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Making Sense of Behaviour
Published in Cathy Laver-Bradbury, Margaret J.J. Thompson, Christopher Gale, Christine M. Hooper, Child and Adolescent Mental Health, 2021
Although often presented as the preeminent model in mental ‘health’ teams, the biological model has its limitations. It offers a mechanistic and simple way to understand behaviour without having to engage with psychological complexity. It allows us to translate complex psychological phenomena into the language of biology, creating an illusion of understanding. Low levels of serotonin are not just a biological phenomenon associated with the psychological phenomenon of low mood. In the biological model, they are thought of as the same phenomenon as low mood and eventually the cause of it. We could explain a complex phenomenon such as crying as an imbalance between the production of serum by the lacrimal glands and the capacity of the lacrimal duct to evacuate such serum, just as we could explain depression as an imbalance in serotonin in the brain. In both cases, we reduce a complex psychological phenomenon (crying, low mood) to one of its biological components, such as overflow of serum or imbalance of serotonin. We understand some of the mechanics, but we are none the wiser as to what it means or why it happens.
Brain Motor Centers and Pathways
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The basal ganglia have been implicated in a wide range of functions, as evidenced by the distribution of the inputs they receive. Practically all areas of the cerebral cortex project essentially topographically to the dorsal striatum, thence to other nuclei, and back through the feedback loops via the thalamus to the same cortical areas of origin of the given input to the basal ganglia. The dorsal striatum also receives: (i) feedback input from thalamic nuclei, (ii) dopaminergic input from the ventral tegmental area of the midbrain, which is believed to be part of the “reward” system in the brain, and (iii) serotonergic input from the raphe nuclei, which are a group of nuclei in the brainstem that are a major source of serotonin to the rest of the brain. Serotonin is a neurotransmitter that influences many brain functions, including mood, behavior, sleep, memory, and learning.
Bioactive Compounds in Coffee: Health Benefits of Macronutrients and Micronutrients
Published in Megh R. Goyal, Durgesh Nandini Chauhan, Assessment of Medicinal Plants for Human Health, 2020
Tryptophan is a protein that is found in green beans. Tryptophan content will affect the increase in serotonin levels.6 Serotonin is an appetite controller. Serotonin function will reduce the intake of food by a person. Conversely, decreased serotonin levels will increase appetite.4 Patients with depression will experience deficiency of serotonin levels so that more food is intaken than energy expenditure, resulting in visceral fat accumulation and proinflamasi cytokines.26,27
Amelioration of modified chronic unpredictable stress using Celastrus paniculatus seed oil alone and in combination with fluoxetine
Published in Drug and Chemical Toxicology, 2023
Sanjana Chahuan, Sania Grover, Shamsher Singh
In depressive patients, learning and memory impairment, mood swings, alteration in thinking power are most commonly seen which may be due to the disruption of neurotransmission system (Liu et al. 2018). On the other hand, depression is caused by excessive stress, altered neurotransmitters level either by increased degradation due to activation of MAO or their reduced synthesis. Both preclinical and clinical report showed reduced level of serotonin in depressive state (Angoa-Pérez et al. 2014, Liu et al. 2018). Clinically, FLU has been recommended to improve serotonin level in depressive patients but long-term use of FLU produces adverse effects and causes Serotonin syndrome (Little et al. 2018), mania (Akaltun and Ayaydin 2020), dysregulate electrolyte balance in the patients (Riznic et al. 2017). However, in our protocol, animals treated with CPSO 100 mg/kg + FLU 10 mg/kg and CPSO 50 mg/kg + FLU 10 mg/kg significantly improved serotonin as well as catecholamine level (dopamine and nor-epinephrine) as compared to CPSO alone and depressive control group.
The current state-of-the-art in pharmacotherapy for pediatric generalized anxiety disorder
Published in Expert Opinion on Pharmacotherapy, 2023
Peter J. Castagna, Elita Farahdel, Marc N. Potenza, Michael J. Crowley
In our review of the current state-of-the-art in pharmacotherapy for pediatric GAD, we examined evidence obtained from ten RCTs and six open-label trials between the years of 1991 and 2015, inclusive. We found that the most frequently studied pharmacotherapies included selective serotonin reuptake inhibitors (SSRIs). Specifically, most studies investigated fluoxetine (n = 6), fluvoxamine (n = 4) or sertraline (n = 3). The findings suggest efficacy of these agents, as well as for selective norepinephrine reuptake inhibitors (SNRIs) like atomoxetine, venlafaxine, and duloxetine. Limitations include heterogeneous samples, often with mixed anxiety disorders, complicating comparisons across studies. Nonetheless, based on results of these studies, expert opinions may be generated.
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.