ATP-SENSITIVE K-INDUCED OR MORPHINE-INDUCED ANTINOCICEPTION AT THE SPINAL LEVEL - A STUDY USING EMG PLANIMETRY OF FLEXOR REFLEX IN RATS( CHANNELS ARE INVOLVED IN THE MEDIATION OF INTRATHECAL NOREPINEPHRINE)

The effects of intrathecally (IT) administered glibenclamide (Gli), an ATP-sensitive K+ (K-ATP) channel blocker, on the antinociception prod uced by IT norepinephrine (NE), serotonin (5-HT), morphine (Mor), or a denosine agonist, 5'-N-ethylcarboxamide adenosine (NECA) were investig ated using integrated EMG measurement of hindlimb flexor reflex (FR) i n lightly pentobarbital-anesthetized rats. The results showed that: 1) NE (3, 6, or 12 nmol) or 5-HT (60, 120, or 240 nmol) each produced a dose-dependent suppression of FR EMG, respectively; 2) pretreatment wi th Gli (5, 10, or 20 nmol) antagonized the NE (6 nmol)-induced antinoc iception in a dose-dependent manner and failed to modulate the 5-HT (1 20 nmol)-induced suppression of FR EMG; 3) pretreatment with Gli (5, 1 0, or 20 nmol) also antagonize the Mor (2 nmol)-induced suppression of FR EMG in a dose-dependent manner; 4) pretreatment with naloxone (Nal , 60, 120, or 240 nmol) also antagonize the NE (6 nmol)-induced suppre ssion of FR EMG in a dose-dependent manner; and 5) NECA (0.5, 1.0, or 2.0 nmol) produced a dose-dependent suppression of FR EMG, while pretr eatment with Gli (5, 10, or 20 nmol) failed to modulate the NECA (1.0 nmol)-induced suppression of FR EMG. The results show that (a) ATP-sen sitive K+ channels are involved in the NE-and Mor-induced antinocicept ion but not 5-HT- or NECA-induced antinociception at the spinal level; (b) endogenous opioids might act as a successor of NE and then activa te K-ATP channels to producing the antinociception. (C) 1998 Elsevier Science Inc.