Dear readers of, please forgive the disruption. needs about $53200 in 2024. In 2023 we received donations from third parties of about $ 32200. Unfortunately, 99.8% of our readers do not donate. If everyone who reads this request makes a small contribution, our fundraising campaign for 2024 would be over after a few days. This donation request is displayed 19,000 times a week, but only 40 people donate. If you find useful, please take a minute and support with your donation. Thank you!

Since 01.06.2021 is supported by the non-profit ADxS e.V..

$3391 of $53200 - as of 2024-02-01
Header Image
Motivation in ADHD - Neurophysiological correlates


Motivation in ADHD - Neurophysiological correlates

ADHD shows an aberrant response to expected reward as well as to received reward.

1. Neurophysiological correlates of reward expectancy

Dopaminergic projections from the VTA to the ventral striatum (the nucleus accumbens) influence reward and motivation, while dopaminergic projections from the substantia nigra to the dorsal striatum influence voluntary movements and habit learning .1

1.1. Striatum and reward expectancy: underactivated in ADHD and stress

1.1.1. Striatum in reward expectancy: underactivated in ADHD

In rats that performed actions required to obtain a reward, dopamine levels continued to rise as the reward approached and peaked with the receipt of the reward. Afterwards, when they consumed the reward, it quickly dropped again.2

ADHD correlates with reduced activity on expected rewards in brain regions of the reward center (including nucleus accumbens). Motivation triggered by (appropriately high) personally interesting rewards reduces ADHD symptoms.

Adult males with ADHD-HI were found to have decreased activation of the ventral striatum during gain anticipation and increased activation of the orbitofrontal cortex in response to gain. The lower activation of the ventral striatum during gain anticipation, the higher hyperactivity and impulsivity were.34 Children with ADHD-HI showed significantly decreased ventral striatum volume bilaterally and a correlation of right ventral striatum reduction with hyperactivity/impulsivity.5

Brain activity on reward expectancy and reward maintenance appears to be subtype specific. ADHD-I showed bilateral underactivation of the ventral striatum during reward expectancy compared to ADHD-C and healthy controls. In contrast, ADHD-C showed underactivation of the OFC in response to reward compared with ADHD-I and controls.6

One study found underactivation of the striatum during reward anticipation in ADHD-C only in adults but not in children.7

Another study found in ADHD-HI that hyperactivity/impulsivity correlated with (relatively) decreased ventral striatum activity during reward expectancy and increased ventral striatum activity as a reward response. In contrast, unaffected subjects showed increased activity of the ventral striatum during reward expectancy.8

ADHD symptoms correlated with decreased striatum activation in reward expectancy in children, independent of ADHD symptom severity.9

Dihydro-β-erythroidine (DHβE) is a herbal competetive antagonist of nicotinic receptors. It is an inhibitor of nicotinic acetylcholine receptors containing β2-units (β2* NAChRs; β2-nicotinic receptors). DHβE decreases phasic dopamine release in the dorsolateral striatum10
It follows that reward anticipation, which is controlled by phasic dopamine in the striatum and even more so in the nucleus accumbens, is also increased by β2-nicotinic receptor agonists-such as nicotine .

1.1.2. Striatum in reward expectation and stress Striatum during reward anticipation: increased activation during acute stress

Acute stress also increases dopamine, including in the nucleus accumbens, which triggers motivational expectancy. Mediation of the increased motivational expectancy appears to occur through CRH release in the nucleus accumbens.11 A CRH1 antagonist blocks this reinforcing effect of acute stress on reward motivation.12 High chronic stress abolishes - after up to 90 days after cessation of the stressor - the ability of CRH to increase dopamine in the nucleus accumbens and at the same time caused a switch from appetitive to aversive motivation,13 as is also observed in major depression MDD.14 Striatum in reward expectation: underactivated in chronic stress

Chronic stress reduces striatal dopaminergic activity over the long term. Institutional neglect, early childhood stress, or maltreatment inhibit striatal reward function, which is dopaminergically mediated.15161718

See more at Alteration of the dopaminergic system by chronic stress Striatum in reward expectation: underactivated after early childhood stress

Early childhood stress (e.g., postnatal deprivation, maternal separation) resulted in decreased mesolimbic dopamine levels in the striatum and decreased motivation to pursue rewards in adult rats and monkeys.19 Monkeys with early childhood stress experience showed decreased interest in rewards. However, reward consumption remained unchanged. Increased urinary norepinephrine depletion was found.20

In humans, early childhood stress is also associated with decreased activity in relation to reward in the ventral striatum21, which is associated with increased symptoms of anhedonia22, although the data did not differentiate between reward expectation and reward receipt. It would be conceivable that reduced reactivity to received rewards in particular correlates with anhedonia or depression.

Adolescents who were maltreated as children showed reduced dopaminergic activation of the pallidum (part of the striatum) in reward expectancy concomitant with more severe depression symptoms.23

Further studies confirm that early childhood stress (with no direct link to depression) correlates with decreased activation of the striatum during reward expectancy but not during reward maintenance.2417 This is consistent with changes in ADHD in both reward expectancy and reward maintenance.

See more at Early childhood stress permanently alters the dopaminergic system

1.2. ACC, PFC, cerebellum in reward expectancy: overactivated in ADHD

A larger study found increased responses in adolescents and young adults with ADHD during reward expectancy in the25

  • Anterior cingulate cortex (ACC)
  • PFC
  • Cerebellum

In the unaffected siblings, the results were identical, except for the cerebellum.

1.3. Ventral anterior thalamus in reward expectancy: underactivated in ADHD

Cues that predicted reward caused greater activation in the ventral anterior thalamus in the control group than cues that did not predict reward, whereas in ADHD, just the opposite, cues that predicted reward caused less activation than cues that did not predict reward.26

1.4. OFC activity in reward expectancy: increased in ADHD

An fMRI study found a significant signal increase in OFC to large versus small expected rewards in all subjects. Responses were significantly stronger in ADHD and also correlated with hyperactivity/impulsivity. High cognitive ability normalized OFC responses.27

1.5. Further changes during reward and loss expectancy in early childhood stress

A study that reexamined children with high and low early childhood stress after 10 years found:28

Early childhood stress correlated with

  • With expectation of loss
    • Reduced activation of the putamen
    • Reduced activation of the insula
  • When suffering losses
    • Increased activation of the left inferior frontal gyrus
  • With reward expectation
    • Reduced activation of the posterior cingulate cortex
    • Reduced activation of the precuneus
    • Reduced activation of the middle temporal gyrus
    • Reduced activation of the superior occipital cortex

1.6. Stress, anhedonia and the VTA-BLA-NAc pathway

A signaling pathway between ventral tegmentum, basolateral amygdala, and nucleus accumbens seems to be activated by (sexual) reward. Blockade of this signaling pathway caused anhedonic behavior. Chronic stress (from exercise restriction in rats) inhibited the responsiveness of VTA dopaminergic neurons to sexual reward. Reactivation of ventral tegmentum cells associated with sexual reward experience acutely counteracted stress-induced impairment of reward-seeking behavior (anhedonia).29

(Severe) one-time stress can cause long-lasting neuroadaptive changes in VTA dopamine neurons. Thus, even one-time acute stress can alter the responsiveness of VTA dopamine neurons to future stressors or rewards.30

2. Neurophysiological correlates of reward reception

2.1. OFC in reward maintenance: overactivation in ADHD

A larger study found increased responses in adolescents and young adults with ADHD during receipt of reward in the25

  • OFC
  • Occipital lobe
  • Ventral striatum

In the unaffected siblings, the results were identical except for the ventral striatum.

ADHD-HI symptom severity predicted higher orbitofrontal activity in response to immediate reward.31

2.2. Caudate nucleus and frontal eye field in reward maintenance in ADHD

Feedback that no reward was received caused stronger activation in the left caudate nucleus and frontal eye field than feedback about rewards received in the control group, whereas in the ADHD-HI group, exactly the opposite, feedback that no reward was received caused weaker activation in the left caudate nucleus and frontal eye field than feedback about rewards received.26

2.3. Nucleus accumbens and reward response

Mice in which dopamine was chemically reduced in the nucleus accumbens showed a reduced response to offered rewards. The nucleus accumbens appears to dopaminergically moderate the response to rewards and aversive stimuli.32 In this context, motivational control by the nucleus accumbens appears to be stimulated by the mPFC via norepinephrine. Norepinephrine deficiency in the mPFC leads to dopamine deficiency in the nucleus accumbens with resultant changes in motivational control.33

2.4. Connectivity of the ventral striatum during reward reception: increased in ADHD

ADHD sufferers show increased activity in the ventral striatum and superior frontal gyrus when receiving rewards, as well as increased connectivity between the ventral striatum and regions of motor control.34

3. Control of motivation by dopamine

Motivation is controlled by increased dopamine in the ventral striatum (nucleus accumbens).
The increase in dopamine levels can be triggered by various mechanisms.

3.1. Phasic pulses from dopaminergic cells of the VTA

Mesolimbic dopamine projection from the VTA to the nucleus accumbens is central to reward-driven learning and to motivation to be active for more reward.

The dorsolateral striatum, nucleus accumbens nucleus, and nucleus accumbens shell responded in vitro with different dopamine releases to electrical stimulation of different numbers (single pulse (tonic), 5 pulses, 20 pulses (phasic) at 20 Hz each and 0.5 to 1 ms in length):35

  • Single pulse (tonic signal)
    • Dorsolateral striatum: high dopaminergic response
    • Nucleus accumbens nucleus: medium dopaminergic response
    • Nucleus accumbens shell: low dopaminergic response
  • 5 Impulses
    • Dorsolateral striatum: high dopaminergic response
    • Nucleus accumbens nucleus: medium dopaminergic response
    • Nucleus accumbens shell: medium dopaminergic response
  • 20 pulses (phasic signal)
    • Dorsolateral striatum: smallest increase of the dopaminergic response
    • Nucleus accumbens nucleus: mean increase in dopaminergic response
    • Nucleus accumbens shell: greatest increase in dopaminergic response

The dorsolateral striatum responded to tonic stimuli with an enhancement of the dopaminergic signal and to phasic stimuli with an attenuation, whereas the nucleus accumbens shell aut responded to tonic stimulation with a weak dopamine signal and to phasic stimulation with a strong dopamine signal.

During very slow tonic stimulation at 0.2 Hz followed by a 5-pulse burst at 20 Hz, dopamine amplitude is higher in the dorsolateral striatum than in the nucleus accumbens shell, and dopamine release to the phasic stimulus is higher in both regions than to the preceding tonic stimulation. In the nucleus accumbens shell, the increase in dopamine release from the tonic to the phasic stimulus is higher than in the dl striatum.

The usual tonic firing frequency of dopaminergic neurons is about 4 Hz10 36

  • Running single pulses of 3.3 Hz (tonic signal)
    • Dopamine response began to blur
    • Static dopaminergic background level
  • 5 pulses at 20 Hz
    • Dorsolateral striatum: only slightly increased dopaminergic response
    • Nucleus accumbens nucleus: markedly increased dopaminergic response
    • Nucleus accumbens shell: very marked increased dopaminergic response

A strong phasic dopamine response is a respresentative of an unexpected positive perception that turns out better than expected, e.g., for a surprising reward. Expected rewards do not correlate with phasic dopamine bursts in the striatum.37

3.2. Increase tonic extracellular dopamine by varicosities?

There is evidence that motivation-related dopamine dynamics do not result from firing of VTA dopamine cells but may reflect local influences on forebrain dopamine varicosities:38

The mesolimbic dopamine projection sent from the VTA to the nucleus accumbens encodes reward prediction errors. These are important as learning signals for behavioral adaptation.
However, the actual release of dopamine in the nucleus accumbens is more consistent with the value of reward expectancy, a motivational signal that promotes approach behavior.
This discrepancy could be due to changes in tonic firing of dopamine neurons, or a fundamental disconnect between firing and release.

Dopamine release in the nucleus accumbens nucleus and ventral prelimbic cortex correlates with reward expectancy.
In contrast, the firing rate of dopamine neurons in the VTA does not correlate with reward expectancy but with transient, error-like responses to unexpected cues, thus encoding reward prediction errors.

  1. Keath, Iacoviello, Barrett, Mansvelder, McGehee (2007): Differential modulation by nicotine of substantia nigra versus ventral tegmental area dopamine neurons. J Neurophysiol. 2007 Dec;98(6):3388-96. doi: 10.1152/jn.00760.2007. PMID: 17942622.

  2. Berke (2018): What does dopamine mean? Nat Neurosci. 2018 Jun;21(6):787-793. doi: 10.1038/s41593-018-0152-y. PMID: 29760524; PMCID: PMC6358212.

  3. Ströhle, Stoy, Wrase, Schwarzer, Schlagenhauf, Huss, Hein, Nedderhut, Neumann, Gregor, Juckel, Knutson, Lehmkuhl, Bauer, Heinz (2008): Reward anticipation and outcomes in adult males with attention-deficit/hyperactivity disorder. Neuroimage. 2008 Feb 1;39(3):966-72. doi: 10.1016/j.neuroimage.2007.09.044. PMID: 17996464. n = 20

  4. Scheres, Milham, Knutson, Castellanos (2007): Ventral striatal hyporesponsiveness during reward anticipation in attention-deficit/hyperactivity disorder. Biol Psychiatry. 2007 Mar 1;61(5):720-4. doi: 10.1016/j.biopsych.2006.04.042. PMID: 16950228. n = 22

  5. Carmona, Proal, Hoekzema, Gispert, Picado, Moreno, Soliva, Bielsa, Rovira, Hilferty, Bulbena, Casas, Tobeña, Vilarroya (2009): Ventro-striatal reductions underpin symptoms of hyperactivity and impulsivity in attention-deficit/hyperactivity disorder. Biol Psychiatry. 2009 Nov 15;66(10):972-7. doi: 10.1016/j.biopsych.2009.05.013. Epub 2009 Jul 3. PMID: 19576573. n = 84

  6. Edel, Enzi, Witthaus, Tegenthoff, Peters, Juckel, Lissek (2013): Differential reward processing in subtypes of adult attention deficit hyperactivity disorder. J Psychiatr Res. 2013 Mar;47(3):350-6. doi: 10.1016/j.jpsychires.2012.09.026. PMID: 23201229. n = 36

  7. Kappel V, Lorenz RC, Streifling M, Renneberg B, Lehmkuhl U, Ströhle A, Salbach-Andrae H, Beck A. Effect of brain structure and function on reward anticipation in children and adults with attention deficit hyperactivity disorder combined subtype. Soc Cogn Affect Neurosci. 2015 Jul;10(7):945-51. doi: 10.1093/scan/nsu135. PMID: 25338631; PMCID: PMC4483558. N = 60

  8. Furukawa, Bado, Tripp, Mattos, Wickens, Bramati, Alsop, Ferreira, Lima, Tovar-Moll, Sergeant, Moll (2014): Abnormal striatal BOLD responses to reward anticipation and reward delivery in ADHD. PLoS One. 2014 Feb 26;9(2):e89129. doi: 10.1371/journal.pone.0089129. PMID: 24586543; PMCID: PMC3935853. n = 29

  9. van Hulst, de Zeeuw, Bos, Rijks, Neggers, Durston (2017): Children with ADHD symptoms show decreased activity in ventral striatum during the anticipation of reward, irrespective of ADHD diagnosis. J Child Psychol Psychiatry. 2017 Feb;58(2):206-214. doi: 10.1111/jcpp.12643. PMID: 27678006. n = 76

  10. Zhang, Zhang, Liang, Siapas, Zhou, Dani (2009): Dopamine signaling differences in the nucleus accumbens and dorsal striatum exploited by nicotine. J Neurosci. 2009 Apr 1;29(13):4035-43. doi: 10.1523/JNEUROSCI.0261-09.2009. PMID: 19339599; PMCID: PMC2743099.

  11. Peciña, Schulkin, Berridge (2006): Nucleus accumbens corticotropin-releasing factor increases cue-triggered motivation for sucrose reward: paradoxical positive incentive effects in stress? BMC Biol. 2006 Apr 13;4:8. doi: 10.1186/1741-7007-4-8. PMID: 16613600; PMCID: PMC1459217.

  12. Liu (2015): Enhanced motivation for food reward induced by stress and attenuation by corticotrophin-releasing factor receptor antagonism in rats: implications for overeating and obesity. Psychopharmacology (Berl). 2015 Jun;232(12):2049-60. doi: 10.1007/s00213-014-3838-1. PMID: 25510859; PMCID: PMC4433618.

  13. Lemos, Wanat, Smith, Reyes, Hollon, Van Bockstaele, Chavkin, Phillips (2012): Severe stress switches CRF action in the nucleus accumbens from appetitive to aversive. Nature. 2012 Oct 18;490(7420):402-6. doi: 10.1038/nature11436. PMID: 22992525; PMCID: PMC3475726.

  14. Ironside, Kumar, Kang, Pizzagalli (2018): Brain mechanisms mediating effects of stress on reward sensitivity. Curr Opin Behav Sci. 2018 Aug;22:106-113. doi: 10.1016/j.cobeha.2018.01.016. PMID: 30349872; PMCID: PMC6195323.

  15. Hanson, Hariri, Williamson (2015): Blunted Ventral Striatum Development in Adolescence Reflects Emotional Neglect and Predicts Depressive Symptoms. Biol Psychiatry. 2015 Nov 1;78(9):598-605. doi: 10.1016/j.biopsych.2015.05.010. PMID: 26092778; PMCID: PMC4593720.

  16. Takiguchi, Fujisawa, Mizushima, Sait, Okamoto, Shimada, Koizumi, Kumazaki, Jung, Kosaka, Hiratani, Ohshima, Teicher, Tomoda (2015): Ventral striatum dysfunction in children and adolescents with reactive attachment disorder: functional MRI study. BJPsych Open. 2015 Oct 14;1(2):121-128. doi: 10.1192/bjpo.bp.115.001586. PMID: 27703736; PMCID: PMC4995568.

  17. Mehta, Gore-Langton, Golembo, Colvert, Williams, Sonuga-Barke (2010): Hyporesponsive reward anticipation in the basal ganglia following severe institutional deprivation early in life. J Cogn Neurosci. 2010 Oct;22(10):2316-25. doi: 10.1162/jocn.2009.21394. PMID: 19929329.

  18. Dillon, Holmes, Birk, Brooks, Lyons-Ruth, Pizzagalli (2009): Childhood adversity is associated with left basal ganglia dysfunction during reward anticipation in adulthood. Biol Psychiatry. 2009 Aug 1;66(3):206-13. doi: 10.1016/j.biopsych.2009.02.019. PMID: 19358974; PMCID: PMC2883459.

  19. Pizzagalli (2014): Depression, stress, and anhedonia: toward a synthesis and integrated model. Annu Rev Clin Psychol. 2014;10:393-423. doi: 10.1146/annurev-clinpsy-050212-185606. PMID: 24471371; PMCID: PMC3972338.

  20. Pryce, Dettling, Spengler, Schnell, Feldon (2004): Deprivation of parenting disrupts development of homeostatic and reward systems in marmoset monkey offspring. Biol Psychiatry. 2004 Jul 15;56(2):72-9. doi: 10.1016/j.biopsych.2004.05.002. PMID: 15231438.

  21. Hanson, Albert, Iselin, Carré, Dodge, Hariri (2016): Cumulative stress in childhood is associated with blunted reward-related brain activity in adulthood. Soc Cogn Affect Neurosci. 2016 Mar;11(3):405-12. doi: 10.1093/scan/nsv124. PMID: 26443679; PMCID: PMC4769626.

  22. Corral-Frías, Nikolova, Michalski, Baranger, Hariri, Bogdan (2015): Stress-related anhedonia is associated with ventral striatum reactivity to reward and transdiagnostic psychiatric symptomatology. Psychol Med. 2015;45(12):2605-17. doi: 10.1017/S0033291715000525. PMID: 25853627; PMCID: PMC4700837.

  23. Dennison, Sheridan, Busso, Jenness, Peverill, Rosen, McLaughlin (2016): Neurobehavioral markers of resilience to depression amongst adolescents exposed to child abuse. J Abnorm Psychol. 2016 Nov;125(8):1201-1212. doi: 10.1037/abn0000215. Erratum in: J Abnorm Psychol. 2017 Jan;126(1):136. PMID: 27819477; PMCID: PMC5119749.

  24. Dillon, Holmes, Birk, Brooks, Lyons-Ruth, Pizzagalli (2009): Childhood adversity is associated with left basal ganglia dysfunction during reward anticipation in adulthood. Biol Psychiatry. 2009 Aug 1;66(3):206-13. doi: 10.1016/j.biopsych.2009.02.019. PMID: 19358974; PMCID: PMC2883459.

  25. von Rhein, Cools, Zwiers, van der Schaaf, Franke, Luman, Oosterlaan, Heslenfeld, Hoekstra, Hartman, Faraone, van Rooij, van Dongen, Lojowska, Mennes, Buitelaar (2015):. Increased neural responses to reward in adolescents and young adults with attention-deficit/hyperactivity disorder and their unaffected siblings. J Am Acad Child Adolesc Psychiatry. 2015 May;54(5):394-402. doi: 10.1016/j.jaac.2015.02.012. PMID: 25901776; PMCID: PMC4417499. n = 350

  26. Metin, Tas, Çebi, Büyükaslan, Soysal, Hatıloglu, Tarhan (2018): Reward Processing Deficits During a Spatial Attention Task in Patients With ADHD: An fMRI Study. J Atten Disord. 2018 May;22(7):694-702. doi: 10.1177/1087054717703188. PMID: 28423978.

  27. Tegelbeckers, Kanowski, Krauel, Haynes, Breitling, Flechtner, Kahnt (2018): Orbitofrontal Signaling of Future Reward is Associated with Hyperactivity in Attention-Deficit/Hyperactivity Disorder. J Neurosci. 2018 Jul 25;38(30):6779-6786. doi: 10.1523/JNEUROSCI.0411-18.2018. PMID: 29954849; PMCID: PMC6067073.

  28. Birn, Roeber, Pollak (2017): Early childhood stress exposure, reward pathways, and adult decision making. Proc Natl Acad Sci U S A. 2017 Dec 19;114(51):13549-13554. doi: 10.1073/pnas.1708791114. PMID: 29203671; PMCID: PMC5754769.

  29. Sun, You, Cui, Sun, Wang, Wang, Wang, Liu, Xu, Qiu, Liu, Yan (2021): The VTA-BLA-NAc circuit for sex reward inhibited by VTA GABAergic neurons under stress in male mice, bioRxiv

  30. Holly, Miczek (2016): Ventral tegmental area dopamine revisited: effects of acute and repeated stress. Psychopharmacology (Berl). 2016 Jan;233(2):163-86. doi: 10.1007/s00213-015-4151-3. PMID: 26676983; PMCID: PMC4703498. REVIEW

  31. Pretus, Picado, Ramos-Quiroga, Carmona, Richarte, Fauquet, Vilarroya (2018): Just-in-time response to reward as a function of ADHD symptom severity. Psychiatry Clin Neurosci. 2018 Sep;72(9):731-740. doi: 10.1111/pcn.12689. PMID: 29888833.

  32. Bergamini, Sigrist, Ferger, Singewald, Seifritz, Pryce (2016): Depletion of nucleus accumbens dopamine leads to impaired reward and aversion processing in mice: Relevance to motivation pathologies. Neuropharmacology. 2016 Oct;109:306-319. doi: 10.1016/j.neuropharm.2016.03.048. PMID: 27036890.

  33. Ventura, Morrone, Puglisi-Allegra (2007): Prefrontal/accumbal catecholamine system determines motivational salience attribution to both reward- and aversion-related stimuli. Proc Natl Acad Sci U S A. 2007 Mar 20;104(12):5181-6. doi: 10.1073/pnas.0610178104. PMID: 17360372; PMCID: PMC1820518.

  34. Ma, van Holstein, Mies, Mennes, Buitelaar, Cools, Cillessen, Krebs, Scheres (2016): Ventral striatal hyperconnectivity during rewarded interference control in adolescents with ADHD. Cortex. 2016 Sep;82:225-236. doi: 10.1016/j.cortex.2016.05.021.PMID: 27399612.

  35. Zhang, Doyon, Clark, Phillips, Dani (2009): Controls of tonic and phasic dopamine transmission in the dorsal and ventral striatum. Mol Pharmacol. 2009 Aug;76(2):396-404. doi: 10.1124/mol.109.056317. PMID: 19460877; PMCID: PMC2713129.

  36. Clark, Chiodo (1988): Electrophysiological and pharmacological characterization of identified nigrostriatal and mesoaccumbens dopamine neurons in the rat. Synapse. 1988;2(5):474-85. doi: 10.1002/syn.890020503. PMID: 2903568.

  37. Schultz, Dayan, Montague (1997): A neural substrate of prediction and reward. Science. 1997 Mar 14;275(5306):1593-9. doi: 10.1126/science.275.5306.1593. PMID: 9054347.

  38. Mohebi, Pettibone, Hamid, Wong, Kennedy, Berke (2018): Forebrain dopamine value signals arise independently from midbrain dopamine cell firing. bioRxiv 2018, doi: 10.1101/334060

Diese Seite wurde am 20.05.2023 zuletzt aktualisiert.