Evidence for N-methyl-d-aspartate and AMPA subtypes of the glutamate receptor on substantia nigra dopamine neurons: Possible preferential role for N-methyl-d-aspartate receptors

Christoffersen, Curt; Meltzer, Leonard T.

doi:10.1016/0306-4522(95)00047-m

Cited by 105 publications

(55 citation statements)

References 39 publications

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“…Soltis et al, 1994;Gotz et al, 1997;Kita et al, 2004;Kita et al, 2005), STN (e. g. Mouroux and Feger, 1993;Gotz et al, 1997;Nambu et al, 2000;Wilson et al, 2004;Zhu et al, 2004) and SNc (e.g. Mereu et al, 1991;Christoffersen and Meltzer, 1995). Further supporting the notion that glutamatergic transmission is mediated by a combination of AMPA and NMDA receptor, both types of receptors subunits co-localize at individual glutamatergic synapses (Fig.…”

Section: Ionotropic Receptorsmentioning

confidence: 72%

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

2006

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GABA and glutamate, the main transmitters in the basal ganglia, exert their effects through ionotropic and metabotropic receptors. The dynamic activation of these receptors in response to released neurotransmitter depends, among other factors, on their precise localization in relation to corresponding synapses. The use of high resolution quantitative electron microscope immunocytochemical techniques has provided in-depth description of the subcellular and subsynaptic localization of these receptors in the CNS. In this article, we review recent findings on the ultrastructural localization of GABA and glutamate receptors and transporters in the basal ganglia, at synaptic, extrasynaptic and presynaptic sites. The anatomical evidence supports numerous potential locations for receptor-neurotransmitter interactions, and raises important questions regarding mechanisms of activation and function of synaptic versus extrasynaptic receptors in the basal ganglia.

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Section: Ionotropic Receptorsmentioning

confidence: 72%

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

2006

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“…There are no D1 DA receptors on dopaminergic (DAergic) neurons, however; D1 DA receptors in the VTA are localized on glutamate and GABA afferents to the VTA (Harrison et al, 1990;Herkenham et al, 1991;Yung et al, 1995;Lu et al, 1997), and the effect of DA at these receptors is to facilitate the release of these neurotransmitters (Starr, 1987;Cameron and Williams, 1993;Kalivas and Duffy, 1995). Glutamate excites VTA DAergic and non-DAergic neurons (Albin et al, 1992;Nakanishi, 1992;Carr and Sesack, 2000) and GABAergic neurons (Overton and Clark, 1992;Zhang et al, 1994;Christoffersen and Meltzer, 1995). GABA inhibits both DAergic neurons (Kalivas, 1993) and nearby GABAergic projection neurons, some of which, in turn, inhibit their dopaminergic neighbors, probably via local collaterals (Tepper et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

“…Dendritically released DA in the VTA acts on D1 receptors located on the terminals of GABAergic and glutamatergic inputs originating in forebrain regions (Sesack and Pickel, 1992;Smith et al, 1996;Steffensen et al, 1998). GABA and glutamate in the VTA modulate the activity of dopaminergic and GABAergic output cells (Albin et al, 1992;Nakanishi, 1992;Overton and Clark, 1992;Kalivas, 1993;Zhang et al, 1994;Christoffersen and Meltzer, 1995). Thus, by modulating the release of GABA and glutamate, which in turn modulate DA cell activity and output, dendritically released DA could play a significant role in cocaine reward.…”

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confidence: 99%

Blockade of D1 Dopamine Receptors in the Ventral Tegmental Area Decreases Cocaine Reward: Possible Role for Dendritically Released Dopamine

Ranaldi

Wise

2001

J. Neurosci.

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This study was designed to assess the involvement of D1 dopamine actions in the ventral tegmental area (VTA) on intravenous cocaine self-administration. Rats were trained to selfadminister intravenous injections of cocaine (1.0 mg/kg per injection) on a fixed-ratio 1 (FR-1) schedule or a progressive ratio (PR) schedule of reinforcement and then were tested under the influence of bilateral VTA injections of the D1 dopamine receptor antagonist SCH 23390 or the 5-HT2 receptor antagonist ketanserin. SCH 23390 increased cocaine selfadministration on the FR-1 schedule but decreased it on the PR schedule. Injections of ketanserin were ineffective, as were injections of SCH 23390 in a site 1 mm dorsal or 1 mm rostral to the effective VTA site. These data suggest a role for dendritically released dopamine, presumably acting through D1 receptors located on the axons of GABAergic or glutamatergic inputs to the VTA, in the effectiveness of cocaine reward.Key words: drug abuse; reinforcement; dendritic release; motivation; operant learning; progressive ratio schedule Brain dopamine (DA) plays important roles in the rewarding effects of natural rewards such as food Ettenberg and Camp, 1986a), water (Gerber et al., 1981;Ettenberg and Camp, 1986b), and sexual contact (Pfaus and Phillips, 1989) and in the laboratory reward of lateral hypothalamic electrical stimulation (Fouriezos and Wise, 1976;Franklin, 1978;Wise and Rompré, 1989). The mesocorticolimbic DA system, which originates in the ventral tegmental area (VTA) and terminates in various forebrain structures (Bjorklund and Lindvall, 1986), is also implicated in the rewarding effects of several drugs of abuse, including cocaine, amphetamine, heroin, and nicotine (Wise, 1996;Bardo, 1998). Each of these drug reinforcers causes elevations in extracellular dopamine levels at the axon terminals of the mesocorticolimbic DA system (Zetterström et al., 1983;Di Chiara and Imperato, 1988;Moghaddam and Bunney, 1989). In the case of cocaine, the enhanced extracellular DA concentrations are caused by a blockade of the reuptake of DA back into presynaptic terminals. Destruction of dopaminergic terminals (Roberts et al., 1977) or dopaminergic synaptic targets (Zito et al., 1985) in the nucleus accumbens (NAcc), a mesolimbic terminal region, disrupts responding maintained by cocaine. Injection of D1 dopamine receptor antagonists into the NAcc (Maldonado et al., 1993;McGregor and Roberts, 1993), the medial prefrontal cortex (McGregor and Roberts, 1995), or, to a lesser extent, the amygdala (McGregor and Roberts, 1993), reduces cocaine reward. Thus it is widely assumed that it is dopamine released at the terminals of the mesocorticolimbic system that is important for reward function (Fibiger, 1978;Wise, 1978;Koob and Bloom, 1988;Wise, 1996;Berridge and Robinson, 1998).In addition to increasing extracellular levels of DA at the level of the axon terminals of the mesocorticolimbic system, cocaine also increases extracellular DA at the level of the dendrites in the VTA (Bradberry and Roth, 1989;...

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“…The AMPA/NMDA ratio was positively correlated with locomotor activity, and Jones and Bonci (2005) speculated that an increase in the synaptic AMPA response could result in an enhancement of the response of dopamine neurons to reward related stimuli. In addition, iontophoretic administration of AMPA has been shown to increase both the frequency and the fraction of spikes fired in bursts in chloral hydrate anesthetized rats (Christoffersen and Meltzer 1995).…”

Section: Rationale For Examining the Effect Of Doubling The Ampa Condmentioning

confidence: 99%

An Increase in AMPA and a Decrease in SK Conductance Increase Burst Firing by Different Mechanisms in a Model of a Dopamine Neuron In Vivo

Canavier¹,

Landry²

2006

Journal of Neurophysiology

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Canavier, C. C. and R. S. Landry. An increase in AMPA and a decrease in SK conductance increase burst firing by different mechanisms in a model of a dopamine neuron in vivo. J Neurophysiol 96: 2549 -2563. First published August 2, 2006 doi:10.1152/jn.00704.2006. A stylized, symmetric, compartmental model of a dopamine neuron in vivo shows how rate and pattern can be modulated either concurrently or differentially. If two or more parameters in the model are varied concurrently, the baseline firing rate and the extent of bursting become decorrelated, which provides an explanation for the lack of a tight correlation in vivo and is consistent with some independence of the mechanisms that generate baseline firing rates versus bursts. We hypothesize that most bursts are triggered by a barrage of synaptic input and that particularly meaningful stimuli recruit larger numbers of synapses in a more synchronous way. An example of concurrent modulation is that increasing the short-lived AMPA current evokes additional spikes without regard to pattern, producing comparable increases in spike frequency and fraction fired in bursts. On the other hand, blocking the SK current evokes additional bursts by allowing a depolarization that previously produced only a single spike to elicit two or more and elongates existing bursts by the same principle, resulting in a greater effect on pattern than rate. A probabilistic algorithm for the random insertion of spikes into the firing pattern produces a good approximation to the pattern changes induced by increasing the AMPA conductance, but not by blocking the SK current, consistent with a differential modulation in the latter case. Furthermore, blocking SK produced a longer burst with a greater intra-burst frequency in response to a simulated meaningful input, suggesting that reduction of this current may augment reward-related responses.

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Evidence for N-methyl-d-aspartate and AMPA subtypes of the glutamate receptor on substantia nigra dopamine neurons: Possible preferential role for N-methyl-d-aspartate receptors

Cited by 105 publications

References 39 publications

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

Glutamate and GABA receptors and transporters in the basal ganglia: What does their subsynaptic localization reveal about their function?

Blockade of D1 Dopamine Receptors in the Ventral Tegmental Area Decreases Cocaine Reward: Possible Role for Dendritically Released Dopamine

An Increase in AMPA and a Decrease in SK Conductance Increase Burst Firing by Different Mechanisms in a Model of a Dopamine Neuron In Vivo

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