Acute antinociceptive tolerance and partial cross-tolerance to endomorphin-1 and endomorphin-2 given intrathecally in the mouse

Wu, Hsiang‐En; Darpolor, Moses M.; Nagase, Hiroshi; Tseng, Leon F.

doi:10.1016/s0304-3940(03)00748-1

Cited by 18 publications

(21 citation statements)

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“…Spinal pretreatment with antisense oligodeoxynucleotides against exon-1, -4, or -8 of MOR-1 to knockdown different isoforms of the -opioid receptor, differentially attenuates the antinociception induced by EM-1 and EM-2 . In addition, mice or rats made antinociceptive tolerant to EM-1 exhibit no cross-tolerance to EM-2, whereas mice or rats made tolerant to EM-2 exhibit a cross-tolerance to EM-1 to produce antinociception (Wu et al, 2001;Hung et al, 2002). These findings strongly indicate that different subtypes of -opioid receptors are involved in the pharmacological actions produced by EM-1 and EM-2.…”

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confidence: 83%

Differential Conditioned Place Preference Responses to Endomorphin-1 and Endomorphin-2 Microinjected into the Posterior Nucleus Accumbens Shell and Ventral Tegmental Area in the Rat

Terashvili¹,

Wu²,

Leitermann³

et al. 2004

J Pharmacol Exp Ther

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An unbiased conditioned place preference (CPP) paradigm was used to evaluate the reward effects of endogenous -opioid receptor ligands endomorphin-1 (EM-1) and endomorphin-2 (EM-2) from the mesolimbic posterior nucleus accumbens (Acb) shell and the ventral tegmental area (VTA) in CD rats. EM-1 (1.6 -8.1 nmol) microinjected into posterior Acb shell produced CPP, whereas EM-2 (8.7-17.5 nmol) given into the same Acb shell produced conditioned place aversion (CPA). EM-1 (1.6 -16.3 nmol) microinjected into the VTA produced CPP, whereas EM-2 (8.7 and 17.5 nmol) given into the same VTA site did not produce any effect, but at a high dose (35 nmol) produced CPP. EM-1 (3.3 nmol) or EM-2 (17.5 nmol) microinjected into the nigrostriatal substantia nigra was not significantly different from vehicle-injected groups. D-Phe-Cys-Tyr-D-Trp-Orn-Thr-PenThr-NH 2 (CTOP) at 94.13 pmol or 3-methoxynaltrexone at 0.64 pmol microinjected into the posterior Acb shell blocked EM-1-induced CPP and EM-2-induced CPA. At a higher dose, CTOP (941.3 pmol) and 3-methoxynaltrexone (6.4 pmol) produced CPA and CPP, respectively. Coadministration with antiserum against dynorphin A(1-17) (Dyn) (10 g) microinjected into the posterior Acb shell blocked EM-2-induced CPA. However, it did not affect EM-1-induced CPP. It is concluded that EM-1 and EM-2 produce site-dependent CPP and CPA, respectively, by stimulation of different subtypes of -opioid-receptors; stimulation of one subtype of -opioid-receptor at the posterior Acb shell and VTA by EM-1 induces CPP, whereas stimulation of another subtype of -opioid receptor at the posterior Acb shell, but not the VTA, by EM-2 induces the release of Dyn to produce CPA.

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confidence: 83%

Differential Conditioned Place Preference Responses to Endomorphin-1 and Endomorphin-2 Microinjected into the Posterior Nucleus Accumbens Shell and Ventral Tegmental Area in the Rat

Terashvili¹,

Wu²,

Leitermann³

et al. 2004

J Pharmacol Exp Ther

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“…or i.t. administered endomorphin-1 or endomorphin-2, respectively (Wu et al, 2001Hung et al, 2002;Labuz et al, 2002). Interestingly, endomorphins induced the development of tolerance much faster than morphine, although endomorphin-1 required a longer pretreatment time than endomorphin-2 before the acute antinociceptive tolerance was observed.…”

Section: A Biological Effects Of Endomorphinsmentioning

confidence: 97%

“…Interestingly, endomorphins induced the development of tolerance much faster than morphine, although endomorphin-1 required a longer pretreatment time than endomorphin-2 before the acute antinociceptive tolerance was observed. It was proposed that these diverse effects might result from different peptide halflives or differences in the -opioid receptor selectivity or divergent neuronal mechanisms and not from the degree of receptor stimulation by endomorphins or differences in the opioid receptor desensitization (Wu et al, 2001). Labuz et al (2002) reported on results obtained in a cross-tolerance study, in which the antinociceptive effects of endomorphins and morphine were compared in tail-flick and paw pressure tests in rats.…”

Section: A Biological Effects Of Endomorphinsmentioning

confidence: 99%

The Endomorphin System and Its Evolving Neurophysiological Role

Fichna

Janecka²,

Costentin³

et al. 2007

Pharmacol Rev

219

171

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“…For groups of mice injected with antiserum against Dyn versus NRS, F interaction, treatment, time ϭ 2.96, 37.65, 8.57; ‫,ء‬ p Ͻ 0.01, ‫,ءء‬ p Ͻ 0.001 compared with NRS-injected groups. cross-tolerant to EM-2, whereas mice or rats made tolerant to EM-2 are partially cross-tolerant to EM-1 (Wu et al, 2001;Hung et al, 2002). Intrathecal pretreatment with antisense oligodeoxynucleotides against exon-1 or -4 of -opioid receptor clone is about equally effective in attenuating the antinociception induced by EM-1 and EM-2.…”

Section: Em-2 At Subantinociceptive Doses Produces Antianalgesia Agaimentioning

confidence: 98%

“…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…”

Section: Introductionmentioning

confidence: 95%

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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Acute antinociceptive tolerance and partial cross-tolerance to endomorphin-1 and endomorphin-2 given intrathecally in the mouse

Cited by 18 publications

References 10 publications

Differential Conditioned Place Preference Responses to Endomorphin-1 and Endomorphin-2 Microinjected into the Posterior Nucleus Accumbens Shell and Ventral Tegmental Area in the Rat

Differential Conditioned Place Preference Responses to Endomorphin-1 and Endomorphin-2 Microinjected into the Posterior Nucleus Accumbens Shell and Ventral Tegmental Area in the Rat

The Endomorphin System and Its Evolving Neurophysiological Role

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

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