Regulation of opioid binding sites in the superficial dorsal horn of the rat spinal cord following loose ligation of the sciatic nerve: comparison with sciatic nerve section and lumbar dorsal rhizotomy.

摘要: The aim of the present study was to quantify time-related modifications in μ and δ opioid binding sites superficial layers (laminae I II) L4 lumbar segment a rat model mononeuropathy induced by loose ligation sciatic nerve. We have shown 28% (P < 0.01) 24% decrease ipsi/contralateral side ratios for tritiated (Tyr*-d-Ala-Gly-NMe-Phe-Gly-ol) ([3H]DAMGO) (Tyr*-d-Thr-Gly-Phe-Leu-Thr) ([3H]DTLET) respectively, at two weeks postlesion which correspond delay maximal hyperalgesia alteration fine diameter primary afferent fibers. In contrast, no change [3H]U.69593 specific could be detected this delay. For longer survival delays (four, eight 15 postlesion), return towards control values (approximately equal 1), probably reflecting occurrence long-term neuroplasticity (i.e. new equilibrium metabolism neurons, or collateral sprouting from intact afferents) following nerve ligation. addition, comparison results obtained with those measured after section dorsal rhizotomy performed order compare degree loss these three types lesion. days an 18% ratio [3H]DAMGO [3H]DTLET, respectively. At ligands, (four 12 weeks), progressive recovery observed. Thus, it appears that both lesions we studied result similar intensity time course 12–15 postlesion. unilateral nine consecutive roots (T13-S2), is known induce massive degeneration fibers, followed dramatic (53%, P 0.001) [3H]DTLET (45%, postlesion. These data suggest more deprived horn ipsilateral as compared contralateral side. However, when considering concentration, must emphasized regulation can occur independently direct A significant up-regulation found every only section. This seems bilateral although, on side, effect masked fiber degeneration. propose activation endogenous systems due nociceptive sensory input. Our are discussed view recent controversy arising efficacy opiates neuropathic pains.