1997
DOI: 10.1016/s0924-977x(97)00411-2
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Implication of β1- and β2-adrenergic receptors in the antinociceptive effect of tricyclic antidepressants

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Cited by 32 publications
(12 citation statements)
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“…Our data indicate that both kynurenine/tryptophan and serotonin/tryptophan ratios in the hippocampus were closely regulated by IDO1 activity. This regulatory mechanism appears to have two important functional implications: on the one hand, increased IDO activity lowers the endogenous serotonin level (43), which leads to depression (44) and diminishes the descending inhibition of pain modulation (45,46); on the other hand, increased IDO activity increases kynurenine derivatives such as quinolinic acid, contributing to neurotoxicity and nociception via the interaction with glutamate receptors (47). Therefore, IDO is situated in a key tryptophan metabolic pathway, and alteration of IDO activity results in changes in the content of endogenous kynurenine and serotonin, both of which play a critical role in the mechanisms of pain and depression (Supplemental Figure 2).…”
Section: Figurementioning
confidence: 99%
“…Our data indicate that both kynurenine/tryptophan and serotonin/tryptophan ratios in the hippocampus were closely regulated by IDO1 activity. This regulatory mechanism appears to have two important functional implications: on the one hand, increased IDO activity lowers the endogenous serotonin level (43), which leads to depression (44) and diminishes the descending inhibition of pain modulation (45,46); on the other hand, increased IDO activity increases kynurenine derivatives such as quinolinic acid, contributing to neurotoxicity and nociception via the interaction with glutamate receptors (47). Therefore, IDO is situated in a key tryptophan metabolic pathway, and alteration of IDO activity results in changes in the content of endogenous kynurenine and serotonin, both of which play a critical role in the mechanisms of pain and depression (Supplemental Figure 2).…”
Section: Figurementioning
confidence: 99%
“…In fact, both α-adrenoreceptor [10] and 5-HT receptor [11] antagonists have been shown to inhibit antidepressantsmediated antinociception. Moreover, both p-chlorophenylalanine and alpha-methyl-p-tyrosine [12] were shown to inhibit antidepressants-mediated antinociception, by depleting respectively central noradrenaline and serotonin system.…”
Section: Central Mechanisms Of Analgesic Action the Monoamine Hypothesismentioning
confidence: 98%
“…Other aspects of monoaminergic systems have been implicated in the analgesic action of antidepressants. Beta-adrenoceptors have been demonstrated to mediate the analgesic effects of desipramine and nortriptyline (Mico et al, 1997). TCAs may reduce hyperalgesia but not tactile allodynia because different neuronal mechanisms underlie different manifestations of neuropathic pain (Jett et al, 1997).…”
Section: Antidepressantsmentioning
confidence: 98%