D1 and D2 dopamine receptors differentially regulate c-fos expression in striatonigral and striatopallidal neurons

Robertson, George S.; Vincent, Steven R.; Fibiger, Hans C.

doi:10.1016/0306-4522(92)90096-k

Cited by 317 publications

(106 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The present experimental preparation cannot tell about the neuronal substrate(s) of this D 1 /D 2 receptor interaction but presents neurochemical evidence that this interaction is relevant for the control of the striatal efferent pathways. Indeed, the increase of nigral GLU release induced by raclopride is consistent with blockade of the inhibitory tone mediated by D 2 receptors on striatopallidal neurons (Albin et al 1989) and disinhibition of the indirect pathway (Robertson et al 1992;Ferrè et al 1994). Thus, disinhibition of the striatopallidal pathway induced by D 2 receptor blockade may require functional D 1 receptors.…”

Section: )supporting

confidence: 61%

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Marti

Mela

Bianchi

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

Dual probe microdialysis was employed in conscious rats to investigate whether endogenous dopamine is involved in the stimulation of glutamate release in the substantia nigra pars reticulata following striatal NMDA receptor activation. Intrastriatal perfusion with NMDA (1 and 10 lM) facilitated nigral glutamate release (dizocilpine-and tetrodotoxin-sensitive). The D 2 dopamine receptor antagonist raclopride increased spontaneous nigral glutamate release and caused a leftward shift in the NMDA sensitivity, lowering NMDA effective concentrations to submicromolar levels. Conversely, the D 1 antagonist SCH23390 prevented the effect of NMDA (1 lM) and caused a rightward shift in the NMDA sensitivity. It was tested whether the antagonist effects were due to dopamine receptor blockade or increased tone on D 1 /D 2 receptors. SCH23390 prevented the raclopride-induced enhancement of spontaneous but not NMDA-evoked glutamate release while raclopride left unchanged the SCH23390-induced inhibition. The physiopathological relevance of the dopaminergic modulation was strengthened by perfusing NMDA in the dopaminedepleted striatum of hemiparkinsonian rats. Nigral glutamate responsiveness to NMDA was enhanced as with raclopride. We conclude that endogenous striatal dopamine regulates both spontaneous and NMDA-induced nigral glutamate release via an opposite control mediated by D 1 facilitatory and D 2 inhibitory receptors. Alterations of this control may subserve the motor symptoms of Parkinson's disease.

show abstract

Section: )supporting

confidence: 61%

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Marti

Mela

Bianchi

et al. 2002

Journal of Neurochemistry

View full text Add to dashboard Cite

show abstract

“…In particular, because DA has greater affinity for the D 2 than for the D 1 class of receptors (Creese et al, 1983), D 2 receptors are very sensitive to low tonic DA levels, whereas large increases in DA are required to functionally stimulate D 1 receptors (e.g., levels of DA release no-go cells from inhibition (via lack of binding to D 2 receptors), allowing them to become more excited than their go counterparts and driving Hebbian learning in the opposite direction of DA bursts. Supporting this hypothesis, blockade of D 2 receptors is associated with enhanced no-go activity and associated increases in long-term potentiation (Calabresi et al, 1997;Finch, 1999;Robertson, Vincent, & Fibiger, 1992).…”

Section: Bg-damentioning

confidence: 87%

Anatomy of a decision: Striato-orbitofrontal interactions in reinforcement learning, decision making, and reversal.

Frank¹,

Claus²

2006

Psychological Review

523

505

View full text Add to dashboard Cite

The authors explore the division of labor between the basal ganglia-dopamine (BG-DA) system and the orbitofrontal cortex (OFC) in decision making. They show that a primitive neural network model of the BG-DA system slowly learns to make decisions on the basis of the relative probability of rewards but is not as sensitive to (a) recency or (b) the value of specific rewards. An augmented model that explores BG-OFC interactions is more successful at estimating the true expected value of decisions and is faster at switching behavior when reinforcement contingencies change. In the augmented model, OFC areas exert top-down control on the BG and premotor areas by representing reinforcement magnitudes in working memory. The model successfully captures patterns of behavior resulting from OFC damage in decision making, reversal learning, and devaluation paradigms and makes additional predictions for the underlying source of these deficits.Keywords: decision making, neural network, basal ganglia, orbitofrontal cortex, reinforcement learning What enables humans to make choices that lead to long-term gains, even when having to incur short-term losses? Such decisionmaking skills depend on the processes of action selection (choosing between one of several possible responses) and reinforcement learning (modifying the likelihood of selecting a given response on the basis of experienced consequences). Although all mammals can learn to associate their actions with consequences, humans are particularly advanced in their ability to flexibly modify the relative reinforcement values of alternative choices to select the most adaptive behavior in a particular behavioral, spatial, and temporal context.The behavioral and cognitive neurosciences have identified two neural systems that are involved in such adaptive behavior. On the one hand, the basal ganglia (BG) and the neuromodulator dopamine (DA) are thought to participate in both action selection and reinforcement learning

show abstract

“…However, as striatopallidal neurons preferentially express D2 dopamine receptors and D2 receptor stimulation reduces the response of medium spiny neurons to cortical input (Gerfen et al, 1990;Robertson et al, 1992;Cepeda et al, 1993), it is consistent that dopaminergic denervation of the striatopallidal neurons would lead to increased response to cortical input. Selective loss of spines on D2 bearing striatal neurons provides an additional mechanism that could contribute to altered processing of cortical activity by striatopallidal neurons (Day et al, 2006).…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 87%

Phase relationships support a role for coordinated activity in the indirect pathway in organizing slow oscillations in basal ganglia output after loss of dopamine

et al. 2007

View full text Add to dashboard Cite

The goal of the present study was to determine the phase relationships of the slow oscillatory activity that emerges in basal ganglia nuclei in anesthetized rats after dopamine cell lesion in order to gain insight into the passage of this oscillatory activity through the basal ganglia network. Spike train recordings from striatum, subthalamic nucleus (STN), globus pallidus (GP), and substantia nigra pars reticulata (SNpr) were paired with simultaneous local field potential (LFP) recordings from SNpr or motor cortex ipsilateral to a unilateral lesion of substantia nigra dopamine neurons in urethane anesthetized rats. Dopamine cell lesion induced a striking increase in incidence of slow oscillations (0.3-2.5 Hz) in firing rate in all nuclei. Phase relationships assessed through paired recordings using SNpr LFP as a temporal reference showed that slow oscillatory activity in GP spike trains is predominantly antiphase with oscillations in striatum, and slow oscillatory activity in STN spike trains is in-phase with oscillatory activity in cortex but predominantly antiphase with GP oscillatory activity. Taken together, these results imply that after dopamine cell lesion in urethane anesthetized rats, increased oscillatory activity in GP spike trains is shaped more by increased phasic inhibitory input from the striatum than by phasic excitatory input from STN. In addition, results show that oscillatory activity in SNpr spike trains is typically antiphase with GP oscillatory activity and in-phase with STN oscillatory activity. While these observations do not rule out additional mechanisms contributing to the emergence of slow oscillations in the basal ganglia after dopamine cell lesion in the anesthetized preparation, they are compatible with 1) increased oscillatory activity in the GP facilitated by an effect of dopamine loss on striatal 'filtering' of slow components of oscillatory cortical input, 2) increased oscillatory activity in STN spike trains supported by convergent antiphase inhibitory and excitatory oscillatory input from GP and cortex, respectively, and 3) increased oscillatory activity in SNpr spike trains organized by convergent antiphase inhibitory and excitatory oscillatory input from GP and STN, respectively. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errorsmaybe discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2012 May 17. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript KeywordsParkinson's disease; subthalamic nucleus; substantia nigra; globus pallidus; striatum; bursting; local field potentials Dopa...

show abstract

D1 and D2 dopamine receptors differentially regulate c-fos expression in striatonigral and striatopallidal neurons

Cited by 317 publications

References 49 publications

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Anatomy of a decision: Striato-orbitofrontal interactions in reinforcement learning, decision making, and reversal.

Phase relationships support a role for coordinated activity in the indirect pathway in organizing slow oscillations in basal ganglia output after loss of dopamine

Contact Info

Product

Resources

About

D1 and D2 dopamine receptors differentially regulate c-fos expression in striatonigral and striatopallidal neurons

Cited by 317 publications

References 49 publications

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D1 and D2 receptors

Anatomy of a decision: Striato-orbitofrontal interactions in reinforcement learning, decision making, and reversal.

Phase relationships support a role for coordinated activity in the indirect pathway in organizing slow oscillations in basal ganglia output after loss of dopamine

Contact Info

Product

Resources

About

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors

Striatal dopamine–NMDA receptor interactions in the modulation of glutamate release in the substantia nigra pars reticulata in vivo: opposite role for D₁ and D₂ receptors