Transforming growth factor-1 (TGF-1) protects against neuroinflammatory events underlying neuropathic pain. TGF- signaling enhancement is a phenotypic characteristic of mice lacking the TGF- pseutodoreceptor BAMBI (BMP and activin membrane-bound inhibitor), which leads to an increased synaptic release of opioid peptides and to a naloxone-reversible hypoalgesic/antiallodynic phenotype. Herein, we investigated the following: (1) the effects of BAMBI deficiency on opioid receptor expression, functional efficacy, and analgesic responses to entodogenous and exogenous opioids; and (2) the involvement of the opioid system in the antiallodynic effect of TGF-1. BAMBI-KO mice were subjected to neuropathic pain by sciatic nerve crash injury (SNI). Gene (PCR) and protein (Western blot) expressions of - and -opioid receptors were determined in the spinal cord. The inhibitory effects of agonists on the adenylyl cyclase pathway were investigated.
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