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The story of modern tranquilliser drugs
Published in Adam Doble, Ian L Martin, David Nutt, Calming the Brain: Benzodiazepines and related drugs from laboratory to clinic, 2020
Adam Doble, Ian L Martin, David Nutt
During the 1980s, a lot of interest was shown in the potential use of drugs acting on the serotonergic system for the treatment of anxiety disorders and insomnia. The only drug to have been marketed as a result of this programme has been buspirone (Rickels, 1990), a 5-HT1A receptor agonist used for the treatment of generalised anxiety disorders. Buspirone has clear anxiolytic properties, but, unlike benzodi-azepines, has a delayed onset of action (around two weeks) that makes it less interesting in this indication than benzodiazepine anxiolytics that act immediately. Ritanserin, a 5-HT2A receptor antagonist, received extensive investigation for the treatment of both anxiety and sleep disorders. However, unequivocal demonstration of efficacy was lacking and this agent has never been marketed. Interest in drugs acting at serotonin receptors has now been on the wane for several years, although this may change if deramciclane, a 5-HT2 receptor antagonist currently in clinical development for the treatment of anxiety disorders, demonstrates interesting efficacy.
Serotonin Metabolism in Functional Somatic Illness
Published in Peter Manu, The Psychopathology of Functional Somatic Syndromes, 2020
The monoamine hypothesis of depression, which was proposed more than 30 years ago, states that the biological basis of affective disorders is a deficiency in serotonergic and noradrenergic neurotransmission (Hirschfeld, 2000). Most research activities have focused on the serotonergic system, a complex neurofunctional apparatus with dozens of receptor subtypes in cortical and subcortical structures (Mann, 1999). Impairments in the serotonergic system occur at many levels and may involve decreased concentrations of serotonin, altered affinity and numbers of serotonin receptors and uptake sites, and postreceptor abnormalities (Leonard, 2000). In this chapter, we review the work testing the components and function of the serotonergic system in functional illnesses to determine whether patients with functional somatic syndromes show evidence of serotonergic deficiency and whether such deficiency correlates with the somatic and psychological manifestations of these conditions.
Clinical and Medical Management of Conditions Caused by MDMA or ‘Ecstasy’
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
MDMA can alter sleep patterns, both acutely and chronically. Jones, Callan, Blagrove, and Parrott (2008) described the patterns of self-reported sleep after weekend Ecstasy/MDMA. They noted significant reductions in sleep time and sleep quality for several days afterward, with sleep patterns returning to normal after five or six days. In relation to chronic sleep effects in abstinent users, Allen, McCann, and Ricaurte (1993) found a reduction in total sleep time, due mainly to less stage 2 non-REM sleep. In a review, McCann and Ricaurte (2007) concluded that abstinent Ecstasy/MDMA users were at increased risk for chronic sleep disturbances. In a later study, McCann et al. (2009) revealed the medical disorder ‘sleep apnoea’ in young recreational users, with incidence rates related to lifetime MDMA usage. The authors noted that serotonin was important in the control of breathing and hypothesized that this particular sleep disorder might be another reflection of serotonergic neurotoxicity. Ogeil et al. (2013) noted that around 70% of Ecstasy/MDMA users reported sleep disturbances. In relation to therapy, it is recommended not to administer sleep medications, since they all tend to be problematic when used chronically, because of tolerance or withdrawal problems. The best advice is abstinence—in the hope that sleep may gradually improve, although the limited evidence suggests that this disorder can be enduring (Taurah et al., 2013) and may possibly be permanent.
Almond intake during pregnancy in rats improved the cognitive performance of adult male offspring
Published in Nutritional Neuroscience, 2023
Zahra Bahaeddin, Fariba Khodagholi, Forough Foolad, Fatemeh Emadi, Fatemeh Alijaniha, Shima Zareh Shahamati, Romina Tavassoli Yousef Abadi, Mohsen Naseri
On the other hand, Haider and colleagues revealed an increase in the brain tryptophan and serotonergic turnover of rat’s brains following oral intake of almonds leading to memory improvement in rats [45]. Enhanced serotonin activity of the brain has been shown to improve cognitive performance in both animals and human studies, whereas decreased serotonergic levels by acute tryptophan depletion would impair cognition [46,47]. The role of the serotonergic system in neuroplasticity has been explored, which is critical during brain development [48]. Serotonin acts as a growth factor during embryogenesis and is involved in brain structural changes. The serotonergic system interacts with chemical messengers of the GABAergic, glutamatergic, and dopaminergic neurotransmitters [49]. Given the above-mentioned data, tryptophan can be considered an effective part of almond in improving the memory of adult offspring rats.
Ginsenoside Re attenuates 8-OH-DPAT-induced serotonergic behaviors in mice via interactive modulation between PKCδ gene and Nrf2
Published in Drug and Chemical Toxicology, 2023
Eun-Joo Shin, Ji Hoon Jeong, Bao-Trong Nguyen, Naveen Sharma, Cuong Ngoc Kim Tran, Seung-Yeol Nah, Yi Lee, Jae Kyung Byun, Sung Kwon Ko, Hyoung-Chun Kim
The 5-HT1A receptor agonist (±)-8-hydroxy-dipropylaminotetralin (8-OH-DPAT) has been well-recognized to elicit ‘traditional serotonin syndrome behaviors’ (Haberzettl et al.2013). Serotonin syndrome is a serious disorder/toxic state due to the excessive serotonergic function in the brain, most commonly after the overdose of antidepressants or after the combination of several neuropsychiatric prescriptions (Boyer and Shannon 2005). Serotonin syndrome has become a common health problem, reflecting the frequent application of drugs that activate serotonergic transmission (Isbister et al.2004). Serotonin syndrome can be induced by an excess of serotonin (5-hydroxytryptophan, 5-HT) precursor or receptor agonists, increased release of 5-HT, or reduced 5-HT reuptake or metabolism (Kalueff et al.2008). Indeed, increased prescription of antidepressants (i.e., selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs)) augmented the incidence of serotonin syndrome (Boyer and Shannon 2005, Isbister and Buckley 2005). Therefore, it is highly important that sustained exposure to antidepressant drugs has the potential to cause serotonin syndrome.
Why lithium should be used in patients with bipolar disorder? A scoping review and an expert opinion paper
Published in Expert Review of Neurotherapeutics, 2022
Gaia Sampogna, Delfina Janiri, Umberto Albert, Filippo Caraci, Giovanni Martinotti, Gianluca Serafini, Alfonso Tortorella, Alessandro Zuddas, Gabriele Sani, Andrea Fiorillo
Lithium does not bind serum protein and has a distribution volume of about 0.7–1.0 L/kg. It is not metabolized by liver cytochromes and is eliminated as free ion at renal level. Several interactions – both pharmacokinetic and pharmacodynamic [43] – have been described. The most clinically relevant pharmacokinetic drug interactions occur when lithium is co-administered with drugs reducing renal elimination, such as thiazide and loop diuretics, nonsteroidal anti-inflammatory drugs [NSAIDs] and angiotensin-converting enzyme [ACE] inhibitors [44]. Pharmacodynamic drug interactions are less frequent and may occur when combining lithium with: i) selective serotonin reuptake inhibitors (SSRI) (i.e., increased risk of serotonergic syndrome); ii) first-generation antipsychotics (i.e., haloperidol) with increased laboratory markers of oxidative stress and neurotoxicity [43]. In particular, some drugs, such as SSRI, NSAIDs, ACE inhibitors, angiotensin-II receptor antagonists, thiazides, spironolactone, furosemide, metronidazole, tetracyclines, topiramate, may increase serum levels of lithium concentrations. On the contrary, theophylline, caffeine, sodium bicarbonate, and products containing sodium chloride may decrease lithium concentrations. Antipsychotics may worsen lithium neurotoxicity, while calcium channel blockers may cause ataxia, confusion, and somnolence.