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Central Nervous System Effects of Essential Oil Compounds
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Elaine Elisabetsky, Domingos S. Nunes
Linalool 9 showed antidepressant effects in mice and rats (Nestler and Hyman, 2010; Strekalova and Steinbusch, 2010; Berton et al., 2012; dos Santos et al., 2018). The effect is consistent with some linalool-bearing species used traditionally, such as the Mexican Mazahua people who use L. glaucescens along with other species to prepare a decoction used to treat sadness, nervousness, anger, and susto (“fright”) (Guzmán-Gutiérrez et al., 2012). Serotonin postsynaptic 5-HT1A receptors and α2 adrenergic receptors were implicated in the antidepressant-like effects (Guzmán-Gutiérrez et al., 2015).
Flavonoids with Preclinical Antidepressant-Like Effects
Published in Scott Mendelson, Herbal Treatment of Major Depression, 2019
The flavanone glycoside, hesperidin, is found in citrus fruit, onion, and peppermint. The aglycone form is hesperitin. Both have been shown to have antidepressant-like effects, with hesperidin being particularly well-studied. A number of studies have demonstrated antidepressant effects of hesperidin and shown plausible mechanisms by which this might occur. Intraperitoneal administration of hesperidin decreased immobility time of mice in the forced swim and tail suspension tests, and these antidepressant-like effects were blocked by the 5-HT1A receptor antagonist, WAY100635. Moreover, combining sub-effective doses of hesperidin and the SSRI fluoxetine produced an antidepressant-like effect. Together, those data suggest that stimulation of the 5-HT1A receptor played a role.35 In a similar study of mice, hesperidin reduced immobility in the forced swim test, and this effect was blocked by naloxone and the selective κ-opioid receptor antagonist, DIPPA. Thus, kappa opiate receptors may also be involved in this antidepressant effect.36
Anxious Patient in the Emergency Ward
Published in R. Thara, Lakshmi Vijayakumar, Emergencies in Psychiatry in Low- and Middle-Income Countries, 2017
Janardhanan C. Narayanaswamy, Y.C. Janardhan Reddy
Buspirone, a non-benzodiazepine anxiolytic that has partial agonist properties at 5-HT1A receptors, does not have the side-effects associated with the benzodiazepines, such as sedation, impairment of memory, slowed reaction time, or physiological dependence (Bernstein et al. 2006). Its anti-anxiety action is of delayed onset (a few weeks). It has a short half-life and thus requires multiple daily dosing (10–30 mg per day in 2–3 divided doses).
Early outcomes, associated factors and predictive values of clinical outcomes of tandospirone in generalized anxiety disorder: a post-hoc analysis of a randomized, controlled, multicenter clinical trial
Published in Current Medical Research and Opinion, 2023
Yi Fu, Jian Lin Ji, Shen Xun Shi, Hai Yin Zhang, Guo Zhen Lin, Ying Li Zhang, Xiuli Li, Wen Yuan Wu
At present, GAD treatment is mainly based on medication. Commonly used anxiolytic drugs in the clinic include anxiolytics (benzodiazepines and 5-HT1A receptor partial agonists) and antidepressants with anxiolytic effects. 5-HT1A receptor partial agonists mainly produce anxiolytic effects by regulating 5-HT function. Tandospirone is a representative 5-HT1A receptor partial agonist. In vitro and in vivo studies have shown that tandospirone is mainly metabolized by cytochrome P450 (CYP) 3A4. In vivo, tandospirone is metabolized to 1-(2-pyrimidine) -piperazine by CYP3A4. Trials have demonstrated the anxiolytic effects of tandospirone7,8. The currently approved indications of tandospirone in China are anxiety caused by various neuroses, including GAD, essential hypertension, peptic ulcer and other physical diseases. The recommended dose of tandospirone is 30-60 mg/d9. Several national and international guidelines have recommended 5-HT1A receptor partial agonists for the first-line treatment of anxiety disorders, especially GAD10–12. Tandospirone is highly effective and safe, and represents a more promising drug for clinical application compared with traditional anti-anxiety drugs13–15.
Sexual dysfunction with major depressive disorder and antidepressant treatments: impact, assessment, and management
Published in Expert Opinion on Drug Safety, 2022
Joan Winter, Kimberly Curtis, Bo Hu, Anita H. Clayton
Serotonin binding at the post-synaptic 5-HT1A receptor produces antidepressant and anxiolytic effects, while increased binding at the 5-HT2A and 5-HT2C receptors leads to increased anxiety, insomnia, and sexual dysfunction. Multiple antidepressants (eg. mirtazapine, trazodone, several TCAs, and norquetiapine – the active metabolite of quetiapine) with fewer sexual side effects exhibit antagonism at 5-HT2. The release of dopamine and norepinephrine in the cortex is inhibited by stimulation of 5-HT2A and 5-HT2C receptors [9–10]. Norepinephrine and nitric oxide promote tumescence of sexual organs and lubrication. Dopamine is a key neurotransmitter of the reward system, which includes the nucleus accumbens/ventral striatum, ventral tegmental area (VTA), pre-frontal cortex, orbitofrontal cortex, anterior cingulate cortex, and amygdala. Dopamine promotes sexual function at varying concentrations at progressive stages of sexual engagement: from sexual desire to increased parasympathetic activation required for erections, and finally climax. Dopamine may also be involved in the medial preoptic area of the hypothalamus (mPOA) in the initial disinhibition of genital reflexes[12]. In addition to central effects, serotonin acts in the peripheral nervous system by directly suppressing spinal ejaculatory centers [10–11]. Thus, the increase of serotonin at the synaptic cleft as a result of antidepressant action can impact many levels of sexual functioning: decreased interest and arousal, inhibited/delayed orgasm, and diminished intensity and frequency of orgasm[13].
The serotonin toxidrome: shortfalls of current diagnostic criteria for related syndromes
Published in Clinical Toxicology, 2022
Angela L. Chiew, Nicholas A. Buckley
There are at least seven families of 5-HT receptors (5-HT1 to 5-HT7), some of which have multiple subtypes [4,5]. It is likely that no single receptor is responsible for serotonin toxicity. However, stimulation of the 5-HT1A and 5-HT2A receptors have been implicated in serotonin toxicity. The 5-HT1A receptors possibly contribute to some of the milder symptoms of serotonin toxicity including anxiety and hyperactivity [8,9]. Activation of 5HT2A receptors at high serotonin concentrations is implicated in severe serotonin toxicity in animal studies [10,11]. The 5-HT1A receptors have a higher affinity for serotonin than the low-affinity 5-HT2A receptors and are likely to be nearly fully occupied at much lower extracellular 5-HT concentrations [10]. This means that changes in 5-HT1A receptor occupancy and effects are likely to be dominant with small increases in 5-HT.