISSN	0270-6474
DOI	10.1523/JNEUROSCI.4071-08.2009
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Article: BDNF modulates sensory neuron synaptic activity by a facilitation of GABA transmission in the dorsal horn.

Pezet, Sophie / Cunningham, Joanna / Patel, Jaykumar / Grist, John / Gavazzi, Isabella / Lever, Isobel J / Malcangio, Marzia

Molecular and cellular neurosciences

2002 Volume 21, Issue 1, Page(s) 51–62

Abstract: Topical application of brain-derived neurotrophic factor (BDNF) to the adult rat isolated dorsal horn with dorsal root attached preparation inhibited the electrically evoked release of substance P (SP) from sensory neurons. This effect of BDNF was dose ... ...

Abstract	Topical application of brain-derived neurotrophic factor (BDNF) to the adult rat isolated dorsal horn with dorsal root attached preparation inhibited the electrically evoked release of substance P (SP) from sensory neurons. This effect of BDNF was dose dependent (EC(50) 250 pM) and reversed by the tyrosine kinase inhibitor, K-252a. BDNF-induced inhibition of SP release was blocked by the GABA(B) receptor antagonist CGP 55485 but not by naloxone. Acute application of BDNF significantly increased potassium-stimulated release of GABA in the dorsal horn isolated in vitro and this effect was blocked by K-252a. Intrathecal injection of BDNF into the rat lumbar spinal cord induced a short-lasting increase in hindpaw threshold to noxious thermal stimulation that was blocked by CGP 55485 and was associated with activation of ERK in dorsal horn. These data suggest that exogenous BDNF can indirectly modulate primary sensory neuron synaptic efficacy via facilitation of the release of GABA from dorsal horn interneurons.
MeSH term(s)	Afferent Pathways/drug effects ; Afferent Pathways/metabolism ; Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Brain-Derived Neurotrophic Factor/pharmacology ; Cells, Cultured ; Ganglia, Spinal/drug effects ; Ganglia, Spinal/metabolism ; Injections, Spinal ; Male ; Narcotic Antagonists/pharmacology ; Neural Inhibition/drug effects ; Neural Inhibition/physiology ; Pain/drug therapy ; Pain/metabolism ; Pain/physiopathology ; Pain Threshold/drug effects ; Pain Threshold/physiology ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/metabolism ; Rats ; Rats, Wistar ; Reaction Time/drug effects ; Reaction Time/physiology ; Receptors, Opioid/metabolism ; Substance P/metabolism ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology ; gamma-Aminobutyric Acid/metabolism ; gamma-Aminobutyric Acid/pharmacology
Chemical Substances	Brain-Derived Neurotrophic Factor ; Narcotic Antagonists ; Receptors, Opioid ; Substance P (33507-63-0) ; gamma-Aminobutyric Acid (56-12-2)
Language	English
Publishing date	2002-10-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1006/mcne.2002.1166
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Article: Noxious stimulation induces Trk receptor and downstream ERK phosphorylation in spinal dorsal horn.

Pezet, Sophie / Malcangio, Marzia / Lever, Isobel J / Perkinton, Michael S / Thompson, Stephen W N / Williams, Robert J / McMahon, Stephen B

Molecular and cellular neurosciences

2002 Volume 21, Issue 4, Page(s) 684–695

Abstract: Several lines of evidence suggest that the brain-derived neurotrophic factor (BDNF) acts as central pain neuromodulator. We examined the ability of different types of peripheral stimulation to activate the BDNF high-affinity receptor, TrkB, in the spinal ...

Abstract	Several lines of evidence suggest that the brain-derived neurotrophic factor (BDNF) acts as central pain neuromodulator. We examined the ability of different types of peripheral stimulation to activate the BDNF high-affinity receptor, TrkB, in the spinal cord. We found that noxious chemical, mechanical, or thermal stimuli, but not innocuous stimuli, caused Trk phosphorylation in the spinal cord. These changes were rapid and transient and restricted to somatotopically appropriate spinal segments. We observed, both in vitro and in vivo, that exogenous BDNF induced a rapid activation of ERK, a signaling kinase important in the development of acute pain. Finally, we found that sequestering BDNF in vivo with a TrkB-IgG fusion molecule significantly reduced the activation of ERK evoked by noxious stimulation. These data suggest that BDNF, once released with activity from primary afferent nociceptors, exerts a neuromodulatory role in pain processing through stimulation of postsynaptic TrkB receptors and subsequent activation of ERK.
MeSH term(s)	Afferent Pathways/drug effects ; Afferent Pathways/metabolism ; Animals ; Animals, Newborn ; Brain-Derived Neurotrophic Factor/metabolism ; Male ; Mitogen-Activated Protein Kinases/drug effects ; Mitogen-Activated Protein Kinases/metabolism ; Mustard Plant ; Nerve Fibers, Unmyelinated/drug effects ; Nerve Fibers, Unmyelinated/metabolism ; Nociceptors/drug effects ; Nociceptors/metabolism ; Pain/chemically induced ; Pain/metabolism ; Pain/physiopathology ; Pain Measurement ; Phosphorylation ; Physical Stimulation ; Plant Extracts ; Plant Oils ; Posterior Horn Cells/drug effects ; Posterior Horn Cells/metabolism ; Precipitin Tests ; Presynaptic Terminals/drug effects ; Presynaptic Terminals/metabolism ; Rats ; Rats, Wistar ; Receptor, trkB/drug effects ; Receptor, trkB/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Synaptic Transmission/drug effects ; Synaptic Transmission/physiology
Chemical Substances	Brain-Derived Neurotrophic Factor ; Plant Extracts ; Plant Oils ; Receptor, trkB (EC 2.7.10.1) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; mustard oil (TYY1MA9BSY)
Language	English
Publishing date	2002-12-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1006/mcne.2002.1205
Database	MEDical Literature Analysis and Retrieval System OnLINE

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