Pharmacological insights into impulsive‐compulsive spectrum disorders associated with dopaminergic therapy

Impulsive‐compulsive spectrum disorders are associated with dopamine agonist therapy in some patients. These untoward outcomes occur with direct‐acting, full and partial agonists at D2 dopamine family receptors. The disorders typically emerge during chronic treatment, and exhibit common features tha...

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Bibliographic Details
Published in:The European journal of neuroscience 2019-08, Vol.50 (3), p.2492-2502
Main Authors: Napier, T. Celeste, Persons, Amanda L.
Format: Article
Language:English
Subjects:
Agonists
aripiprazole
D2 receptor
D3 receptor
Dopamine
Dopamine D2 receptors
Dopamine receptors
Impulsivity
Nervous system
Neurosciences
Plasticity
pramipexole
Receptor mechanisms
ropinirole
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Summary:Impulsive‐compulsive spectrum disorders are associated with dopamine agonist therapy in some patients. These untoward outcomes occur with direct‐acting, full and partial agonists at D2 dopamine family receptors. The disorders typically emerge during chronic treatment, and exhibit common features that are independent of the neurological or psychiatric pathology for which the initial therapy was indicated. It is well‐documented that the brain is ‘plastic’, changing in response to alterations to internal factors (e.g., disease processes), as well as external factors (e.g., therapies). The complexities of these clinical scenarios have eluded a clear depiction of the neurobiology for impulsive‐compulsive spectrum disorders and engendered considerable debate regarding the mechanistic underpinnings of the disorders. In this opinion, we use pharmacological concepts related to homeostatic compensation subsequent to chronic receptor activation to provide a unifying construct. This construct helps explain the occurrence of impulsive‐compulsive spectrum disorders across disease states, and during therapy with full and partial agonists. Impulsive‐compulsive spectrum disorders are associated with chronic therapy using full agonists to D2/D3 dopamine receptors (D2R/D3R). Emerging clinical reports describe similar disorders with partial agonist therapy used to dial back overactive dopamine transmission. This review describes pharmacological mechanisms to explain how partial agonism with e.g., aripiprazole can also exaggerate dopamine D2R/D3R transmission when administered to those with a history of antipsychotic therapy.
ISSN:0953-816X
1460-9568
DOI:10.1111/ejn.14177