Ultrastructural immunocytochemical localization of the dopamine D2 receptor within GABAergic neurons of the rat striatum

Donne, Karen T. Delle; Sesack, Susan R.; Pickel, Virginia M.

doi:10.1016/s0006-8993(96)01226-7

Cited by 93 publications

(64 citation statements)

References 71 publications

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“…Finally, in the rat striatum D 2 receptor immunoreactivity has been found both presynaptically (in both dopaminergic and glutamatergic terminals) and postsynaptically. At the postsynaptic level, D 2 receptor immunoreactivity has not only been observed at symmetric synapses but also perisynaptically at asymmetric synapses (Yung et al, 1995;Delle Donne et al, 1997). In summary, these morphological findings strongly suggest that the three receptors, A 2A , mGluR 5 , and D 2 , are colocalized in the striatopallidal GABAergic efferent neuron, postsynaptically and perisynaptically at dopaminergic and glutamatergic synapses (Fig.…”

Section: Receptor/receptor Interactions In the Striatopallidalmentioning

confidence: 59%

Molecular Mechanisms and Therapeutical Implications of Intramembrane Receptor/Receptor Interactions among Heptahelical Receptors with Examples from the Striatopallidal GABA Neurons

et al. 2003

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Section: Receptor/receptor Interactions In the Striatopallidalmentioning

confidence: 59%

Molecular Mechanisms and Therapeutical Implications of Intramembrane Receptor/Receptor Interactions among Heptahelical Receptors with Examples from the Striatopallidal GABA Neurons

et al. 2003

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“…However, sulpiride will inhibit both presynaptic and postsynaptic DA D 2 -type receptors. Because there are differences in function and expression of DATs and D 2 receptors along the dorsal-to-ventral extent of the striatum (Delle Donne et al, 1997;Centonze et al, 2003), there is potential for varied distributions and roles of D 2 receptors. Despite that potential, the first-order influence of sulpiride is probably inhibition of D 2 autoreceptors that regulate DA release.…”

Section: Tonic and Phasic Dopamine Transmission In The Striatummentioning

confidence: 99%

Controls of Tonic and Phasic Dopamine Transmission in the Dorsal and Ventral Striatum

et al. 2009

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Dopamine (DA) release varies within subregions and local environments of the striatum, suggesting that controls intrinsic and extrinsic to the DA fibers and terminals regulate release. While applying fast-scan cyclic voltammetry and using tonic and phasic stimulus trains, we investigated the regulation of DA release in the dorsolateral to ventral striatum. The ratio of phasic-to-tonic-evoked DA signals varied with the average ongoing firing frequency, and the ratio was generally higher in the nucleus accumbens (NAc) compared with the dorsolateral striatum. At the normal average firing frequency, burst stimulation produces a larger increase in the DA response in the NAc than the dorsolateral striatum. This finding was comparable whether the DA measurements were made using in vitro brain slices or were recorded in vivo from freely moving rodents. Blockade of the dopamine transporters and dopamine D 2 receptors particularly enhanced the tonic DA signals. Conversely, blockade of nicotinic acetylcholine receptors (nAChRs) containing the ␤ 2 subunit (␤ 2 *) predominantly suppressed tonic DA signals. The suppression of tonic DA release increased the contrast between phasic and tonic DA signals, and that made the frequencydependent DA dynamics between the dorsolateral striatum and NAc more similar. The results indicate that intrinsic differences in the DA fibers that innervate specific regions of the striatum combine with (at least) DA transporters, DA receptors, and nAChRs to regulate the frequency dependence of DA release. A combination of mechanisms provides specific local control of DA release that underlies pathway-specific information associated with motor and reward-related functions. Dopamine (DA) neurons operate in distinct tonic and phasic timescales to differentiate behaviorally relevant information (Schultz, 2007). DA neurons discharge tonically at low frequencies that consist of individual action potentials without bursts . Periodically, DA neurons fire in phasic bursts of near 20 Hz and greater (Hyland et al., 2002;Robinson et al., 2004). Evidence indicates that phasic or burst firing induces greater extracellular DA release compared with tonic, single-spike firing activity (Gonon, 1988;Grace, 1991;Floresco et al., 2003). Those tonic and phasic signals arise from midbrain DA neurons of the substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) that innervate the whole dorsal to ventral extent of the striatum. Although the DA neurons that project to the prefrontal cortex may have higher discharge rates (Chiodo et al., 1984;Lammel et al., 2008), many midbrain DA neurons often exhibit similar overall firing properties (Schultz, 1986;Clark and Chiodo, 1988;Gariano et al., 1989;Robinson et al., 2004). Reward-related sensory input, however, such as that initiated by an addictive drug, enhances DA release to varying degrees depending on the dopaminergic pathway and target region (Pontieri et al., 1996;Nisell et al., 1997;Shi et al., 2000;Di Chiara et al., 2004;Janhunen and Ahtee, 2007). Th...

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“…Accordingly, in vivo, blockade of ongoing GABAergic inhibition of medium spiny neurons significantly elevates basal activity (Nisenbaum and Berger 1992), supporting the idea that psychostimulants, by inhibiting GABAergic inhibition, would substantially enhance the ability of cortical activity to evoke spiking in medium spiny neurons. Recurrent collaterals of projection neurons and GABAergic interneurons, such as fast-spiking and parvalbumin-immunoreactive cells contact striatal spiny neurons in their somato-dendritic region (Wilson and Groves 1980;Yung et al 1996;Bennet and Bolam 1994;Plentz and Kitai 1998;Koos and Tepper 1999) and express D2 DA receptors (Lenz et al 1994;Delle Donne et al 1997;Aizman et al 2000). It is therefore conceivable that terminals from all these different cell types would also possess D2 DA receptor and be sensitive to a similar extent to the pharmacological action of psychostimulants.…”

Section: Anatomo-functional Characteristics Of Synaptic Inputs To Strmentioning

confidence: 99%

Cocaine and Amphetamine Depress Striatal GABAergic Synaptic Transmission through D2 Dopamine Receptors

Centonze

Picconi

Baunez

et al. 2002

Neuropsychopharmacology

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The striatum is a brain area implicated in the pharmacological action of drugs of abuse. To test the possible involvement of both cocaine and amphetamine in the modulation of synaptic transmission in this nucleus, we coupled whole-cell patch clamp recordings from striatal spiny neurons to the focal stimulation of glutamatergic or GABAergic nerve terminals. We found that neither cocaine (1-600 M) nor amphetamine (0.3-300 M) significantly affected the glutamate-mediated EPSCs recorded from these cells. Conversely, both pharmacological agents depressed GABA-mediated IPSCs in a dose-dependent manner. This effect was mediated by the stimulation of dopamine (DA) D2 receptors since it was prevented by 3 M L-sulpiride (a DA D2-like receptor antagonist), mimicked by the DA D2-like receptor agonist quinpirole (0.3-30 M), and absent in mice lacking DA D2 receptors. A presynaptic mechanism was likely involved in this action since both cocaine and amphetamine depress GABAergic transmission by increasing paired-pulse facilitation. Cocaine and amphetamine failed to affect GABAergic IPSCs after 6-OHDA-induced nigral lesion, indicating that both drugsFollowing psychostimulant administration, markers of brain activity are altered in many areas (Stein and Fuller 1993;Lyons et al. 1996;Breiter et al. 1997), suggesting that the diverse cognitive, emotional, and motor effects of these drugs are caused by the interaction with multiple neuronal systems in the central nervous system. Increasing evidence indicates that not only cortical but also subcortical areas play a role in the cocaine-and amphetamine-mediated effects. In particular, the increased locomotor activity and stereotypy caused by psychostimulants seem to involve specifically the nucleus striatum (Kelly et al. 1975;Amalric and Koob 1993;Berke and Hyman 2000), a structure that receives virtually all the cortical information directed to the basal ganglia (Penney and Young 1983;Albin et al. 1989;McGeorge and Faull 1989;Calabresi et al. 1996 Kaneko et al. 2000). The nucleus striatum also receives profuse dopaminergic innervation from the substantia nigra and has a very high density of D1 and D2 dopamine (DA) receptors but also of D3, D4 and D5 receptors (Mansour and Watson 1995;Surmeier et al. 1996;Bordet et al. 1997;LaHoste et al. 2000). Amphetamine and cocaine cause in the striatum rapid induction of c-fos, a commonly used molecular marker for neuronal activity. Interestingly, this effect is sensitive to dopamine (DA) receptor blockade (Graybiel et al. 1990;Moratalla et al. 1993), suggesting that increased release of DA in the striatum is responsible, at least in part, for the action of these drugs. In this regard, while the full diversity of drug effects is mediated by multiple neurotransmitters acting in multiple brain regions, most drugs abused by humans share the common property of increasing DA release in this brain area (Di Chiara and Imperato 1988; Kuczenshi et al. 1991;Yamamoto and Spanos 1988;Koob et al. 1998;Ito et al. 2000). Cocaine increases DA availability in th...

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Ultrastructural immunocytochemical localization of the dopamine D2 receptor within GABAergic neurons of the rat striatum

Cited by 93 publications

References 71 publications

Molecular Mechanisms and Therapeutical Implications of Intramembrane Receptor/Receptor Interactions among Heptahelical Receptors with Examples from the Striatopallidal GABA Neurons

Molecular Mechanisms and Therapeutical Implications of Intramembrane Receptor/Receptor Interactions among Heptahelical Receptors with Examples from the Striatopallidal GABA Neurons

Controls of Tonic and Phasic Dopamine Transmission in the Dorsal and Ventral Striatum

Cocaine and Amphetamine Depress Striatal GABAergic Synaptic Transmission through D2 Dopamine Receptors

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