From the Guidelines
Dopamine release is triggered by psychostimulants, such as methylphenidate and dextroamphetamine, which indirectly cause the release of dopamine and norepinephrine from presynaptic terminals. When considering the triggers of dopamine release, it is essential to prioritize the most recent and highest quality evidence. However, based on the available study from 1, it appears that psychostimulants play a significant role in dopamine release. Some key points to consider include:
- Psychostimulants, including methylphenidate and dextroamphetamine, stimulate adrenergic receptors directly as agonists and indirectly cause the release of dopamine and norepinephrine from presynaptic terminals 1
- These medications are scheduled as controlled drugs due to their rapid onset of action, immediate behavioral effects, and tendency to develop tolerance with continued use, leading to increased risk for abuse and dependence in vulnerable individuals 1
- While the study focuses on the use of psychostimulants for cancer-related fatigue, the mechanism of action provides insight into the triggers of dopamine release
- It is crucial to note that other factors, such as pleasurable experiences, certain foods, physical activity, and some medications, may also trigger dopamine release, but the available evidence does not provide a comprehensive overview of these triggers
- In real-life clinical practice, it is essential to consider the potential risks and benefits of psychostimulants and other dopamine-releasing agents, prioritizing the patient's morbidity, mortality, and quality of life.
From the FDA Drug Label
Prior to discontinuation of ropinirole, patients should be informed about potential withdrawal symptoms, and monitored during and after discontinuation. In case of severe withdrawal symptoms, a trial re-administration of a dopamine agonist at the lowest effective dose may be considered. Augmentation is a phenomenon in which dopaminergic medication causes a worsening of symptom severity above and beyond the level at the time the medication was started
The FDA drug label does not answer the question.
From the Research
Dopamine Release Triggers
- Exercise: Voluntary exercise has been shown to boost striatal dopamine release, with evidence suggesting a necessary and sufficient role for brain-derived neurotrophic factor (BDNF) in this process 2. Aerobic exercise has also been found to increase caudate dopamine release and ventral striatal activation in individuals with Parkinson's disease 3.
- Music: Listening to music can trigger dopamine release, with studies demonstrating that dopamine modulates the reward experiences elicited by music 4. The anticipation and experience of peak emotion to music have been found to be associated with anatomically distinct dopamine release in the striatum 5.
- Dopamine Precursors: The administration of dopamine precursors, such as levodopa, has been shown to increase dopamine release and enhance the hedonic experience of music 4.
- Anticipation of Rewards: The anticipation of abstract rewards, such as music, can result in dopamine release in an anatomical pathway distinct from that associated with the peak pleasure itself 5.
Neurotransmitter Interactions
- BDNF: Brain-derived neurotrophic factor has been found to play a crucial role in exercise-enhanced striatal dopamine release, with evidence suggesting that BDNF is necessary and sufficient for this process 2.
- Dopamine-Semiquinones: Pramipexole, a non-ergot dopamine agonist, has been found to scavenge dopamine-semiquinones generated in a dose-dependent manner, which may contribute to its neuroprotective effects against abnormal dopamine metabolism 6.