α2-Adrenoceptors inhibit a nociceptive response in neonatal rat spinal cord
1991; Elsevier BV; Volume: 192; Issue: 2 Linguagem: Inglês
10.1016/0014-2999(91)90055-u
ISSN1879-0712
AutoresJoan J. Kendig, Maarit K.T. Savola, Scott J. Woodley, Mervyn Maze,
Tópico(s)Veterinary Pharmacology and Anesthesia
Resumoα2-Adrenoceptors mediate analgesia in vivo. The present study explored the actions of the α2-adrenoceptor agonists dexmedetomidine and clonidine on a nociceptive response in isolated neonatal rat spinal cord. Stimulation of a dorsal root generates a slow ventral root potential (slow VRP) at the corresponding ipsilateral ventral root. The slow VRP meets several criteria for a nociceptive response. Dexmedetomidine (10 nM) and clonidine (200 nM) depressed the slow VRP by approximately 80%. Dexmedetomidine's action was approximately linear over the concentration range 0.5–500 nM, whereas clonidine (20 nM-5 μM) exerted biphasic effects. The profile of agonist and antagonist effectiveness characterized the receptor(s) as α2-adrenoceptors; the subtype could not be identified as either α2A or α2B. Naloxone pretreatment partially blocked dexmedetomidine's effect, suggesting a possible endogenous opiate involvement. Dexmedetomidine (0.5–2.0 nM) also depressed the VRP evoked by application of substance P to the cord, implicating postsynaptic as well as possible presynaptic actions. At high concentrations, dexmedetomidine (50–500 nM) depressed the monosynaptic reflex, probably through non-α2-receptor(s). Results from the neonatal spinal cord correlate well with those from in vivo analgesia studies. They suggest an important direct spinal contribution to α2-adrenoceptor-mediated analgesia.
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