Implication of endogenous opioid system in the learned helplessness model of depression

Micó, J.A.; Maldonado, Rafaël; Roques, Bernárd P.; Gibert-Rahola, J.

doi:10.1016/0091-3057(95)00067-7

Cited by 110 publications

(52 citation statements)

References 44 publications

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“…Therefore, we could suggest that endomorphins produce their antidepressant-like effect by the activation of the m-opioid receptors. This observation is in good agreement with the previous studies, showing that a wide variety of the m-opioid receptor agonists, including b-endorphin and buprenorphine, possess antidepressant-like behavioral effects (Mansour et al, 1988;Darko et al, 1992;Bodkin et al, 1995;Tejedor-Real et al, 1995;Besson et al, 1996;Stoll and Rueter, 1999;Vilpoux et al, 2002) and that morphine, an alkaloid opiate with substantial affinity to the m-opioid receptors, produces a significant antidepressant effect in the forced-swimming test after subcutaneous injections (Eschalier et al, 1987). Endomorphins and the m-opioid receptors are localized in the brain regions involved in the physiopathology of depression, such as the limbic system (septum, nucleus accumbens, amygdala), thalamic nuclei, locus coeruleus, and some regions of brain stem (Schreff et al, 1998;MartinSchild et al, 1999;Zadina, 2002).…”

Section: Discussionsupporting

confidence: 82%

Antidepressant-Like Effect of Endomorphin-1 and Endomorphin-2 in Mice

Fichna

Janecka

Piestrzeniewicz

et al. 2006

Neuropsychopharmacol

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Endomorphin-1 (Tyr-Pro-Trp-Phe-NH 2 ) and endomorphin-2 (Tyr-Pro-Phe-Phe-NH 2 ) are two recently isolated m-opioid selective peptides with a potent antinociceptive activity, involved in a number of physiological processes, including food intake, vasomotricity, sexual behavior, as well as neuroendocrine and cardiorespiratory functions. The neuroanatomical distribution of endomorphins prompted us to study their antidepressant activity in two animal behavioral models of depression: forced-swimming and tail-suspension tests. In both tests, the intracerebroventricular (i.c.v.) injection of either endomorphin-1 or endomorphin-2 significantly decreased the duration of immobility, interpreted as an expression of 'behavioral despair', which could be related to the depression syndrome. These effects of endomorphins did not result from the stimulation of the animal motor activity. We have also demonstrated that the antidepressant-like effect of endomorphins was antagonized by the universal opioid antagonist, naloxone and the m-opioid receptor selective antagonist, b-funaltrexamine. In contrast, this effect was not antagonized by d-and k-opioid receptor selective antagonists, naltrindole and nor-binaltorphimine, respectively. The results of the present study demonstrate that endomorphin-1 and endomorphin-2 produce potent antidepressant-like effects after i.c.v. injection in mice. We may suggest that endomorphins and the m-opioid receptors might be involved in the physiopathology of depressive disorders, and that the endomorphinergic system could serve as a novel target for the development of antidepressant drugs. Neuropsychopharmacology (2007) 32, 813-821.

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Section: Discussionsupporting

confidence: 82%

Antidepressant-Like Effect of Endomorphin-1 and Endomorphin-2 in Mice

Fichna

Janecka

Piestrzeniewicz

et al. 2006

Neuropsychopharmacol

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“…Increased enkephalin levels after pharmacological blockade of enkephalin-degrading enzymes resulted in a reduction of depression-related behaviors in animal models (Tejedor-Real et al, 1993, 1995. This effect is probably mediated by an enhanced delta opioid receptor (DOPr) activity, because similar results have been obtained by application of DOPr agonists (Broom et al, 2002) and because DOPr knockout mice showed an increased frequency of depression-like behavior in the forced swimming test (Filliol et al, 2000).…”

Section: Introductionsupporting

confidence: 59%

“…It has been proposed that endogenous opioids, particularly enkephalins, contribute to the antidepressant effect of reference compounds, because their efficacy was antagonized by the non-specific opioid receptor antagonist naloxone (Tejedor-Real et al, 1995) or the DOPr-specific antagonist naltrindole (Zomkowski et al, 2005). Interestingly, the tricyclic catecholamine uptake inhibitor imipramine increased brain enkephalin level by antagonizing the activity of the neutral endopeptidase (de Gandarias et al, 1999).…”

Section: Preproenkephalin Knockout Mice In Models Of Depressionmentioning

confidence: 99%

Preproenkephalin Knockout Mice Show No Depression-Related Phenotype

Bilkei-Gorzó

Michel

Noble

et al. 2007

Neuropsychopharmacol

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Clinical, preclinical, and pharmacological studies have suggested that decreased enkephalin tone is associated with depression-like symptoms and increase in enkephalin signaling could have a therapeutic value in the treatment of depression. In this study we demonstrate that, surprisingly, animals lacking enkephalin (preproenkephalin, Penk1 À/À ) showed no depression-related phenotype in the Porsolt forced swimming or tail suspension tests. Moreover, Penk1 À/À mice had a lower frequency of depression-related behavior in stress-induced hypoactivity and ultrasonic vocalization models of depression, similar to animals treated with antidepressant drugs, although this effect was specific to the genetic background. In addition, there was no significant difference in the efficacy of antidepressant reference compounds in wild-type and knockout animals. Nialamide and amitriptyline were even slightly more effective in animals with genetic deletion of Penk1, whereas the minimal effective dose of imipramine and fluoxetine was the same in the two genotypes. The dual peptidase inhibitor RB-101 was also effective in Penk1 À/À as well as in Penk1/Pdyn À/À animals, although its efficacy was somewhat reduced compared with wild-type animals. This result was also surprising because the antidepressant effects of RB-101 were thought to be due to the elevation of enkephalin levels.

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“…Importantly, opioids can also modify the action of antidepressants and a significant attenuation of the behavioural effects of two TCAs, clomipramine and desipramine, was observed in mice treated with the non-selective opioid antagonist naloxone (Devoize et al, 1984). This antagonistic effect was corroborated in subsequent studies, demonstrating a reduction in the antidepressant efficacy of tricyclic and non-tricyclic antidepressants in response to opioid pretreatment (Baamonde et al, 1992;Berrocoso et al, 2004;Besson et al, 1999;Tejedor-Real et al, 1995).…”

Section: The Opioid Systemsupporting

confidence: 62%