Dopaminergic regulation of striatal cholinergic interneurons: an in vivo microdialysis study

Damsma, G.; Deboer, P; Westerink, Bhc; Fibiger, H.C.

doi:10.1007/bf00169040

Cited by 91 publications

(22 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, these studies are complicated by the necessity to use cholinesterase inhibition. The dose of the inhibitor (34) and the ionic composition of the perfusion medium (35) have been shown to influence the responsiveness of striatal acetylcholine release. The increase in dopamine release induced by the high dose of NT (1 ELM) that reflects an extracellular NT concentration =100 times above the Kd value of local NT receptors is instead postulated to be caused by a direct action of NT on voltage-dependent Ca2+ channels, since this effect is blocked by TTX and has been shown to be insensitive to dopamine autoreceptor activation (31).…”

Section: Introductionmentioning

confidence: 99%

Evidence for a substrate of neuronal plasticity based on pre- and postsynaptic neurotensin-dopamine receptor interactions in the neostriatum.

Fuxé

O’Connor

Antonelli

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The major mechanism underlying the neuroleptic action of the tridecapeptide neurotensin (NT) appears to be an interaction with dopamine receptor mechanisms based on biochemical binding and behavioral experiments. In vivo microdialysis was used in conscious rats to investigate the effects of local perfusion with NT on the sensitivity of striatal dopamine DI and D2 receptors for their selective agonists by monitoring extracellular dopamine, 3,4-dihydroxyphenylacetic acid, homovanilic acid, and r-aminobutyric acid levels in the awake unrestrained male rat. Perfusion with NT (10 nM) counteracted the inhibitory effects of the dopamine D2 agonist pergolide (500 nM) on extracellular levels of dopamine and y-aminobutyric acid. In contrast, NT (10 nM) significantly enhanced the reduction of extracellular striatal levels of dopamine after perfusion with the DI agonist SKF 38393 (5 IpM), and this combined treatment also resulted in a significant increase in the extracellular striatal levels of y-aminobutyric acid. These results provide in vivo evidence that NT regulates central dopamine transmission by reducing pre-and postsynaptic dopamine D2 and enhancing DI receptor sensitivity possibly through an antagonistic NT receptor-D2 receptor interaction. This heteroregulation has the potential to substantially increase the plasticity within the dopamine synapse.within the nerve cell membrane between NT and dopamine D2 receptors (10-12).In the present study we tested the hypothesis that in the neostriatum of the awake unrestrained rat (15), NT selectively reduces dopamine D2 receptor control of dopamine release, which leads to a switching of dopamine transmission toward dopamine D1 receptor-mediated responses. Toward this aim we investigated the effects of local perfusion with NT on the sensitivity of dopamine D1 and D2 receptors for their selective agonists by monitoring extracellular dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanilic acid (HVA), and GABA levels. Thus, we evaluated the effects of local perfusion of the neostriatum with NT alone (a high and a low dose) and with pergolide (a preferential dopamine D2 receptor agonist) or SKF 38393 (a preferential dopamine D1 receptor agonist) (16, 17) by measuring extracellular levels of dopamine, DOPAC, HVA (18), and GABA (19) from a microdialysis probe (20,21) permanently implanted into the neostriatum of the awake unrestrained male rat. Basal extracellular striatal dopamine and GABA levels measured using this technique have been shown (22-24) to be both voltage-and calcium-sensitive and as such can be considered to be derived predominantly from neuronal origin.The dopaminergic system in mammalian forebrain has been implicated in disorders such as schizophrenia and Parkinson disease. Therefore, the regulation of this system may have important implications for the pathophysiology and development of treatments of these disorders. The tridecapeptide neurotensin (NT) has been shown to be closely associated with this dopamine system and to display a neuroleptic or ...

show abstract

Section: Introductionmentioning

confidence: 99%

Evidence for a substrate of neuronal plasticity based on pre- and postsynaptic neurotensin-dopamine receptor interactions in the neostriatum.

Fuxé

O’Connor

Antonelli

et al. 1992

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…They are modulated by dopaminergic, glutamatergic, and GABAergic mechanisms, and by cholinergic autoregulation (Penney and Young, 1983;Starke et al, 1989). Many aspects of the modulation have been demonstrated by brain microdialysis under in vivo conditions (Damsma et al, 1990;DeBoer and Westerink, 1994;Anderson et al, 1994). However, most dialysis studies focus on the release of acetylcholine (ACh) and do not consider changes in extracellular choline (Ch) levels.…”

mentioning

confidence: 99%

Relations Between the Extracellular Concentrations of Choline and Acetylcholine in Rat Striatum

Ikarashi

Takahashi

Ishimaru

et al. 1997

Journal of Neurochemistry

View full text Add to dashboard Cite

Changes in extracellularlevels of acetylcholine (ACh) and choline (Ch) in the striatum of rats were examined by in vivo microdialysis after intraperitoneal injections of drugs. A dopamine D 2 antagonist, sulpiride (20 mg/kg), and a muscarinic antagonist, atropine (3.5 mgI kg), increased ACh levels and decreased Ch levels. On the contrary, the D2 agonist (±)-2-(N-phenylethyl-N-propyl)amino-5-hydroxytetralin (N-434; 5mg/kg) and an anesthetic, pentobarbital (50 mg/kg), decreased ACh levels and increased Ch levels. Perfusion of 10 p~Mhemicholi-nium-3 (HC-3), a Ch uptake inhibitor, through the striaturn induced a complete inhibition of ACh release and increased Ch levels in all drug-treated groups. The degree of relative increase in the level of Ch induced by HC-3 differed among the drug-pretreated groups; compared with the control group, the relative increase was larger in the sulpiride-and atropine-treated groups and smaller in the N-434 and pentobarbital-treated groups. Thus, we demonstrated reciprocal relations between extracellular concentrations of Ch and ACh after treatments by drugs. The data suggest that in the striatum, which is rich in cholinergic innervation, the extracellularCh concentration is to a large extent determined by activity of the cholinergic transmission reflected in high-affinity choline uptake.

show abstract

“…Presynaptic localization of DA receptors is associated with an inhibitory effect on the release of DA (Zetterstr6m et al 1986;Imperato and Di Chiara 1988), NA (Galzin et al 1982;Misu et al 1985) and acetylcholine (Damsma et al 1990;De Boer et al 1992), and these DA receptors possess the pharmacological characteristics of the D2 subtype. DA receptor subtypes involved in the regulation of 5-HT release, however, remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Functional regulation by dopamine receptors of serotonin release from the rat hippocampus: in vivo microdialysis study

Matsumoto

Yoshioka

Togashi

et al. 1996

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

The functional regulation by dopamine (DA) receptors of serotonin (5-HT) release from the rat hippocampus was investigated by use of in vivo microdialysis. Dialysate 5-HT levels were reduced by co-perfusion of 10 microM tetrodotoxin (TTX) and were elicited by K+ (60 and 120 mM) stimulation in a concentration-dependent manner. Local perfusion (10 microM) and peripheral administration (20 mg/kg, i.p.) of fluoxetine produced increases in 5-HT levels. These results indicate that the spontaneous 5-HT levels in the rat hippocampus can be used as indices of neuronal origin from the serotonergic nerve terminals. The nonselective dopamine (DA) receptor agonist apomorphine (1, 10 and 100 microM), when perfused through the probe over a period of 40 min, increased 5-HT release in a concentration-dependent manner. Apomorphine-induced (100 microM) increases in 5-HT release was abolished by pretreatment with the selective D2 receptor antagonist, S(-)-sulpiride (1 and 10 microM), but not prevented by pretreatment with the selective D1 receptor antagonist, R(+)-SCH-23390 (R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2, 3, 4, 5-tetrahydro-1H-3-benzazepine) (1 microM). S(-)-Sulpiride and R(+)-SCH-23390 by themselves did not alter the spontaneous 5-HT levels. The 5-HT release was elevated by perfusion of the selective DA reuptake inhibitor GBR 12909 (1-[2-[bis(4-fluorophenyl) methoxy]ethyl]-4-[3-phenyl-propyl]piperazine) (1, 10 and 100 microM), indicating the possibility of not only exogenous but also endogenous DA-mediated facilitatory effects on 5-HT release in vivo. The 5-HT release was also elevated by perfused (+/-)-PPHT ((+/-)-2-(N-phenylethyl-N-propyl)-amino-5-hydroxytetralin) (1, 10 and 100 microM), the selective D2 receptor agonist, in a concentration-dependent manner. On the other hand, (+/-)-PPHT (100 microM) failed to increase 5-HT release in catecholamine (CA)-lesioned rats pretreated with 6-hydroxydopamine (6-OHDA)(200 micrograms/rat, i.c.v.). The (+/-)-PPHT-induced (100 microM) increase in 5-HT release was prevented not only by pretreatment with 10 microM S(-)-sulpiride but also by pretreatment with the alpha 2-adrenoceptor antagonist idazoxan (10 microM). These findings suggest that the functional regulation of 5-HT release via D2 receptors exists in the rat hippocampus. Furthermore our results indicate that the facilitatory effect of 5-HT release via D2 receptors may be mediated indirectly by noradrenergic neurons, but not mediated directly through D2 receptors located on serotonergic nerve terminals.

show abstract

Dopaminergic regulation of striatal cholinergic interneurons: an in vivo microdialysis study

Cited by 91 publications

References 23 publications

Evidence for a substrate of neuronal plasticity based on pre- and postsynaptic neurotensin-dopamine receptor interactions in the neostriatum.

Evidence for a substrate of neuronal plasticity based on pre- and postsynaptic neurotensin-dopamine receptor interactions in the neostriatum.

Relations Between the Extracellular Concentrations of Choline and Acetylcholine in Rat Striatum

Functional regulation by dopamine receptors of serotonin release from the rat hippocampus: in vivo microdialysis study

Contact Info

Product

Resources

About