Dopamine action in the nucleus accumbens

DeFrance, Jon F.; Sikes, Robert W.; Chronister, R.B.

doi:10.1152/jn.1985.54.6.1568

Cited by 63 publications

(35 citation statements)

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“…While this paper does not attempt to integrate this important and complex literature into the current discussion, it will be of interest in the future to determine whether and how these presynaptic interactions might contribute to a selective gating function). As described above, and noted by others, DA appears to amplify the activity of neurons receiving strong corticostriatal input (and, within the accumbens, cells receiving coincident input from frontal and hippocampal regions [86]) while filtering-out activity at weakly-activated synapses [27,33,48,67,88,120,124]. A disruption in striatal DA activity may, therefore, interfere with corticostriatal information processing either by disrupting the transmission of strong input signals, or by permitting the transmission of weak signals that would not normally be permitted to compete for basal ganglia processing beyond the level of the striatum.…”

Section: Da Neurons Respond To Salient Unexpected Eventssupporting

confidence: 53%

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

Horvitz

2002

Behavioural Brain Research

187

148

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Section: Da Neurons Respond To Salient Unexpected Eventssupporting

confidence: 53%

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

Horvitz

2002

Behavioural Brain Research

187

148

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“…Such a selection process may be accomplished by a dopaminergic enhancement of the signal-to-noise ratio in accumbens neurons (DeFrance et al, 1985;Kiyatkin and Rebec, 1996;O'Donnell and Grace, 1996;Nicola et al, 2000). In behaviorally relevant contexts, increased dopamine transmission may reduce background activity and suppress responses to weak or irrelevant inputs in accumbens cells, while facilitating transmission from contextually appropriate inputs Pennartz et al, 1994;O'Donnell and Grace, 1996;Nicola and Malenka, 1997).…”

Section: Functional Considerationsmentioning

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).…”

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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“…For instance, in the medial prefrontal cortex, a structure important for attention, dopamine can inhibit the entry of information, including entry from the hippocampus (Jay et al, 1995;Thierry et al, 2000). Dopamine also inhibits the inputs to the nucleus accumbens, including those from the prefrontal cortex (Carr et al, 1999) and the hippocampus (DeFrance et al, 1985). A short dopamine pulse from the VTA therefore would cause a decrease of excitatory drive of accumbal inhibitory neurons.…”

Section: Properties Of Vta Cells That Supply Dopaminergic Input To Thmentioning

confidence: 99%

Storage, recall, and novelty detection of sequences by the hippocampus: Elaborating on the SOCRATIC model to account for normal and aberrant effects of dopamine

2001

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ABSTRACT:In order to understand how the molecular or cellular defects that underlie a disease of the nervous system lead to the observable symptoms, it is necessary to develop a large-scale neural model. Such a model must specify how specific molecular processes contribute to neuronal function, how neurons contribute to network function, and how networks interact to produce behavior. This is a challenging undertaking, but some limited progress has been made in understanding the memory functions of the hippocampus with this degree of detail. There is increasing evidence that the hippocampus has a special role in the learning of sequences and the linkage of specific memories to context. In the first part of this paper, we review a model (the SOCRATIC model) that describes how the dentate and CA3 hippocampal regions could store and recall memory sequences in context. A major line of evidence for sequence recall is the "phase precession" of hippocampal place cells. In the second part of the paper, we review the evidence for theta-gamma phase coding. According to a framework that incorporates this form of coding, the phase precession is interpreted as cued recall of a discrete sequence of items from long-term memory. The third part of the paper deals with the issue of how the hippocampus could learn memory sequences. We show that if multiple items can be active within a theta cycle through the action of a short-term "buffer," NMDA-dependent plasticity can lead to the learning of sequences presented at realistic item separation intervals. The evidence for such a buffer function is reviewed. An important underlying issue is whether the hippocampal circuitry is configured differently for learning and recall. We argue that there are indeed separate states for learning and recall, but that both involve theta oscillations, albeit in possibly different forms. This raises the question of how neuromodulatory input might switch the hippocampus between learning and recall states and more generally how different neuromodulatory inputs reconfigure the hippocampus for different functions. In the fifth part of this paper we review our studies of dopamine and dopamine/NMDA interactions in the control of synaptic function. Our results show that dopamine dramatically reduces the direct cortical input to CA1 (the perforant path input), while having little effect on the input from CA3. In order to interpret the functional consequences of this pathway-specific modulation, it is necessary to understand the function of CA1 and the role of dopaminergic input from the ventral tegmental area (VTA). In the sixth part of this paper we consider several possibilities and address the issue of how dopamine hyperfunction or NMDA hypofunction, abnormalities that may underlie schizophrenia, might lead to the symptoms of the disease. Relevant to this issue is the demonstrated role of the hippocampus in novelty detection, a function that is likely to depend on sequence recall by the hippocampus. Novelty signals are generated when reality does not match ...

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Dopamine action in the nucleus accumbens

Cited by 63 publications

References 0 publications

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

Dopamine gating of glutamatergic sensorimotor and incentive motivational input signals to the striatum

Dopaminergic Modulation of Prefrontal Cortical Input to Nucleus Accumbens NeuronsIn Vivo

Storage, recall, and novelty detection of sequences by the hippocampus: Elaborating on the SOCRATIC model to account for normal and aberrant effects of dopamine

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