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Herbs with Antidepressant Effects
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
In several studies, antidepressant-like effects were noted. Salvinorin A reduced immobility in the forced swim test with rats, and in the tail suspension test with mice. These effects could be blocked by either the κ-opioid receptor antagonist nor-binaltorphimine or the CB1 cannabinoid receptor antagonist AM251. Treatment with Salvinorin A also suggested anxiolytic effects in rats in the elevated plus maze.11 Chronic treatment of rats with salvinorin A also reversed the reduction in preference for sucrose – considered a form of depression-like anhedonia – that was induced by chronic unpredictable stress.12
Brain site-specific regulation of hedonic intake by orexin and DYN peptides: role of the PVN and obesity
Published in Nutritional Neuroscience, 2022
P. Mattar, S. Uribe-Cerda, C. Pezoa, T. Guarnieri, C. M. Kotz, J. A. Teske, E. Morselli, C. Perez-Leighton
This study aimed to determine how OXA and DYN-A1–13 peptides regulate palatable food choice and intake in PVN and whether in obesity, the brain expression of KOR and orexin receptors correlates with food choice and intake. We first determined the effect of OXA on hedonic intake caused by injection of DYN-A1–13 in PVN. Second, we tested whether injection of OXA or DYN-A1–13 in VTA to determine if their effects on hedonic intake were opposite to those observed in PVN. Third, we determined if endogenous opioid activity in PVN was necessary for hedonic intake and whether it inhibited the potential effect of OXA on hedonic intake. To do this, we measured palatable food intake in mice injected into PVN with norBNI, (nor-Binaltorphimine, mixed KOR and MOR antagonist that can block DYN-A1–13 activity [14]) followed by OXA injection into PVN. Fourth, we tested whether the individual preference for palatable foods modulated hedonic intake caused by DYN-A1–13 in PVN. Finally, we determined whether food preference and intake in obese mice with extended access to a cafeteria (CAF) diet (free access to a rotation of palatable foods made for humans that causes hedonic intake with large individual food preferences [19,28]) correlated with expression of KOR and orexin receptors across different brain sites.
Emerging concepts on the use of ketamine for chronic pain
Published in Expert Review of Clinical Pharmacology, 2020
Yunpeng Yang, Dermot P. Maher, Steven P. Cohen
Additional evidence from rodent models of depression indicate that the clinical manifestations of ketamine may be the result of interactions with dopamine D2 and D3 receptors, but not D1[55]. The opioid receptor system seems to partially mediate ketamine-induced antinociceptive effects in rodents, which may be translatable to pain patients. NMDA NR1 subunits and mu opioid receptors co-localize and functionally associate on neurons in the periaqueductal gray area, which is involved in the processing of pain. Pacheco Dda and colleagues found that administration of the pan-opioid receptor antagonist naloxone, the μ-opioid receptor-specific antagonist clocinnamox and the δ-opioid receptor-specific antagonist naltrindole, but not the κ-opioid receptor antagonist nor-binaltorphimine, antagonized ketamine-induced central antinociception in a dose-dependent manner in mice[56]. The synergistic involvement of opioid receptors in the analgesic effects of ketamine has been described by several other investigators [57,58]. In humans, however, the administration of naloxone failed to prevent ketamine-induced reductions in secondary hyperalgesia, which may indicate differences in hyperalgesic mechanisms between species[59].
Can pharmacotherapy improve treatment outcomes in people with co-occurring major depressive and cocaine use disorders?
Published in Expert Opinion on Pharmacotherapy, 2021
Gustavo A. Angarita, Hasti Hadizadeh, Ignacio Cerdena, Marc N. Potenza
As with D3R investigations, KOR antagonists (LY2444296, buprenorphine combined with naltrexone, and nor-binaltorphimine) have been more extensively studied in animal models of CUD and MDD. Findings support their capacity to decrease cocaine self-administration and foot-shock-induced reinstatement of cocaine-seeking [97,105,106]. They may also reduce anxiety and depressive-like behaviors (e.g. decrease escape failure, decrease immobility time, increase swimming time) on learned helplessness, forced swim, and elevated plus maze tests [97,99,107]. Some KOR-antagonist studies test and display both antidepressant actions and the capacity to block stress-induced reinstatement of cocaine use [92]. Combinations that block KOR signaling show promise in treating MDD and CUD. These combinations include buprenorphine (a partial mu-opioid receptor (MOR) agonist and KOR antagonist) combined with samidorphan (a potent MOR antagonist) and buprenorphine combined with naltrexone (a potent MOR and weaker KOR and delta-opioid receptor antagonist). In rodents, buprenorphine/naltrexone decreased the self-administration of cocaine without producing opioid dependence [105]. Clinically, in a multisite double-blind RCT involving 292 individuals with CUD and past or current opioid use disorder, 8 weeks of [buprenorphine+naloxone] (16 mg) and naltrexone (vs. placebo) were associated with more frequent negative urine toxicology tests, although results for the primary outcome were negative [108]. A multicenter RCT with sequential parallel-comparison design in adults with MDD with inadequate response to selective serotonin reuptake inhibitors (SSRIs) or serotonin norepinephrine reuptake inhibitors (SNRIs) showed a beneficial effect of 4 weeks of treatment with buprenorphine/samidorphan over placebo [109]. Later, two global phase-3 multicenter trials with similar designs also showed significant effects of buprenorphine/samidorphan over placebo in the treatment of refractory MDD [110].