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Degenerative Diseases of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
James A. Mastrianni, Elizabeth A. Harris
Dyskinesias are abnormal involuntary movements occurring as a complication of dopaminergic therapy. The cause is unclear, but may be related to: Upregulation of dopamine receptors.Postsynaptic changes associated with both PD and exposure to levodopa.Influences of glutamatergic projections and other transmitter systems including serotonergic, alpha-2 adrenergic, histaminergic, and cannabinoid pathways.
Biological Basis of Behavior
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
The various actions of dopamine are mediated by specific receptors. There are five subtypes of dopamine receptors, D1, D2, D3, D4, and D5, which are members of the large G-protein coupled receptor superfamily. The dopamine receptor subtypes are divided into two major subclasses: the D1-like group, which include types 1 and 5; and the D2-like group, which includes dopamine receptor types 2, 3, and 4. Whereas the D2 receptor subtype seems to be the major site of action for traditional antipsychotic agents, the D1 and D4 subtypes are implicated in the action of the newer, atypical antipsychotics like clozapine.
Basic psychopharmacology
Published in Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson, Pocket Prescriber Psychiatry, 2019
Jonathan P Rogers, Cheryl CY Leung, Timothy RJ Nicholson
The five dopamine receptors (D1, D2, D3, D4 and D5) are categorised as the D1 type (D1 and D5) and the D2 type (D2, D3 and D4).
Antiglycoxidative properties of amantadine – a systematic review and comprehensive in vitro study
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
Miłosz Nesterowicz, Małgorzata Żendzian-Piotrowska, Jerzy Robert Ładny, Anna Zalewska, Mateusz Maciejczyk
Amantadine (C10H17N; 1-adamantanamine; Figure 1) is a synthetic tricyclic amine, a derivative of adamantane15. It is an antidyskinetic drug used in Parkinson’s disease and Parkinsonian syndromes, as well as in the prevention/treatment of influenza A16. Although the mechanism of the drug’s action is not precisely known, amantadine increases the extracellular concentration of dopamine by enhancing its release in the striatum and blocking its reuptake by presynaptic neurons17. Dopamine regulates motor activity and cognitive function like memory and learning18. Loss of dopaminergic cells is the essence of the Parkinson’s disease19. Pharmacotherapy of Parkinson’s disease requires the use of levodopa, which is a precursor of dopamine, as well as dopamine receptor agonists (e.g. ropinirole and pramipexole)20.
Treatment of tardive dyskinesia: a review and update for dermatologists managing delusions of parasitosis
Published in Journal of Dermatological Treatment, 2022
Christian Cheng, Nicholas Brownstone, John Koo
There have been several proposed etiologies regarding the pathogenesis of TD. The most accepted explanation involves the concept of ‘dopamine receptor hypersensitivity state’ (2) (Figure 1, from the reference Citrome 2018). Antipsychotic medications decrease delusions and hallucinations by blocking dopamine receptors and thereby decreasing dopamine-mediated neurotransmission in the brain. Excessive dopamine-mediated neurotransmission appears to cause psychosis, which is manifested by delusions and hallucinations. However, after a prolonged blockage of dopamine receptors by antipsychotic agents, some patients develop hypersensitivity by increasing the number and/or the sensitivity of dopamine receptors in the postsynaptic neuron. This acquired hypersensitivity to dopamine, especially in the motor cortex such as the striatum, is hypothesized as to why TD causes involuntary movements. In addition, there are several other less well substantiated proposed pathogenic pathways of TD including the possibility of oxidative damage to the nerves and the direct neurotoxic effect of antipsychotic agents (3,4).
Innovative screening models for the discovery of new schizophrenia drug therapies: an integrated approach
Published in Expert Opinion on Drug Discovery, 2021
Marinos G. Sotiropoulos, Eleni Poulogiannopoulou, Foteini Delis, Christina Dalla, Katerina Antoniou, Nikolaos Kokras
Unfortunately, fewer integrated schizophrenia models can reliably reproduce negative or cognitive schizophrenia symptoms [2,10]. The continued use of dopaminergic animal models will only result in a self-fulfilling prophecy, as new, better drugs that act on different systems, would be doomed to never being discovered [49]. In fact, despite the variation to some degree of current antipsychotic drugs regarding their receptor targeting, they all share a common mechanism of blocking dopamine receptors [20]. In this context, all current drugs for schizophrenia target ‘psychosis’, i.e. the positive symptoms of the syndrome. In other words, research so far is producing ‘antipsychotic’ but not ‘anti-schizophrenia’ drugs. This has been the case for the past 70 years, mostly due to the practical feasibility of developing and testing such treatments in animals and in human clinical trials.