Patrick W. Mantyh
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Patrick W. Mantyh has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
Scott D. Rogers
Molecular Neurobiology Laboratory, Veterans Affairs Medical Center, Minneapolis, Minnesota 55455, USA
2 shared publications- Stephen P. Hunt
Department of Cell and Developmental Biology, University College London, London, UK
2 shared publications - Christopher M. Peters
Department of Anesthesiology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA
1 shared publication Denis R. Clohisy
Department of Orthopaedic Surgery, Medical School and Cancer Center, University of Minnesota, 420 Delaware Street SE, Minneapolis, Minnesota 55455, USA
1 shared publicationElizabeth H. Kamp
Department of Pharmacology, University of Iowa, Iowa City, IA
1 shared publication- G. F. Gebhart
Department of Pharmacology, College of Medicine, University of Iowa, Iowa City, Iowa 52242-1109, USA
1 shared publication
Latest Publications
- 1 October 2004
- Published by Elsevier in Trends in Neurosciences
- Vol. 27 (10) , 582-584
Setting the tone: superficial dorsal horn projection neurons regulate pain sensitivity
- 1 October 2004
- Published by Elsevier in Trends in Neurosciences
- Vol. 27 (10) , 582-584
Setting the tone: superficial dorsal horn projection neurons regulate pain sensitivity
Endothelin B receptors are expressed by astrocytes and regulate astrocyte hypertrophy in the normal and injured CNS
The ability of mammalian central nervous system (CNS) neurons to survive and/or regenerate following injury is influenced by surrounding glial cells. To identify the factors that control glial cell function following CNS injury, we have focused on the endothelin B receptor (ETBR), which we show is expressed by the majority of astrocytes that are immunoreactive for glial acid fibrillary protein (GFAP) in both the normal and crushed rabbit optic nerve. Optic nerve crush induces a marked increase in ETBR and GFAP immunoreactivity (IR) without inducing a significant increase in the number of GFAP‐IR astrocytes, suggesting that the crush‐induced astrogliosis is due primarily to astrocyte hypertrophy. To define the role that endothelins play in driving this astrogliosis, artificial cerebrospinal fluid (CSF), ET‐1 (an ETAR and ETBR agonist), or Bosentan (a mixed ETAR and ETBR antagonist) were infused via osmotic minipumps into noninjured and crushed optic nerves for 14 days. Infusion of ET‐1 induced a hypertrophy of ETBR/GFAP‐IR astrocytes in the normal optic nerve, with no additional hypertrophy in the crushed nerve, whereas infusion of Bosentan induced a significant decrease in the hypertrophy of ETBR/GFAP‐IR astrocytes in the crushed but not in the normal optic nerve. These data suggest that pharmacological blockade of astrocyte ETBR receptors following CNS injury modulates glial scar formation and may provide a more permissive substrate for neuronal survival and regeneration. GLIA 41:180–190, 2003.
Endothelin B receptors are expressed by astrocytes and regulate astrocyte hypertrophy in the normal and injured CNS
The ability of mammalian central nervous system (CNS) neurons to survive and/or regenerate following injury is influenced by surrounding glial cells. To identify the factors that control glial cell function following CNS injury, we have focused on the endothelin B receptor (ETBR), which we show is expressed by the majority of astrocytes that are immunoreactive for glial acid fibrillary protein (GFAP) in both the normal and crushed rabbit optic nerve. Optic nerve crush induces a marked increase in ETBR and GFAP immunoreactivity (IR) without inducing a significant increase in the number of GFAP‐IR astrocytes, suggesting that the crush‐induced astrogliosis is due primarily to astrocyte hypertrophy. To define the role that endothelins play in driving this astrogliosis, artificial cerebrospinal fluid (CSF), ET‐1 (an ETAR and ETBR agonist), or Bosentan (a mixed ETAR and ETBR antagonist) were infused via osmotic minipumps into noninjured and crushed optic nerves for 14 days. Infusion of ET‐1 induced a hypertrophy of ETBR/GFAP‐IR astrocytes in the normal optic nerve, with no additional hypertrophy in the crushed nerve, whereas infusion of Bosentan induced a significant decrease in the hypertrophy of ETBR/GFAP‐IR astrocytes in the crushed but not in the normal optic nerve. These data suggest that pharmacological blockade of astrocyte ETBR receptors following CNS injury modulates glial scar formation and may provide a more permissive substrate for neuronal survival and regeneration. GLIA 41:180–190, 2003.
- Top Cited Papers
- 1 March 2002
- Published by Springer Nature in Nature Reviews Cancer
- Vol. 2 (3) , 201-209
Molecular mechanisms of cancer pain
Pain is the most disruptive influence on the quality of life of cancer patients. Although significant advances are being made in cancer treatment and diagnosis, the basic neurobiology of cancer pain is poorly understood. New insights into these mechanisms are now arising from animal models, and have the potential to fundamentally change the way that cancer pain is controlled.
- 1 March 2002
- Published by Springer Nature in Nature Reviews Cancer
- Vol. 2 (3) , 201-209
Top Cited PapersMolecular mechanisms of cancer pain
Pain is the most disruptive influence on the quality of life of cancer patients. Although significant advances are being made in cancer treatment and diagnosis, the basic neurobiology of cancer pain is poorly understood. New insights into these mechanisms are now arising from animal models, and have the potential to fundamentally change the way that cancer pain is controlled.
- 1 February 2002
- Published by Elsevier in The Journal of Pain
- Vol. 3 (1) , 3-11
Activation of lamina I spinal cord neurons that express the substance P receptor in visceral nociception and hyperalgesia
- 1 February 2002
- Published by Elsevier in The Journal of Pain
- Vol. 3 (1) , 3-11
Activation of lamina I spinal cord neurons that express the substance P receptor in visceral nociception and hyperalgesia
- 1 July 2001
- Published by Springer Nature in Nature Medicine
- Vol. 7 (7) , 772-773
Sensory neurons are PARtial to pain
- 1 July 2001
- Published by Springer Nature in Nature Medicine
- Vol. 7 (7) , 772-773
Sensory neurons are PARtial to pain
- Open Access
- 1 December 2000
- Published by Oxford University Press (OUP) in Pain Medicine
- Vol. 1 (4) , 303-309
Bone Cancer Pain: From Mechanism to Model to Therapy
Although bone cancer pain can be severe and is relatively common, very little is known about the basic mechanisms that generate and maintain this deb
- 1 December 2000
- Published by Oxford University Press (OUP) in Pain Medicine
- Vol. 1 (4) , 303-309
Open AccessBone Cancer Pain: From Mechanism to Model to Therapy
Although bone cancer pain can be severe and is relatively common, very little is known about the basic mechanisms that generate and maintain this deb