Null Mutations Lacking Substance: Elucidating Pain Mechanisms by Genetic Pharmacology
Open Access
- 1 June 1998
- Vol. 20 (6) , 1063-1066
- https://doi.org/10.1016/s0896-6273(00)80487-0
Abstract
No abstract availableKeywords
This publication has 17 references indexed in Scilit:
- Mutant Mice and Neuroscience: Recommendations Concerning Genetic BackgroundNeuron, 1997
- NMDA Channel Regulation by Channel-Associated Protein Tyrosine Kinase SrcScience, 1997
- Inflammatory pain hypersensitivity mediated by phenotypic switch in myelinated primary sensory neuronsNature, 1996
- Alterations in neurokinin 1 receptor gene expression in models of pain and inflammationCanadian Journal of Physiology and Pharmacology, 1995
- Receptor Endocytosis and Dendrite Reshaping in Spinal Neurons After Somatosensory StimulationScience, 1995
- Antinociceptive profiles of non-peptidergic neurokinin1 and neurokinin2 receptor antagonists: a comparison to other classes of antinociceptive agentPain, 1995
- Protein kinase C reduces Mg2+ block of NMDA-receptor channels as a mechanism of modulationNature, 1992
- A Potent Nonpeptide Antagonist of the Substance P (NK 1 ) ReceptorScience, 1991
- Molecular Characterization of a Functional cDNA Encoding the Rat Substance P ReceptorScience, 1990
- Opiate analgesics inhibit substance P release from rat trigeminal nucleusNature, 1977