Dopamine D1-deficient mutant mice do not express the late phase of hippocampal long-term potentiation

Matthies, H; Becker, Axel; Schroeder, Helmut; Kraus, Jürgen; Höllt, Volker; Krug, Manfred

doi:10.1097/00001756-199711100-00023

Cited by 96 publications

(58 citation statements)

References 12 publications

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“…At 100 min, LTP was 121 Ϯ 6% (n ϭ 7) in SCH23390-treated slices and 162 Ϯ 5% in control slices (n ϭ 7, P Ͻ 0.01). Considered together, these results suggest that the activation of D1 receptor is mainly involved in the late maintenance of LTP, which is consistent with the effects of D1 receptor inhibition of Schaffer-collateral LTP in the hippocampal slices (19,20). The D2-type receptor antagonist sulpiride (50 M) had no affect on LTP (Fig.…”

Section: D1 But Not D2 Receptors Are Involved In the Maintenance Ofsupporting

confidence: 86%

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors

Huang

Simpson

Kellendonk

et al. 2004

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

210

169

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To address the role of D1 receptors in the medial prefrontal cortex, we combined pharmacological and genetic manipulations to examine long-term synaptic potentiation (LTP)͞long-term synaptic depression (LTD) in brain slices of rats and mice. We found that the D1 antagonist SCH23390 selectively blocked the maintenance but not the induction of LTP in the prefrontal cortex. Conversely, activation of D1 receptors facilitated the maintenance of LTP, and this effect is impaired in heterozygous D1 receptor knockout mice. Low-frequency stimulation induced a transient depression in the medial prefrontal cortex. This depression could be transformed into LTD by coapplication of dopamine. Coapplication of dopamine, however, shows no facilitating effect on LTD in heterozygous D1 receptor knockout mice. These results provide pharmacological and genetic evidence for a role of D1 receptors in the bidirectional modulation of synaptic plasticity in the medial prefrontal cortex. The absence of this modulation in heterozygous knockout mice shows that a dysregulation of dopamine receptor expression levels can have dramatic effects on synaptic plasticity in the prefrontal cortex.T he prefrontal cortex is thought to be the highest association area in the mammalian cortex and is required for proper executive control. In primates the dorsolateral prefrontal cortex, alone, has been implicated in several different, partly overlapping, cognitive processes, including inhibitory control, working memory, selective attention, attentional-set shifting, rule learning, and strategy switching. In rodents, where the architecture of the cortex is simpler than that of primates, the medial prefrontal cortex (mPFC), the cortex that encompasses the infralimbic and prelimbic areas, is considered to be homologous to the primate dorsolateral prefrontal cortex (1, 2).Consistent with this homology, a variety of studies have shown that dopamine modulates neuronal activity in the prefrontal cortex and affects working memory, attentional performance, attentional-set shifting, and strategy switching (3-9). Some functions of mPFC, such as strategy shifting or rule learning, may be affected by dopaminergic modulation of long-term synaptic plasticity. Dopamine indeed affects long-term plasticity in the prefrontal cortex. It facilitates long-term synaptic depression (LTD) via D1 and D2 receptors (10, 11), and D1 activation has been shown to be required for N-methyl-D-aspartate (NMDA) receptor-dependent long-term synaptic potentiation (LTP) at hippocampal-prefrontal cortex synapses (12).To further our understanding of how dopamine modulates long-term synaptic plasticity in opposite directions, and to develop a model for exploring the underlying molecular signaling pathways, we examined LTP and LTD in slices of the mPFC from rats, wild-type mice, and heterozygous dopamine D1 receptor knockout mice. Heterozygous D1 receptor knockout mice show a 50% reduction in receptor number. They allow us to address specifically the function of the D1 receptor as opposed to both D1 ...

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Section: D1 But Not D2 Receptors Are Involved In the Maintenance Ofsupporting

confidence: 86%

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors

Huang

Simpson

Kellendonk

et al. 2004

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

210

169

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“…In this context, we concluded that D1R plays an important role in detecting spatial novelty encoded by spatial representations of hippocampal place cells, a prerequisite for spatial learning. The present work together with other recent studies (Gasbarri et al, 1996;Matthies et al, 1997;Otmakhova and Lisman, 1996;El-Ghundi et al, 1999;Swanson-Park et al, 1999;Wilkerson and Levin, 1999;Tran et al, 2002Tran et al, , 2005Li et al, 2003;Kentros et al, 2004;Gill and Mizumori, 2006;Stuchlik and Vales, 2006) should help significantly in revealing the mechanisms underlying the involvement of dopamine in learning and memory, from the molecular, to the neuronal, to the behavioral level.…”

Section: Discussionmentioning

confidence: 56%

“…It was found that dopamine D 1 receptor knock-out (D1R-KO) mice had impaired spatial learning and altered spatial activity in the nucleus accumbens (El-Ghundi et al, 1999, Tran et al, 2005. Since dopamine modulates hippocampal synaptic plasticity (Otmakhova and Lisman, 1996;Matthies et al, 1997;Swanson-Park et al, 1999;Li et al, 2003), it is hypothesized that the acquisition of spatial representations in the hippocampus is impaired in D1R-KO mice. The present study tested this hypothesis by comparing place-cell activity in D1R-KO and wild-type (WT) mice in response to spatial cue manipulations in familiar and novel environments.…”

Section: Introductionmentioning

confidence: 99%

Dopamine D₁Receptor Modulates Hippocampal Representation Plasticity to Spatial Novelty

Tran¹,

Uwano²,

Kimura³

et al. 2008

J. Neurosci.

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The human hippocampus is critical for learning and memory. In rodents, hippocampal pyramidal neurons fire in a location-specific manner, forming relational representations of environmental cues. The importance of glutamatergic systems in learning and in hippocampal neural synaptic plasticity has been shown. However, the role of dopaminergic systems in the response of hippocampal neural plasticity to novel and familiar spatial stimuli remains unclear. To clarify this important issue, we recorded hippocampal neurons from dopamine D 1 receptor knock-out (D1R-KO) mice and their wild-type (WT) littermates under the manipulation of distinct spatial cues in a familiar and a novel environment. Here we report that in WT mice, the majority of place cells quickly responded to the manipulations of distal and proximal cues in both familiar and novel environments. In contrast, the influence of distal cues on spatial firing in D1R-KO mice was abolished. In the D1R-KO mice, the influence of proximal cues was facilitated in a familiar environment, and in a novel environment most of the place cells were less likely to respond to changes of spatial cues. Our results demonstrate that hippocampal neurons in mice can rapidly and flexibly encode information about space from both distal and proximal cues to cipher a novel environment. This ability is necessary for many types of learning, and lacking D1R can radically alter this learning-related neural activity. We propose that D1R is crucially implicated in encoding spatial information in novel environments, and influences the plasticity of hippocampal representations, which is important in spatial learning and memory.

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“…Also, there are experimental data supporting the existence of dopamine D1/D5 receptor-NMDA receptor interactions involving plastic changes in hippocampal excitatory synaptic transmission. Thus, D1/ D5 receptors appear to play an important role in the hippocampal "late phase" long-term potentiation (L-LTP) (Frey et al 1993;Huang and Kandel 1995;Matthies et al 1997). The present findings show that, in addition to the VTA and the nucleus accumbens (see introduction), the VH is an important locus of interaction between dopamine and glutamate in relation to the control of motor activity.…”

Section: Discussionmentioning

confidence: 99%

Local Dopaminergic Modulation of the Motor Activity Induced by N-methyl-D-aspartate Receptor Stimulation in the Ventral Hippocampus

Wang

Ögren

Ferré

2002

Neuropsychopharmacology

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Dopaminergic neurotransmission has been implicated in the motor activating effects induced by the local infusion of NMDA in the ventral hippocampus (VH). The nucleus accumbens and the ventral tegmental area (VTA) have been proposed to be the main loci where dopamine is acting as a positive modulator of the VH NMDA receptor-mediated motor activating effects. However, the existence of a relatively high dopamine innervation and dopamine receptor density in the VH suggests the possibility of local dopamine/NMDA receptor interactions. This hypothesis was tested by studying the effects of the bilateral local VH infusion of NMDA (0.05, 0.1, 0.5 and 1.0 g/side), the dopamine D1/D5 receptor antagonist SCH 23390 (1 g/side) and the dopamine D2 receptor antagonist raclopride (1 and 5 g/side). Neither SCH 23390 nor raclopride induced any significant change in motor activity compared with the vehicle control group, but both compounds significantly antagonized the motor activation induced by NMDA. SCH 23390 (1 g/side) was more potent that raclopride (minimal effective dose: 5 g/side). These results demonstrate the existence of a strong tonic facilitating effect of dopamine, acting preferentially at dopamine D1/D5 receptors, on NMDA receptor-mediated effects in the VH.

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Dopamine D1-deficient mutant mice do not express the late phase of hippocampal long-term potentiation

Cited by 96 publications

References 12 publications

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors

Dopamine D₁Receptor Modulates Hippocampal Representation Plasticity to Spatial Novelty

Local Dopaminergic Modulation of the Motor Activity Induced by N-methyl-D-aspartate Receptor Stimulation in the Ventral Hippocampus

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Dopamine D1-deficient mutant mice do not express the late phase of hippocampal long-term potentiation

Cited by 96 publications

References 12 publications

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors

Genetic evidence for the bidirectional modulation of synaptic plasticity in the prefrontal cortex by D1 receptors

Dopamine D1Receptor Modulates Hippocampal Representation Plasticity to Spatial Novelty

Local Dopaminergic Modulation of the Motor Activity Induced by N-methyl-D-aspartate Receptor Stimulation in the Ventral Hippocampus

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Dopamine D₁Receptor Modulates Hippocampal Representation Plasticity to Spatial Novelty