Neuromodulatory action of dopamine in the nucleus accumbens: An in vivo intracellular study

Yim, Chi Yiu; Mogenson, Gordon J.

doi:10.1016/0306-4522(88)90158-3

Cited by 67 publications

(33 citation statements)

References 37 publications

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“…Stimulation of the VTA in vivo or activation of dopamine receptors in vitro attenuates the responses of accumbens neurons to stimulation of the amygdala or hippocampus (Yang and Mogenson, 1984;Yim and Mogenson, 1988;Charara and Grace, 2003). The amplitude of PFC-evoked EPSPs is also decreased after application of dopamine agonists in vitro (Pennartz et al, 1992;O'Donnell and Grace, 1994;Harvey and Lacey, 1996).…”

Section: Vta Modulation Of Cortical Inputs To the Nucleus Accumbensmentioning

confidence: 99%

“…It has been speculated that the depolarization produced by VTA train stimulation is a direct postsynaptic effect in accumbens neurons, whereas the modulation of excitatory inputs may be attributable to presynaptic reduction of glutamate release from afferent terminals Yim and Mogenson, 1988). Such a dissociation may explain why the attenuation of PFC responses can be partially blocked by D 2 antagonism alone, whereas the plateau depolarization in response to VTA train stimulation is shortened only by combined D 1 and D 2 receptor blockade (Goto and O'Donnell, 2001).…”

Section: Mechanisms Of Dopaminergic Modulation Of Pfc Inputsmentioning

confidence: 99%

“…Activation of dopaminergic pathways or receptors has been shown to either increase (Gonon and Sundstrom, 1996) or decrease (DeFrance et al, 1985;White and Wang, 1986) firing activity in accumbens neurons. Although dopamine is typically found to depolarize accumbens neurons (Uchimura et al, 1986;Yim and Mogenson, 1988;Grace, 1994, 1996;Goto and O'Donnell, 2001), these apparently excitatory effects are often accompanied by reduced excitability (O'Donnell and Grace, 1996) or a decrease in action potential firing Goto and O'Donnell, 2001). There is also some evidence that dopamine may exert a tonic inhibition on accumbens neurons (Mulder et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…Synaptic responses in accumbens neurons driven by stimulation of either the amygdala or the hippocampus are attenuated by stimulation of the VTA or local iontophoretic application of dopamine in vivo (Yang and Mogenson, 1984;DeFrance et al, 1985;Yim and Mogenson, 1988). Excitatory accumbens responses to PFC stimulation are also decreased by direct application of dopaminergic receptor agonists in vitro (Pennartz et al, 1992;O'Donnell and Grace, 1994;Harvey and Lacey, 1996;Nicola et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

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Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Brady¹,

O’Donnell²

2004

J. Neurosci.

128

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Dopaminergic transmission in the nucleus accumbens has been proposed to modulate the effects of converging excitatory inputs from the cortex, hippocampus, and amygdala. Here, we used in vivo intracellular recording in anesthetized rats to examine the response of nucleus accumbens neurons to stimulation of the prefrontal cortex (PFC) and the ventral tegmental area (VTA). The EPSP elicited in accumbens neurons by PFC stimulation was attenuated by VTA train stimulation in a pattern mimicking dopamine cell burst firing. PFC-elicited EPSPs were smaller in amplitude and faster to decay after VTA stimulation. These changes could not be explained by membrane depolarization alone, because EPSPs evoked during the sustained depolarization after VTA stimulation were significantly smaller than EPSPs evoked during spontaneously occurring up states. Furthermore, no attenuation of PFC-elicited responses was observed during depolarization produced by positive current injection through the recording electrode. Administration of a D 1 antagonist (SCH 23390; 0.5 mg/kg, i.p.) had no effect on the VTA reduction of PFC-elicited responses, whereas administration of a D 2 antagonist (eticlopride; 0.5 mg/kg, i.p.) reversed the reduction of PFC inputs when the analysis was limited to comparisons with spontaneous up states. These results suggest that the ability of PFC inputs to drive accumbens neurons is dampened by dopamine acting primarily at D 2 receptors. Along with previous reports of dopaminergic attenuation of limbic afferents to the accumbens, these findings support the hypothesis that dopamine mediates the selection and integration of excitatory inputs and thus shapes information processing in accumbens output neurons.

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Section: Vta Modulation Of Cortical Inputs To the Nucleus Accumbensmentioning

confidence: 99%

Section: Mechanisms Of Dopaminergic Modulation Of Pfc Inputsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Brady¹,

O’Donnell²

2004

J. Neurosci.

128

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“…The major cell type in the NAc is the GABAergic medium spiny neuron (DeFrance et al, 1985a;O'Donnell and Grace, 1993). These cells receive excitatory input from a variety of brain regions (DeFrance et al, 1985a,b;Christie et al, 1987;Yim and Mogenson, 1988;Pickel, 1990, 1992;Johnson et al, 1994;O'Donnell and Grace, 1995) and exhibit extensive networks of recurrent axon collaterals that form GABAergic synapses with other NAc cells (Chang and Kitai, 1985;Pennartz and Kitai, 1991;Kawaguchi et al, 1995). Ultrastructural studies of the NAc and striatum have found dopaminergic terminals apposed to both symmetrical and asymmetrical synapses (Bouyer et al, 1984;Sesack and Pickel, 1992), as well as a significant proportion unapposed to any postsynaptic structures (Bouyer et al, 1984;Descarries et al, 1996).…”

Section: Abstract: Amphetamine; Cocaine; Dopamine; Miniature Inhibitmentioning

confidence: 99%

Dopamine Depresses Excitatory and Inhibitory Synaptic Transmission by Distinct Mechanisms in the Nucleus Accumbens

Nicola

Malenka²

1997

J. Neurosci.

174

138

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The release of dopamine (DA) in the nucleus accumbens (NAc) is thought to be critical for mediating natural rewards as well as for the reinforcing actions of drugs of abuse. DA and amphetamine depress both excitatory and inhibitory synaptic transmission in the NAc by a presynaptic D1-like DA receptor. However, the mechanisms of depression of excitatory and inhibitory synaptic transmission appear to be different. DA depressed the frequency of spontaneous miniature EPSCs, but the frequency of miniature IPSCs was depressed only when spontaneous release was made dependent on Ca 2ϩ influx through voltage-dependent Ca 2ϩ channels. Furthermore, the K ϩ channel blocker Ba 2ϩ attenuated the effects of DA on evoked IPSPs, but not on EPSPs. Thus, DA appears to depress inhibitory synaptic transmission in the NAc by reducing Ca 2ϩ influx into the presynaptic terminal, but depresses excitatory transmission by a distinct mechanism that is independent of the entry of Ca 2ϩ .

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CART peptide-immunoreactive neurones in the nucleus accumbens in monkeys: Ultrastructural analysis, colocalization studies, and synaptic interactions with dopaminergic afferents

et al. 1999

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Cocaine‐ and amphetamine‐regulated transcript (CART) is a novel mRNA whose level of expression was found to be increased in the striatum after acute administration of psychomotor stimulants in rats. To define better the potential role of CART peptides in behavioural and physiologic changes induced by psychomotor stimulants, we analyzed the distribution, ultrastructural features, synaptic connectivity, and transmitter content of CART peptide–immunoreactive neurones in the nucleus accumbens in monkeys. Medium‐sized CART peptide–immunoreactive neurones within a rich plexus of labelled varicosities were found mostly in the medial division of the shell of the nucleus accumbens in monkeys. At the electron microscope level, CART peptide immunoreactivity was exclusively associated with neuronal structures that included perikarya, dendrites, spines as well as nerve terminals packed with electron‐lucent and dense‐core vesicles. Most CART peptide‐containing somata displayed the ultrastructural features of striatal output neurones. The majority of labelled terminals formed symmetric axodendritic synapses and displayed γ‐aminobutyric acid (GABA) immunoreactivity. CART peptide–immunoreactive somata were not immunoreactive for parvalbumin and somatostatin, two markers of striatal interneurones, nor for calbindin D‐28k, a marker of a subpopulation of projection neurones. In double‐immunostained sections, CART peptide–immunoreactive dendrites were found to be contacted by tyrosine hydroxylase‐positive terminals which displayed the ultrastructural features of dopamine‐containing boutons. These findings strongly suggest that CART peptides may be a cotransmitter with GABA in a subpopulation of projection neurones in the monkey accumbens. Furthermore, the fact that CART peptide–immunoreactive neurones receive direct synaptic inputs from dopaminergic afferents and are particularly abundant in the caudomedial division of the shell of the nucleus accumbens suggest that CART peptides might be involved in neuronal and behavioural changes that underlie addiction to psychomotor stimulants and feeding in primates. J. Comp. Neurol. 407:491–511, 1999. © 1999 Wiley‐Liss, Inc.

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Neuromodulatory action of dopamine in the nucleus accumbens: An in vivo intracellular study

Cited by 67 publications

References 37 publications

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Dopamine Depresses Excitatory and Inhibitory Synaptic Transmission by Distinct Mechanisms in the Nucleus Accumbens

CART peptide-immunoreactive neurones in the nucleus accumbens in monkeys: Ultrastructural analysis, colocalization studies, and synaptic interactions with dopaminergic afferents

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