D
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            Dopamine Receptor-regulated Gene Expression of Striatonigral and Striatopallidal Neurons

Gerfen, Charles R.; Engber, Thomas M.; Mahan, Lawrence C.; Susel, Zvi; Chase, Thomas N.; Monsma, Frederick J.; Sibley, David R.

doi:10.1126/science.2147780

Cited by 2,709 publications

(1,821 citation statements)

References 32 publications

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“…D 1 and D 2 receptors (and to a lesser extent D 3 , D 4 , D 5 receptors) are variably expressed on striatal spiny projection neurons that can be classified into subpopulations based on that expression (Gerfen et al, 1990;Bergson et al, 1995;Wong et al, 1999;Aizman et al, 2000;Nicola et al, 2000). DA can influence the activity of striatal spiny neurons by modulating voltage-dependent ion channels as well as excitatory and inhibitory synaptic inputs (Nicola et al, 2000).…”

Section: Dopamine Receptors In the Striatummentioning

confidence: 99%

Cholinergic interneuron characteristics and nicotinic properties in the striatum

2002

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ABSTRACT:The neostriatum (dorsal striatum) is composed of the caudate and putamen. The ventral striatum is the ventral conjunction of the caudate and putamen that merges into and includes the nucleus accumbens and striatal portions of the olfactory tubercle. About 2% of the striatal neurons are cholinergic. Most cholinergic neurons in the central nervous system make diffuse projections that sparsely innervate relatively broad areas. In the striatum, however, the cholinergic neurons are interneurons that provide very dense local innervation. The cholinergic interneurons provide an ongoing acetylcholine (ACh) signal by firing action potentials tonically at about 5 Hz. A high concentration of acetylcholinesterase in the striatum rapidly terminates the ACh signal, and thereby minimizes desensitization of nicotinic acetylcholine receptors. Among the many muscarinic and nicotinic striatal mechanisms, the ongoing nicotinic activity potently enhances dopamine release. This process is among those in the striatum that link the two extensive and dense local arbors of the cholinergic interneurons and dopaminergic afferent fibers. During a conditioned motor task, cholinergic interneurons respond with a pause in their tonic firing. It is reasonable to hypothesize that this pause in the cholinergic activity alters action potential dependent dopamine release. The correlated response of these two broad and dense neurotransmitter systems helps to coordinate the output of the striatum, and is likely to be an important process in sensorimotor planning and learning.

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Section: Dopamine Receptors In the Striatummentioning

confidence: 99%

Cholinergic interneuron characteristics and nicotinic properties in the striatum

2002

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“…A substantial literature suggests that the role of DA in incentive learning, as typified by place preference conditioning, is mediated by actions at the D1 receptor subtype (Di Chiara et al 1991;Beninger and Miller 1998). As DA has some excitatory actions at D1 receptors (Gerfen et al 1990;Gerfen 2000), D1 antagonists would tend to decrease the activity of target neurons in the nucleus accumbens, and as NMDA receptors are also excitatory, they would share this property with NMDA receptor antagonists. The psychotomimetic and psychostimulant actions of DA agonists, however, are known to be mediated through the D2 receptor subtype (Creese et al 1976;Ralph et al 1999;Caine et al 2000).…”

Section: Mechanisms Of Acpc Effects On the Acquisition Of Drug-conditmentioning

confidence: 99%

“…The psychotomimetic and psychostimulant actions of DA agonists, however, are known to be mediated through the D2 receptor subtype (Creese et al 1976;Ralph et al 1999;Caine et al 2000). As DA is inhibitory at D2 receptors (Gerfen et al 1990;Gerfen 2000), in this case it is D2 agonists that would share with NMDA antagonists the tendency to decrease activity in cells where D2 receptors and NMDA receptors are co-localized.…”

Section: Mechanisms Of Acpc Effects On the Acquisition Of Drug-conditmentioning

confidence: 99%

“…D1 and D2 receptors are largely segregated in different populations of medium spiny cells, throughout the striatum (Le Moine and Bloch 1995;Smith and Kieval 2000;Gerfen 2000), and associated with different output pathways (Alexander and Crutcher 1990;Gerfen et al 1990). It follows that the blockade of place conditioning by NMDA antagonists may involve NMDA receptors located on D1-receptor containing accumbens cells, while the psychotomimetic and psychostimulant effects of NMDA antagonists may involve NMDA receptors located on, or interacting functionally with, D2-receptor containing cells.…”

Section: Mechanisms Of Acpc Effects On the Acquisition Of Drug-conditmentioning

confidence: 99%

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Selective Blockade of Drug-induced Place Preference Conditioning by ACPC, a Functional NDMA-receptor Antagonist

Papp

Gruca

Willner

2002

Neuropsychopharmacology

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ACPC (1-aminocyclopropanecarboxylic acid) is a partial agonist at the strychnine-insensitive glycine receptor site on the NMDA receptor complex, and a functional NMDA antagonist. A series of experiments was conducted to assess the effects of ACPC in a biased place conditioning paradigm. As previously reported, ACPC itself did not support either appetitive or aversive place conditioning. However, co-administration of ACPC (200 mg/kg) blocked the acquisition of place preferences conditioned using a variety of psychoactive drugs (amphetamine, cocaine, nomifensine, diazepam, morphine, nicotine). No tolerance was seen to this effect following two weeks of chronic ACPC administration. Overall, ACPC did not affect the expression of place conditioning when administered immediately before the post-conditioning test. However, these effects appeared somewhat variable between drugs, and further analysis showed that ACPC did block the expression of preferences conditioned with some drugs (diazepam, morphine, nicotine), but not others (amphetamine, cocaine, nomifensine). The effects of ACPC could not be accounted for by state dependence, as ACPC blocked morphine and cocaine place preferences when administered during both the acquisition and the expression phase of conditioning. In contrast to the blockade by ACPC of drug-induced place preferences, ACPC had no effect on the acquisition of place preferences conditioned using a variety of natural non-drug reinforcers (food, sucrose, social interaction, novelty). ACPC also had no effect on the acquisition of drug-induced place aversions (naloxone, picrotoxin The treatment of drug addiction has two targets: cessation or reduction of use, and maintenance of those gains. During the maintenance phase, a number of factors have been identified that predispose to relapse. These include stimuli associated with drug taking (O'Brien et al. 1998). The place preference conditioning procedure has been used extensively as an animal model for investigating the rewarding properties of drug-conditioned stimuli. In this procedure, 27 , NO . 5 the animal experiences the effects of a drug while confined in a distinctive environment; subsequently the animal is offered a choice between the drug-paired environment and an environment that has been experienced in the drug-free state. Subject to certain methodological considerations, a preference for the drug-paired environment is interpreted to mean that the environment has acquired secondary reinforcing properties as a consequence of its pairing with a primary reinforcer. Drugs that support the development of a conditioned place preference (CPP) are generally those that are abused by people (e.g. psychostimulants, opioids, benzodiazepines, alcohol, nicotine), while drugs that do not support CPP are typically not abused (e.g. neuroleptics, antidepressants, antihistamines) (Carr et al. 1989;Schechter and Calcagnetti 1993;Calcagnetti and Schechter 1998;Tzschentke 1998). In addition to drug rewards, CPP can also be used to study the reinforcing prop...

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“…It is currently accepted (Gerfen 1990) that DA can facilitate motor behavior via stimulation of facilitatory D 1 and inhibitory D 2 receptors preferentially expressed by the striatonigral and striatopallidal GABAergic neurons, respectively. Both subpopulations of GABAergic neurons also express NMDA receptors (Tallaksen-Greene et al 1992;Landwehrmeyer et al 1995) and behavioral evidence that striatal NMDA receptors stimulate both pathways has been presented (Ossowska and Wolfarth 1995;Klockgether and Turski 1993).…”

mentioning

confidence: 99%

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

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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.

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D ₁ and D ₂ Dopamine Receptor-regulated Gene Expression of Striatonigral and Striatopallidal Neurons

Cited by 2,709 publications

References 32 publications

Cholinergic interneuron characteristics and nicotinic properties in the striatum

Cholinergic interneuron characteristics and nicotinic properties in the striatum

Selective Blockade of Drug-induced Place Preference Conditioning by ACPC, a Functional NDMA-receptor Antagonist

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

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D 1 and D 2 Dopamine Receptor-regulated Gene Expression of Striatonigral and Striatopallidal Neurons

Cited by 2,709 publications

References 32 publications

Cholinergic interneuron characteristics and nicotinic properties in the striatum

Cholinergic interneuron characteristics and nicotinic properties in the striatum

Selective Blockade of Drug-induced Place Preference Conditioning by ACPC, a Functional NDMA-receptor Antagonist

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

Contact Info

Product

Resources

About

D ₁ and D ₂ Dopamine Receptor-regulated Gene Expression of Striatonigral and Striatopallidal Neurons

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