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Biological Basis of Behavior
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
The biogenic amines include catecholamines, indolamines, ethylamines, and quaternary amines. Dopamine, epinephrine, and norepinephrine constitute the main catecholamines family of neurotransmitters which are derived from the same precursor molecule (tyrosine). The monoamine theory of mood disorder hypothesizes that altered monoamine activity and related changes in monoamine receptors result in mood abnormalities.
Migraine: diagnosis and treatment
Published in Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby, Headache in Clinical Practice, 2018
Stephen D. Silberstein, Richard B. Upton, Peter J. Goadsby
The currently available antidepressants consist of a number of different classes of drugs with different mechanisms of action: MAOIs: (a) selective and reversible; (b) nonselective and irreversible;monoamine reuptake inhibitors: (a) nonselective TCAs; (b) selective serotonin reuptake inhibitors (SSRIs); (c) selective serotonin and norepinephrine reuptake inhibitors (SNRIs);monoamine receptor targeted drugs: (a) serotonin (trazadone, trazodone); (b) norepinephrine β2 NE antagonist (mirtazepine, mirtazapine); (c) dopamine (bupropion).
Pharmacological management of depression in older people
Published in Stephen Curran, John P Wattis, Practical Management of Affective Disorders in Older People, 2018
Stephen Curran, Andrew Byrne, John P Wattis
For nearly 40 years, the principal theory to explain the biological basis of depression has been the monoamine hypothesis. This theory proposes that depression is due to a deficiency in one or more of three monoamines, namely noradrenaline, serotonin and dopamine in the synaptic clefts of the appropriate neurones. For example, tricyclic antidepressants (TCAs) block the neurotransmitter reuptake pump, causing neurotransmitters to accumulate in the synaptic cleft thus returning the neuron to a ‘normal state’. However, despite the fact that neurotransmitter levels return to normal fairly quickly the clinical effect is delayed as is the down-regulation of receptor sensitivity. A related theory is the monoamine receptor hypothesis. The consequence of neurotransmitter depletion is that postsynaptic receptors become up-regulated (increased in number) and the degree of up-regulation correlates with the degree of depression. In addition, down-regulation correlates with the onset of antidepressant action.10
Lack of bombesin receptor-activated protein homologous protein impairs hippocampal synaptic plasticity and promotes chronic unpredictable mild stress induced behavioral changes in mice
Published in Stress, 2023
Xueping Yao, Xiaoqun Qin, Hui Wang, Jiaoyun Zheng, Zhi Peng, Jie Wang, Horst Christian Weber, Rujiao Liu, Wenrui Zhang, Ji Zeng, Suhui Zuo, Hui Chen, Yang Xiang, Chi Liu, Huijun Liu, Lang Pan, Xiangping Qu
Nervous tissue has a tremendous capacity of plasticity. In response to intrinsic or extrinsic stimuli neural networks change based upon synapse regulation and reorganization of circuitry. Psychosocial stressors or stressful life events have been shown to have profound effects on neural structure and function in susceptible individuals. For example, neuroplasticity hypothesis, which was proposed for understanding the mechanisms of the development of depression, incorporates the continually remodeling of key brain systems in response to various situations. It suggests that a disrupt or dysfunction of neural plasticity contributes to behaviors related to depression (Duman et al., 2016; B. Liu et al., 2017; Pittenger & Duman, 2008; Racagni & Popoli, 2008). Typical antidepressants may improve neuroplasticity through monoamine neurotransmitters’ stimulation of the postsynaptic monoamine receptors (Racagni & Popoli, 2008). In addition, other treatments such as psychotherapy, cognitive behavioral therapy and electroconvulsive shock treatment may also have therapeutic effects on depression through regulating neural plasticity in experimental animals (B. Liu et al., 2017).
The Effectiveness of Cannabinoids in the Treatment of Posttraumatic Stress Disorder (PTSD): A Systematic Review
Published in Journal of Dual Diagnosis, 2020
C. Hindocha, J. Cousijn, M. Rall, M. A. P. Bloomfield
PTSD is a potentially debilitating condition. PTSD affects approximately 1% of the population (Karam et al., 2014) and is overrepresented in military veterans (Richardson, Frueh, & Acierno, 2010). The fundamental features of PTSD include (1) reexperiencing of the trauma through intrusive memories, flashbacks, and/or nightmares; (2) active avoidance of external and internal reminders of the trauma; and (3) hyperarousal (Brewin et al., 2017). At its core, PTSD can be conceptualized as a disorder of memory processing (Brewin, 2001, 2003). Treatment is generally focused on reprocessing and reappraisal of trauma memories and their sequelae through trauma-focused psychotherapies. Pharmacotherapy can also be offered. Currently approved and recommended drugs (NICE, 2018) include serotonin reuptake inhibitors and monoamine receptor antagonists to provide symptomatic relief. However, as many patients struggle to access expert trauma-focused therapies and have suboptimal responses to these pharmacological treatments, there is an urgent need to develop new intervention strategies (Krystal, Rosenheck, & Cramer, 2011).
Rhabdomyolysis, Methamphetamine, Amphetamine and MDMA Use: Associated Factors and Risks
Published in Journal of Dual Diagnosis, 2020
John R. Richards, Colin G. Wang, Roderick W. Fontenette, Rory P. Stuart, Kerry F. McMahon, Samuel D. Turnipseed
Genetic differences in monoamine receptor density, sensitivity, and processing may also be associated with a higher risk of rhabdomyolysis developing. Dopamine D1 and D2 receptor polymorphisms identified in individuals predisposed to the rare neuroleptic malignant syndrome is an example of this phenomenon (Kawanishi, 2003). Pharmacogenetic differences of monoamine receptors may explain the wide range of MA sensitization, addiction, risk-taking behavior, psychomotor effects, and cardiovascular toxicity (Bennett et al., 1998; Richards et al., 2015; Rivest et al., 1995). Genetic polymorphisms may also explain the development of statin-induced rhabdomyolysis in certain predisposed patients (Cervellin et al., 2017).