Dopamine
Original Editor - Lucinda hampton
Top Contributors - Farah Elzanaty, Lucinda hampton, Vidya Acharya, Alexandra Stead, Nikhil Benhur Abburi and Tolulope Adeniji
Introduction

Dopamine is a neurotransmitter that shapes movement, motivation, learning and reward processing, making it directly relevant to physiotherapy practice across neurological and musculoskeletal health settings.[1][2] It is synthesised by a small population of neurons in the midbrain, yet it exerts widespread influence over motor initiation, motor learning and a person's engagement with rehabilitation.[1][3]
This page explains the sites of dopamine synthesis, the consequences of its imbalance and how this knowledge informs clinical reasoning, exercise prescription and the use of feedback and reward during rehabilitation.
Dopamine Origin and Pathways

Dopamine is produced mainly by two midbrain nuclei: the substantia nigra pars compacta and the ventral tegmental area.[1] Neurons from the substantia nigra form the nigrostriatal pathway, which projects to the basal ganglia and supports the initiation, planning and coordination of voluntary movement.[1][3] Neurons from the ventral tegmental area form the mesolimbic and mesocortical pathways, which are activated by anticipated or received rewards and underpin motivation, reinforcement learning and goal-directed behaviour.[1][4]
Although dopaminergic neurons make up a very small proportion of total brain cells, their projections influence circuits throughout the cortex, limbic system and brainstem, which is why dopamine dysfunction can produce such wide-ranging motor and non-motor effects.[1]
Dopamine and Motor Control
Dopamine acts directly on the circuits that plan and execute movement, and so it has particular significance for physiotherapists working with people who have movement disorders.
- Dopamine is essential for motor control. Within the basal ganglia, dopamine modulates the balance between cognitive and habitual movement pathways, allowing learned movements to become efficient and automatic over time.[3][5] [6]
- Reduced striatal dopamine disrupts this balance, contributing to bradykinesia, rigidity and impaired automatic movement seen in Parkinson's disease.[3] [6]
- Dopamine also has a demonstrated role in motor skill acquisition, animal studies show that dopaminergic signalling supports the consolidation of newly learned motor skills, which is one of the core aims of physiotherapy rehabilitation.[7][8]
Dopamine Deficiency
The most clinically significant condition of dopamine deficiency for physiotherapists is Parkinson's disease, in which progressive loss of dopaminergic neurons in the substantia nigra produces the cardinal motor features of bradykinesia, rigidity and resting tremor.[3] [6] Low dopamine availability is also associated with reduced motivation and low mood, which can affect a person's engagement with exercise and rehabilitation programmes.[4]
Dopamine Excess
Physiotherapists working with people on dopaminergic medication should also be aware of the risk of dopamine excess.
Dopamine agonists used to manage Parkinson's disease, are associated with impulse control disorders such as pathological gambling , compulsive shopping, binge eating and hypersexuality.[9] [10] This occurs because these medications stimulate the mesolimbic reward circuits alongside nigrostriatal pathway responsible for motor control.[11]
Physiotherapists are not responsible for diagnosing these conditions, but awareness of the association allows the wider multidisciplinary team to be alerted to behavioural changes, supporting timely medical review.
Dopamine Medication

Two distinct pharmacological uses of dopamine are relevant to clinical practice, and it is important to not conflate them.
Critical Care Use
Intravenous dopamine is used as a vasopressor to manage hypotension, bradycardia and cardiac arrest, working peripherally through dopaminergic and adrenergic receptor effects rather than by acting on the central nervous system, since dopamine itself does not readily cross the blood-brain barrier.[12]
Contemporary critical care evidence favours noradrenaline over dopamine as the first-line vasopressor in most adult shock states, as dopamine has been associated with a higher rate of arrhythmia and, in some analyses, increased mortality in cardiogenic shock; dopamine is still used selectively, including in some neonatal and bradycardia-related contexts.[13]
Levodopa Therapy
Levodopa a dopamine precursor, is used for central nervous system conditions such as Parkinson's disease, because unlike dopamine itself, it readily crosses the blood-brain barrier and is converted to dopamine within the brain.[14]
Levodopa and dopamine agonists remain the mainstay of motor symptom management in Parkinson's disease, but their benefit and side effects fluctuate across the medication cycle, reinforcing the importance of coordinating rehabilitation timing.[4][6][15]
Feedback and Rehabilitation Practice

Research shows how physical activity, dopamine pathways and targeted rewards interact to shape rehabilitation and mental health.
A systematic review of the bidirectional relationship between physical activity and dopamine across adulthood concluded that exercise increases dopaminergic activity, although the reverse relationship (dopamine's effect on physical activity levels) remains less consistent across studies.[16]
Earlier Positron emission tomography research produced mixed results, where one study found no significant change in striatal dopamine release after a single 30 minute bout of treadmill running in healthy adults[17], while more recent imaging work in people with Parkinson's disease has found that habitual, vigorous exercise is associated with greater striatal dopamine release than the same activity performed by sedentary individuals.[18]
A 2024 systematic review and network meta-analysis, found that structured exercise produced clinically meaningful reductions in depressive symptoms, with effects comparable to psychotherapy and antidepressant medication.[19]
A multicentre randomised controlled trial of arm-reaching training after stroke found that adding contingent monetary reward to standard feedback produced greater gains in the Fugl-Meyer Upper Extremity score and the Box and Block Test compared with unrewarded training, although the primary training outcome did not differ significantly between groups.[20]
Relevance for Physiotherapy
Dopamine provides a neurobiological rationale for utilising aerobic exercise and positive reward-based feedback in clinical settings.
- Reward-based feedback appears to enhance both acquisition and retention of motor skills.[21] [20] The same brain circuits that handle rewards also shape how feedback works during rehabilitation.[21] [22] Findings support the deliberate use of positive, performance-contingent feedback during task-specific practice, rather than punishment-based correction, particularly in the early stages of rehabilitation.[21] [20] The reward-based motor learning is therefore increasingly used in rehabilitation, alongside therapist-delivered feedback.
- Reviews of exercise-induced neuroplasticity in Parkinson's disease describe how aerobic and goal-directed exercise can support dopaminergic neurotransmission in the nigrostriatal pathway while limiting the excessive corticostriatal glutamatergic activity that follows dopamine loss, helping to restore a healthier excitation-inhibition balance within basal ganglia circuits.[3] [23] This provides neurobiological rationale for exercise as a complementary intervention alongside pharmacological treatment.[24]
- For physiotherapists, incorporating aerobic exercise into the management of patients with reduced motivation,is an evidence-based rationale, that provides additional musculoskeletal and cardiovascular benefits.[19]
Conclusion
Dopamine links movement, motivation and reward through midbrain circuits that are directly relevant to physiotherapy practice, from exercise-induced neuroplasticity that underlies Parkinson's disease rehabilitation to the reward-based feedback mechanisms that support motor relearning after stroke.[3][21][20] Recognising the signs of dopamine deficiency and excess, understanding how dopaminergic medication timing affects motor performance and using structured aerobic exercise and positive feedback as clinical tools, allows physiotherapists to design rehabilitation that works with the dopaminergic system rather than against it.[4][19]
As research into exercise-induced neuroplasticity and reward-based motor learning continues to develop, physiotherapists should stay alert to emerging evidence that may further refine how dopaminergic mechanisms are used in clinical practice.
References
- ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Speranza L, Miniaci MC, Volpicelli F. The Role of Dopamine in Neurological, Psychiatric, and Metabolic Disorders and Cancer: A Complex Web of Interactions. Biomedicines. 2025 Feb 17;13(2):492.
- ↑ Basso V, Döbrössy MD, Thompson LH, Kirik D, Fuller HR, Gates MA. State of the Art in Sub-Phenotyping Midbrain Dopamine Neurons. Biology (Basel). 2024 Sep 3;13(9):690. doi: 10.3390/biology13090690.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Zikereya T, Shi K, Chen W. Goal-directed and habitual control: from circuits and functions to exercise-induced neuroplasticity targets for the treatment of Parkinson's disease. Front Neurol. 2023 Oct 10;14:1254447.
- ↑ 4.0 4.1 4.2 4.3 Ferrazzoli D, Carter A, Ustun FS, Palamara G, Ortelli P, Maestri R, Yücel M, Frazzitta G. Dopamine Replacement Therapy, Learning and Reward Prediction in Parkinson's Disease: Implications for Rehabilitation. Front Behav Neurosci. 2016 Jun 14;10:121.
- ↑ Turner RS, Desmurget M. Basal ganglia contributions to motor control: a vigorous tutor. Curr Opin Neurobiol. 2010 Dec;20(6):704-16. Epub 2010 Sep 17.
- ↑ 6.0 6.1 6.2 6.3 Höllerhage M, Becktepe J, Classen J, Deuschl G, Ebersbach G, Hopfner F, Lingor P, Löhle M, Maaß S, Pötter-Nerger M, Odin P, Woitalla D; German Parkinson’s Guidelines Group; Trenkwalder C, Höglinger GU. Pharmacotherapy of motor symptoms in early and mid-stage Parkinson's disease: guideline "Parkinson's disease" of the German Society of Neurology. J Neurol. 2024 Nov;271(11):7071-7101. doi: 10.1007/s00415-024-12632-6. Epub 2024 Aug 29.
- ↑ Wood AN. New roles for dopamine in motor skill acquisition: lessons from primates, rodents, and songbirds. J Neurophysiol. 2021 Jun 1;125(6):2361-2374. doi: 10.1152/jn.00648.2020. Epub 2021 May 12.
- ↑ Bastioli G, Arnold JC, Mancini M, Mar AC, Gamallo-Lana B, Saadipour K, Chao MV, Rice ME. Voluntary Exercise Boosts Striatal Dopamine Release: Evidence for the Necessary and Sufficient Role of BDNF. J Neurosci. 2022 Jun 8;42(23):4725-4736. doi: 10.1523/JNEUROSCI.2273-21.2022. Epub 2022 May 16. PMID: 35577554; PMCID: PMC9186798.
- ↑ Zhang JF, Wang XX, Feng Y, Fekete R, Jankovic J, Wu YC. Impulse Control Disorders in Parkinson's Disease: Epidemiology, Pathogenesis and Therapeutic Strategies. Front Psychiatry. 2021 Feb 9;12:635494.
- ↑ Grall-Bronnec M, Victorri-Vigneau C, Donnio Y, Leboucher J, Rousselet M, Thiabaud E, Zreika N, Derkinderen P, Challet-Bouju G. Dopamine Agonists and Impulse Control Disorders: A Complex Association. Drug Saf. 2018 Jan;41(1):19-75.
- ↑ Nils M. Tangedal, Ole-Bjørn Tysnes,Impulse control disorders and dopamine receptor agonism in Parkinson's disease patients: Clinical implications,Parkinsonism & Related Disorders,Volume 143,2026,108147,ISSN 1353-8020, https://doi.org/10.1016/j.parkreldis.2025.108147.
- ↑ Budde H, Dolz N, Mueller-Alcazar A, Schacht F, Velasques B, Ribeiro P, Machado S, Wegner M. A 10 years update of effects of exercise on depression disorders-in otherwise healthy adults: A systematic review of meta-analyses and neurobiological mechanisms. PLoS One. 2025 May 5;20(5):e0317610.
- ↑ Niemelä VH, Jousi M, Petersen JJ, Sillassen C, Faltermeier P, Juul S, Kamp CB, Siddiqui F, Bjerg JL, Couper K, Chia YW, O'Neil BJ, Drennan IR, Berg K, Jakobsen JC, Skrifvars MB; ALS Task Force of ILCOR. The impact of vasopressor choice in patients with hypotension after cardiac arrest: a systematic review. Resuscitation. 2025 Dec;217:110892. doi: 10.1016/j.resuscitation.2025.110892. Epub 2025 Nov 17. PMID: 41237843.
- ↑ Hornykiewicz O. A brief history of levodopa. J Neurol. 2010 Nov;257(Suppl 2):S249-52. doi: 10.1007/s00415-010-5741-y. PMID: 21080185.
- ↑ Pringsheim T, Day GS, Smith DB, Rae-Grant A, Licking N, Armstrong MJ, de Bie RMA, Roze E, Miyasaki JM, Hauser RA, Espay AJ, Martello JP, Gurwell JA, Billinghurst L, Sullivan K, Fitts MS, Cothros N, Hall DA, Rafferty M, Hagerbrant L, Hastings T, O'Brien MD, Silsbee H, Gronseth G, Lang AE; Guideline Subcommittee of the AAN. Dopaminergic Therapy for Motor Symptoms in Early Parkinson Disease Practice Guideline Summary: A Report of the AAN Guideline Subcommittee. Neurology. 2021 Nov 16;97(20):942-957. doi: 10.1212/WNL.0000000000012868. PMID: 34782410; PMCID: PMC8672433.
- ↑ Marques A, Marconcin P, Werneck AO, Ferrari G, Gouveia ÉR, Kliegel M, Peralta M, Ihle A. Bidirectional Association between Physical Activity and Dopamine Across Adulthood-A Systematic Review. Brain Sci. 2021 Jun 23;11(7):829.
- ↑ Wang GJ, Volkow ND, Fowler JS, Franceschi D, Logan J, Pappas NR, Wong CT, Netusil N. PET studies of the effects of aerobic exercise on human striatal dopamine release. J Nucl Med. 2000 Aug;41(8):1352-6.
- ↑ de Laat B, Hoye J, Stanley G, Hespeler M, Ligi J, Mohan V, Wooten DW, Zhang X, Nguyen TD, Key J, Colonna G, Huang Y, Nabulsi N, Patel A, Matuskey D, Morris ED, Tinaz S. Intense exercise increases dopamine transporter and neuromelanin concentrations in the substantia nigra in Parkinson's disease. NPJ Parkinsons Dis. 2024 Feb 9;10(1):34. doi: 10.1038/s41531-024-00641-1. PMID: 38336768; PMCID: PMC10858031.
- ↑ 19.0 19.1 19.2 Noetel M, Sanders T, Gallardo-Gómez D, Taylor P, Del Pozo Cruz B, van den Hoek D, Smith JJ, Mahoney J, Spathis J, Moresi M, Pagano R, Pagano L, Vasconcellos R, Arnott H, Varley B, Parker P, Biddle S, Lonsdale C. Effect of exercise for depression: systematic review and network meta-analysis of randomised controlled trials. BMJ. 2024 Feb 14;384:e075847. doi: 10.1136/bmj-2023-075847. Erratum in: BMJ. 2024 May 28;385:q1024.
- ↑ 20.0 20.1 20.2 20.3 Widmer M, Held JPO, Wittmann F, Valladares B, Lambercy O, Sturzenegger C, Palla A, Lutz K, Luft AR. Reward During Arm Training Improves Impairment and Activity After Stroke: A Randomized Controlled Trial. Neurorehabil Neural Repair. 2022 Feb;36(2):140-150. Epub 2021 Dec 22.
- ↑ 21.0 21.1 21.2 21.3 Palidis DJ, Gardiner Z, Stephenson A, Zhang K, Boruff J, Fellows LK. The Use of Extrinsic Performance Feedback and Reward to Enhance Upper Limb Motor Behavior and Recovery Post-Stroke: A Scoping Review. Neurorehabil Neural Repair. 2025 Feb;39(2):157-173.
- ↑ Weinstein AM. Reward, motivation and brain imaging in human healthy participants - A narrative review. Front Behav Neurosci. 2023 Mar 24;17:1123733.
- ↑ Ishaq S, Shah IA, Lee SD, Wu BT. Effects of exercise training on the nigrostriatal glutamatergic pathway and receptor interactions in Parkinson's disease: a systematic review. Front Aging Neurosci. 2025 Feb 11;17:1512278. doi: 10.3389/fnagi.2025.1512278.
- ↑ Alberts JL, Rosenfeldt AB. The Universal Prescription for Parkinson's Disease: Exercise. J Parkinsons Dis. 2020;10(s1):S21-S27. doi: 10.3233/JPD-202100. PMID: 32925109; PMCID: PMC7592674.