D-2 dopamine-receptors regulate the release of [3H]dopamine in rat cortical regions showing dopamine immunoreactive fibers

Plantjé, Johan F.; Steinbusch, H.W.M.; Schipper, J.; Dijcks, Fred A.; Verheijden, P.F.H.M.; Stoof, Johannes C.

doi:10.1016/0306-4522(87)90009-1

Cited by 51 publications

(19 citation statements)

References 34 publications

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“…Our observation that the lowest dose of Quinpirole caused a slight increase in call durations while the two higher doses caused decreases in call duration is consistent with previous reports of Quinpirole evoking biphasic dose responses due to its actions at pre-synaptic autoreceptors, which have a higher affinity for the drug than post-synaptic D 2 receptors (Lin and Walter, 1994;Plantje et al, 1987). Activation of D 2 autoreceptors has the net effect of suppressing post-synaptic activity at D 2 synapses, and if that was the case here then the results imply that D 2 receptors actively influence the acoustic structure of spontaneously emitted echolocation pulses.…”

Section: Discussionsupporting

confidence: 92%

Regulation of bat echolocation pulse acoustics by striatal dopamine

Tressler

Schwartz

Wellman

et al. 2011

Journal of Experimental Biology

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) but its effects on the mammalian vocal motor pathways have not been described. MPTP has, so far, been shown to be a potent catecholaminergic neurotoxin in primates, cats, rats, mice and pigs but its efficacy and behavioral effects were found Accepted 11 July 2011 SUMMARY The ability to control the bandwidth, amplitude and duration of echolocation pulses is a crucial aspect of echolocation performance but few details are known about the neural mechanisms underlying the control of these voice parameters in any mammal. The basal ganglia (BG) are a suite of forebrain nuclei centrally involved in sensory-motor control and are characterized by their dependence on dopamine. We hypothesized that pharmacological manipulation of brain dopamine levels could reveal how BG circuits might influence the acoustic structure of bat echolocation pulses. A single intraperitoneal injection of a low dose (5mgkg -1 ) of the neurotoxin 1-methyl-4-phenylpyridine (MPTP), which selectively targets dopamine-producing cells of the substantia nigra, produced a rapid degradation in pulse acoustic structure and eliminated the bat's ability to make compensatory changes in pulse amplitude in response to background noise, i.e. the Lombard response. However, high-performance liquid chromatography (HPLC) measurements of striatal dopamine concentrations revealed that the main effect of MPTP was a fourfold increase rather than the predicted decrease in striatal dopamine levels. After first using autoradiographic methods to confirm the presence and location of D 1 -and D 2 -type dopamine receptors in the bat striatum, systemic injections of receptor subtype-specific agonists showed that MPTP's effects on pulse acoustics were mimicked by a D 2 -type dopamine receptor agonist (Quinpirole) but not by a D 1 -type dopamine receptor agonist (SKF82958). The results suggest that BG circuits have the capacity to influence echolocation pulse acoustics, particularly via D 2 -type dopamine receptor-mediated pathways, and may therefore represent an important mechanism for vocal control in bats.

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Section: Discussionsupporting

confidence: 92%

Regulation of bat echolocation pulse acoustics by striatal dopamine

Tressler

Schwartz

Wellman

et al. 2011

Journal of Experimental Biology

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“…A large number of in vitro experiments have consistently shown that stimulus-evoked release of dopamine from all terminal regions, including prefrontal and cingulate cortices (Plantje et al 1985(Plantje et al , 1987) is modulated by D 2 and/or D 3 nerve terminal autoreceptors (for review see Starke et al 1989), although the sensitivity of release to autoreceptor agonists and antagonists in cortex is sometimes reported to be less than in striatum (e.g., Cubeddu et al 1990). In vivo electrophysiological experiments of changes in the excitability of dopamine nerve terminals in response to local infusion of D2 receptor agonists or antagonists or changes in impulse flow revealed that mesoprefrontal dopaminergic neurons responded exactly as did nigrostriatal neurons, reinforcing the idea that these mesoprefrontal dopaminergic neurons also possessed nerve terminal autoreceptors (Tepper et al 1984a,b;Gariano et al 1989a;Tepper and Groves 1990).…”

Section: Are Autoreceptors Ubiquitous Among Dopaminergic Neurons?mentioning

confidence: 99%

Electrophysiological Pharmacology of Mesencephalic Dopaminergic Neurons

Diana¹,

Tepper²

2002

Dopamine in the CNS II

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“…The mesocorticolimbic DA system is involved in the modulation of emotional states and other limbic functions. DA autoreceptors have been demonstrated and most thoroughly characterized in the rat nigrostriatal system, although they also exist in the rat mesocorticolimbic circuit (9,10,(24)(25)(26)(27). The autoreceptor appears to be exclusively a D2-like DA receptor (28).…”

Section: Introductionmentioning

confidence: 99%

“…These so-called autoreceptors are presynaptically located and provide a "short-loop" level of regulatory feedback for a cell (1-7). This feedback tends to be inhibitory; thus the autoreceptor functions to maintain a set level of neurotransmitter synthesis, cell firing, or release (8)(9)(10)(11)(12).Some dopamine (DA)-synthesizing cells synthesize autoreceptors (13,14). The presence and functioning of DA autoreceptors are central to our understanding of certain aspects of the regulation of the brain DA systems.…”

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confidence: 99%

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Differential expression of autoreceptors in the ascending dopamine systems of the human brain.

Meador‐Woodruff

Damask

Watson

1994

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

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The tone and regulation of the brain dopaminergic projections are, in part, determined by the presence or absence of dopamine (DA) autoreceptors: rate of DA synthesis and turnover, as well as both pattern and rate of neuronal firing, are modulated by the expression and activity of these autoreceptors. The expression of dopaminergic receptors in the midbrain DA cell groups, presumably reflecting DA autoreceptors, was determined in the brains of the rat, Old World monkey, and human. In the rat, both the sbstantia nigra (A9) and the ventral tegmental area (A1O) appear to express DA autoreceptors. In the monkey and human, however, only the projections arising from the substantia nia express these receptors; the limbic projections originating in the ventral tegmental area lack this substrate for DA autoregulation. These results indicate that in the human, the nigrostriatal and mesocorticolimbic dopamine systems may be differentially autoregulated.The regulation of neurotransmitter synthesis and release is of central importance to the understanding of brain function. Dysregulation of these processes is likely involved in a number of neuropsychiatric conditions, and many psychotropic drugs exert their effects at this level of cellular physiology. One aspect of neurotransmitter regulation that has been appreciated is that a given transmitter can potentially regulate itself. This autoregulation is generally believed to be mediated via receptors for a given transmitter that are located on the cell synthesizing and releasing that transmitter. These so-called autoreceptors are presynaptically located and provide a "short-loop" level of regulatory feedback for a cell (1-7). This feedback tends to be inhibitory; thus the autoreceptor functions to maintain a set level of neurotransmitter synthesis, cell firing, or release (8)(9)(10)(11)(12).Some dopamine (DA)-synthesizing cells synthesize autoreceptors (13,14). The presence and functioning of DA autoreceptors are central to our understanding of certain aspects of the regulation of the brain DA systems. In those cells with functioning DA autoreceptors, DA appears to have a lower rate of synthesis and turnover, and these neurons manifest a lower rate and intensity ofcellular firing, compared with cells without autoreceptors. Autoreceptor-expressing cells appear to have higher levels of responsiveness to various dopaminergic compounds. Interestingly, cells that lack DA autoreceptors appear to be affected by chronic DA antagonists (i.e., antipsychotic medications) differently than autoreceptorexpressing cells: those cells that lack autoreceptors do not develop either tolerance or depolarization inactivation after chronic antagonist treatment (15-20). DA autoreceptors can then be considered as one cellular mechanism for the modulation of the tone of a given system. Although extensively studied in lower animals, most work has concentrated on the rat. It has been assumed, however, that the human also expresses DA autoreceptors in brain (21, 22).The two major ascending central...

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D-2 dopamine-receptors regulate the release of [3H]dopamine in rat cortical regions showing dopamine immunoreactive fibers

Cited by 51 publications

References 34 publications

Regulation of bat echolocation pulse acoustics by striatal dopamine

Regulation of bat echolocation pulse acoustics by striatal dopamine

Electrophysiological Pharmacology of Mesencephalic Dopaminergic Neurons

Differential expression of autoreceptors in the ascending dopamine systems of the human brain.

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