ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
Noradrenaline is one of the NEUROTRANSMITTERS; neurons that contain noradrenaline are said to be NORADRENERGIC. It is a CATECHOLAMINE neurotransmitter and therefore a member of the even larger family of MONOAMINE neurotransmitters. The full chemical name for noradrenaline is 3,4- DIHYDROXYPHENYLETHANOLAMINE. Noradrenaline, like DOPAMINE, is synthesized from the amino acid LTYROSINE. The enzyme TYROSINE HYDROXYLASE catalyses the conversion of tyrosine to LDOPA (L-3,4- dihydroxyphenylalanine). LDOPA is then converted by AROMATIC LAMINO ACID DECARBOXYLASE to dopamine. In dopaminergic neurons, this is as far as the conversion goes, dopamine being transported and packaged for use as a neurotransmitter. However, further conversion of dopamine produces noradrenaline. The presence of the enzyme DOPAMINE BETA-HYDROXYLASE, involved in the conversion of dopamine to noradrenaline, is the principal way to discriminate noradrenaline- from dopamine- containing neurons. In other neurons a further conversion can occur: the enzyme PHENYLETHANOLAMINE-N-METHYLTRANSFERASE is involved in the production of adrenaline from noradrenaline. There are multiple receptors for noradrenaline (see ADRENOCEPTORS). The synaptic action of noradrenaline is terminated in two ways: destruction by enzymes or by REUPTAKE, for which there are specific noradrenaline transporters. As with dopamine catabolism, enzymatic destruction can be achieved by either of two enzymes: MONOAMINE OXIDASE (MAO) or
The cell
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella in Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
The third mechanism by which drugs may alter synaptic activity involves changes in neurotransmitter re-uptake or degradation. Very well-known examples of drugs in this category are Prozac® (fluoxetine) and the more recently prescribed Cymbalta® (duloxetine) and Wellbutrin® (bupropion), which are used to treat depression. While the complete etiology is unknown, it is widely accepted that depression involves a deficiency of monoamine neurotransmitters (e.g., norepinephrine and serotonin) in the CNS. Prozac, a selective serotonin re-uptake inhibitor, prevents the removal of serotonin from the synaptic cleft. Cymbalta prevents the re-uptake of both serotonin and norepinephrine, whereas Wellbutrin prevents the re-uptake of dopamine and norepinephrine. Therefore, the concentration and activity of these neurotransmitters in the brain are enhanced and the symptoms of depression are relieved.
Resilience and burnout
Anna-leila Williams in Integrating Health Humanities, Social Science, and Clinical Care, 2018
Concurrent with activation of the hypothalamic-pituitary-adrenal axis, stress leads to activation of the sympathetic nervous system and inhibition of the parasympathetic nervous system. Consequently, monoamine neurotransmitters, norepinephrine and dopamine are released in response to stress which facilitates encoding emotionally charged memories at the amygdala. Hypersecretion of norepinephrine is associated with anxiety and post-traumatic stress disorder. Another monoamine neurotransmitter, serotonin, has not had its mode of physiologic influence precisely delineated as of yet. That said, it is widely accepted that serotonin metabolites modulate the amygdala and prefrontal cortex to mitigate physiologic responses to stress. Serotonin effects on the body are known to include regulation of anxiety, mood, aggression, and impulse control, and therefore are presumed to contribute to resilience (Krystal & Neumeister, 2009).
SAR and molecular mechanism studies of monoamine oxidase inhibition by selected chalcone analogs
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Raed Shalaby, Jacobus P. Petzer, Anél Petzer, Usman M. Ashraf, Ealla Atari, Fawaz Alasmari, Sivarajan Kumarasamy, Youssef Sari, Ashraf Khalil
Neuronal signaling is mediated by several neurotransmitters, including monoamine neurotransmitters such as norepinephrine, dopamine, and serotonin. The levels of monoamines in the brain are controlled by a balance between their enzyme-catalyzed synthesis and breakdown, while both reuptake carriers and vesicular transporters regulate the concentrations of these neurotransmitters in the synapse. Alterations of the monoamines homeostasis are associated with many neurological conditions such as depression, autism, drug addiction, and neurodegenerative diseases [Alzheimer’s disease (AD) and Parkinson’s disease (PD)]1. Monoamine oxidases (MAOs, EC 1.4.3.4) are among a family of flavin adenine dinucleotide (FAD)-dependent enzymes that play a key role in the breakdown of endogenous and exogenous amines2. These enzymes are located on the mitochondrial outer membrane, mostly in the brain, and are also present in the liver, gut, intestine, skin, placenta, lymphocytes, and platelets3.
Acute toxic kidney injury
Published in Renal Failure, 2019
Nadezda Petejova, Arnost Martinek, Josef Zadrazil, Vladimir Teplan
Amphetamines are synthetic, widely abused psychoactive drugs with significant stimulant, euphoric, anorectic, empathogenic, entactogenic and hallucinogenic properties. Common in clinical psychiatric practice are amphetamine, methamphetamine and 3,4 methylenedioxymethamphetamine (MDMA, Ecstasy). However, in human history some natural amphetamines have been used for centuries through the ingestion or chewing the leaves of the Catha edulis plant (Khat) in East Africa and Arabia or plants of the genus Ephedra e.g. Ephedra sinica. The biochemical structure of amphetamines is similar to the monoamine neurotransmitters with competitive action at membrane transporters of dopamine, norepinephrine and serotonin. The results of competitive membrane action are blocking of reuptake and induction of the reverse transport of endogenous neurotransmitters [102]. The clinical presentation of MDMA poisoning varies from hyperpyrexia, arrhythmias, serotonin syndrome, neurological symptoms with seizures, sudden death or coma. In vitro study using rat and human proximal tubular cells showed no direct nephrotoxicity of MDMA or methylenedioxyamphetamine (MDA) in varied concentrations, but alpha-methyldopamine (alpha-MeDA) itself and conjugation with glutathione (GSH) to 5-(glutathione-S-yl)-alpha-MeDA were extremely potent nephrotoxicants with approximately 70–80% cell death. Thus, the metabolism of ecstasy on the apical membrane of renal proximal tubular cells with the extracellular event of redox cycling appears to be the possible part of pathophysiological pathway of MDMA nephrotoxicity [103].
Antidepressant-like activities of extracts of the fungus Paecilomyces tenuipes M98
Published in Psychiatry and Clinical Psychopharmacology, 2019
Yaying Li, Long Han, Tong Lu, Muhammad Noman, Weidong Qiang, Xinxin Lan, Tingting Gao, Jinnan Guo, Xiaomei Zhang, Haiyan Li, Jing Yang, Linna Du
According to the monoamine hypothesis, the underlying pathophysiologic bases of depression are the insufficient functional availability of 5-HT, NE and/or dopamine DA [16]. These monoamine neurotransmitters are associated with regulation of mood, self-control, motivation, drive, and cognitive performance [17]. Thus, 5-HT, NE and DA concentrations in hypothalamus of mice were measured. As shown in Figure 3, after 21 days of stimulation, the levels of these three neurotransmitters in mice decreased significantly. Administration of Flu and samples enhanced the level of 5-HT in CUMS mice (Figure 3(A), Flu: p < .05, AE (0.25 g/kg): p < .05, AE (2.50 g/kg): p < .01, WE (three doses): p < .01 vs DM, respectively). Wang et al. reported similar results in terms of 5-HT, NE and DA concentrations in the hypothalamus and hippocampus of mouse [18]. In addition, Flu and extracts administration were able to enhance the concentration of DA in brain significantly (Figure 3(B), Flu: p < .01, AE (2.50 g/kg): p < .01, WE (2.00 and 0.20 g/kg): p < .01, AE (0.25 and 0.05 g/kg): p < .05, WE (0.04 g/kg): p < .05 vs DM, respectively). On the contrary, the NE concentrations of CUMS mice were not enhanced significantly after samples administration (Figure 3(C)).