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Sustained morphine treatment augments prostaglandin E2-evoked Calcitonin Gene-Related Peptide release from primary sensory neurons in a PKA- dependent manner
Tissue damage leads to pain sensitization due to peripheral and central release of excitatory mediators such as prostaglandin E(2) (PGE(2)). PGE(2) sensitizes spinal pain neurotransmitter such as calcitonin gene-related peptide (CGRP) release via activation of cyclic AMP (cAMP)/Protein kinase A (PKA...
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| Autors principals: | , , , |
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| Format: | Artigo |
| Idioma: | Inglês |
| Publicat: |
2010
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| Matèries: | |
| Accés en línia: | https://ncbi.nlm.nih.gov/pmc/articles/PMC2955884/ https://ncbi.nlm.nih.gov/pubmed/20826131 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.ejphar.2010.08.042 |
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