Release of immunoreactive [Met5]enkephalin and cholecystokinin from the spinal cord by β-endorphin administered intraventricularly in the pentobarbital-anesthetized rat

Tseng, Leon F.; Huang, Frederick Y.

doi:10.1016/0014-2999(92)90046-7

Cited by 12 publications

(9 citation statements)

References 7 publications

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“…The doses of antiserum against Dyn were 50 to 300 g and 200 g for other antisera. The doses of antisera used have been shown previously to be sufficient for their specific effects (Tseng and Huang, 1992;Xu and Tseng, 1997;Ohsawa et al, 2001;Wu et al, 2002a). Finally, 5) determine whether the EM-2-induced antianalgesia is selective against opioid -agonists or is generalized to ␦-and -agonists.…”

Section: Methodsmentioning

confidence: 98%

“…The DAMGO was dissolved in 0.9% saline containing 0.01% of Triton X-100 and deltorphin II was dissolved in 0.9% saline containing 1% dimethyl sulfoxide. The antiserum against dynorphin A(1-17), ␤-endorphin, [Leu 5 ]-enkephalin, [Met 5 ]-enkephalin, and CCK-8s were produced by immunization of male New Zealand White rabbits according to the method described in previous publications, and the potencies and cross-immunoreactivity of these antisera have been characterized (Tseng and Huang, 1992;Tseng and Collin, 1993;Wu et al, 2002a).…”

Section: Methodsmentioning

confidence: 99%

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Dynorphinergic Mechanism Mediating Endomorphin-2-Induced Antianalgesia in the Mouse Spinal Cord

Sun²,

Darpolar³

et al. 2003

J Pharmacol Exp Ther

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We have previously demonstrated that both endomorphin-1 (EM-1) and endomorphin-2 (EM-2) at high doses (1.75-35 nmol) given intrathecally (i.t.) or intracerebroventricularly produce antinociception by stimulation of -opioid receptors. Now, we report that EM-2 at small doses (0.05-1.75 nmol), which injected alone did not produce antinociception, produces antianalgesia against opioid agonist-induced antinociception. The tail-flick (TF) response was used to test the antinociception in male CD-1 mice. Intrathecal pretreatment with EM-2 (0.02-1.75 nmol) 45 min before i.t. morphine (3.0 nmol) injection dose dependently attenuated morphine-induced TF inhibition. On the other hand, a similar dose of EM-1 (1.64 nmol) failed to produce any antianalgesic effect. The EM-2 (1.75 nmol)-produced anti-analgesia against morphine-induced TF inhibition was blocked by i.t. pretreatment with the -opioid antagonist naloxone or 3-methoxynaltrexone, but not ␦-opioid receptor antagonist naltrindole, -opioid receptor antagonist nor-binal- Endogenous opioid tetrapeptides endomorphin-1 (EM-1) and endomorphin-2 (EM-2) have been found to be highly selective for -opioid receptors (Zadina et al., 1997). Both EM-1 and EM-2 potently compete with -opioid receptor binding with no appreciable affinity with ␦-and -opioid receptors and selectively activate -opioid receptor-mediated G-proteins with [35 S]guanosine 5Ј-O-(3-thio)triphosphate binding (Goldberg et al., 1998;Narita et al., 1998Narita et al., , 2000Monory et al., 2000). The increases of the [ 35 S]guanosine 5Ј-O-(3-thio)triphosphate binding and antinociceptive effects induced by both EM-1 and EM-2 are selectively blocked by the pretreatment with selective -opioid receptor antagonist ␤-funaltrexamine or D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH 2 , indicating that the effects are mediated by the stimulation of -opioid receptors.However, recent studies indicate that the antinociceptive effects induced by EM-1 and EM-2 are mediated by the stimulation of different subtypes of -opioid receptors. Pretreatment with -opioid receptor antagonist 3-methoxynaltrexone selectively attenuated EM-2-but not EM-1-induced antinociception, whereas ␤-funaltrexamine inhibits both (Sakurada et al., 2000). There is an asymmetric cross-tolerance between EM-1 and EM-2, where mice made acutely tolerant to EM-1 are not cross-tolerant to EM-2, but mice made acutely tolerant to EM-2 cause partial cross-tolerance to EM-1 (Wu et al., 2001). Intrathecal pretreatment with antisense oligodeoxynucleotides against exon-8 of -opioid receptor clone inhibits the antinociception induced by EM-1

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Section: Methodsmentioning

confidence: 98%

Section: Methodsmentioning

confidence: 99%

Dynorphinergic Mechanism Mediating Endomorphin-2-Induced Antianalgesia in the Mouse Spinal Cord

Sun²,

Darpolar³

et al. 2003

J Pharmacol Exp Ther

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“…The TF responses were then measured at 15 min after morphine injection. The doses of antisera used have been shown previously to be sufficient for their specific effects (Tseng and Huang, 1992;Xu and Tseng, 1997;Ohsawa et al, 2001;Wu et al, 2002). 4) Determine whether the morphine-induced antianalgesia is selective against opioid -agonists or is generalized to ␦-and -agonists.…”

Section: Methodsmentioning

confidence: 99%

“…DAMGO was dissolved in 0.9% saline containing 0.01% Triton X-100, and deltorphin II was dissolved in 0.9% saline containing 10% hydroxypropyl-␤-cyclodextrin. The antiserum against dynorphin A(1-17), ␤-endorphin, [Leu]-enkephalin, [Met]-enkephalin, and CCK-8s were produced by immunization of male New Zealand White rabbits according to the method described in previous publications, and the potencies and crossimmunoreactivity of these antisera have been characterized previously (Tseng and Huang, 1992;Tseng and Collin, 1993;Wu et al, 2002). Antiserum against substance P is a kind gift from Dr. J. S. Hong (National Institute of Environmental Health Sciences/National Institutes of Health, Research Triangle Park, NC).…”

Section: Methodsmentioning

confidence: 99%

Nonopioidergic Mechanism Mediating Morphine-Induced Antianalgesia in the Mouse Spinal Cord

Wu¹,

Thompson²,

Sun³

et al. 2004

J Pharmacol Exp Ther

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Intrathecal (i.t.) pretreatment with a low dose (0.3 nmol) of morphine causes an attenuation of i.t. morphine-produced analgesia; the phenomenon has been defined as morphine-induced antianalgesia. The opioid-produced analgesia was measured with the tail-flick (TF) test in male CD-1 mice. Intrathecal pretreatment with low dose (0.3 nmol) of morphine time dependently attenuated i.t. morphine-produced (3.0 nmol) TF inhibition and reached a maximal effect at 45 min. Intrathecal pretreatment with morphine (0.009 -0.3 nmol) for 45 min also dose dependently attenuated morphine-produced TF inhibition. We have previously reported that intrathecal (i.t.) pretreatment with an endogenous -opioid peptide, endomorphin-2 (0.05-1.75 nmol), attenuates the antinociception produced by opioid agonists. The antianalgesic effect is caused by the release of dynorphin A(1-17) through the stimulation of a subtype of -opioid receptors. The unique features of this endomorphin-2-induced antianalgesic action are that there is a lag period before dynorphin A(1-17) is released, and the antianalgesic action of endomorphin-2 corresponds with the time course of dynorphin release Wu et al., 2003). Furthermore, i.t. administered endomorphin-2 at larger doses (5.25-35 nmol) produces analgesia by itself through activation of spinal -opioid receptors (Ohsawa et al., 2001), whereas its delayed antianalgesic action is manifested more easily at small doses of endomorphin-2 by its ability to attenuate the analgesic action of other opioids administered after endomorphin-2 pretreatment.There are indications from the literature that morphine may have an antianalgesic action. Pretreatment with a low dose of naloxone (0.00028 fmol) or dynorphin A antiserum given i.t. enhances the analgesic effect of intracerebroventricularly and i.t.-administered morphine (Fujimoto and Rady, 1989;Holmes and Fujimoto, 1993). Studies performed by Crain and Shen (1990, 2000 indicate that even though generally morphine has a depressant effect on action potential duration in mouse dorsal root ganglion preparations, very low doses (1 fmol-1 pmol) of morphine produce the opposite effect by prolonging the duration of the action potential, an excitatory action. Recent studies also have shown that morphine and opioid compounds not only simply elicit

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“…The antiserum against dynorphin A(1-17) was produced by immunization of male New Zealand white rabbits according to the method described in previous publications. The potencies and cross-immunoreactivities of these antisera have been characterized (Tseng and Huang, 1992;Tseng and Collins, 1993;Wu et al, 2002Wu et al, , 2004. The injections into the centromedial and basolateral amygdala were made by hand with a 30-gauge injection needle attached to a microsyringe via polyethylene tubing.…”

Section: Drugs and Drug Adminstrationmentioning

confidence: 99%

Paradoxical hyperalgesia induced by μ-opioid receptor agonist endomorphin-2, but not endomorphin-1, microinjected into the centromedial amygdala of the rat

Terashvili¹,

Wu²,

Schwasinger³

et al. 2007

European Journal of Pharmacology

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The effects of endomorphin-2 or endomorphin-1 microinjected into the centromedial amygdala on the thermally induced tail-flick response were studied in male CD rats. Microinjection of endomorphin-2 (8.7-35.0 nmol) given into the centromedial amygdala time-and dosedependently decreased the tail-flick latencies. On the other hand, endomorphin-1 (8-32.6 nmol) given into the same site did not cause any change of the tail-flick latency. However, endomorphin-1 (32.6 nmol) or endomorphin-2 (35.0 nmol) given into the basolateral site of amygdala did not affect the tail-flick latency. Pretreatment with the antiserum against dynorphin A(1-17) (200 µg) significantly reversed the decrease of the tail-flick latency induced by endomorphin-2. The decrease of the tail-flick latency induced by endomorphin-2 was also blocked by the endomorphin-2 selective μ-opioid receptor antagonist 3-methoxynaltrexone (6.4 pmol) and by the Nmethyl-D-aspartate (NMDA) receptor antagonist MK-801 (30 nmol), but not by the κ-opioid receptor antagonist nor-binaltorphimine (6.6 nmol). It is concluded that endomorphin-2, but not endomorphin-1, given into the centromedial amygdala stimulates a 3-methoxynaltrexonesensitive μ-opioid receptor subtype to induce the release of dynorphin A(1-17), which then acts on the NMDA receptor, but not κ-opioid receptor for producing hyperalgesia. This conclusion is further supported by the additional findings that dynorphin A(1-17) (2.3 nmol) given into the centromedial amygdala also caused the decrease of the tail-flick latency, which was similarly blocked by the NMDA receptor antagonist MK-801 (30 nmol), but not κ-opioid receptor antagonist nor-binaltorphimine (6.6 nmol).

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Release of immunoreactive [Met5]enkephalin and cholecystokinin from the spinal cord by β-endorphin administered intraventricularly in the pentobarbital-anesthetized rat

Cited by 12 publications

References 7 publications

Dynorphinergic Mechanism Mediating Endomorphin-2-Induced Antianalgesia in the Mouse Spinal Cord

Dynorphinergic Mechanism Mediating Endomorphin-2-Induced Antianalgesia in the Mouse Spinal Cord

Nonopioidergic Mechanism Mediating Morphine-Induced Antianalgesia in the Mouse Spinal Cord

Paradoxical hyperalgesia induced by μ-opioid receptor agonist endomorphin-2, but not endomorphin-1, microinjected into the centromedial amygdala of the rat

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