The Hippocampal-VTA Loop: Controlling the Entry of Information into Long-Term Memory

Lisman, John; Grace, Anthony A.

doi:10.1016/j.neuron.2005.05.002

Cited by 1,681 publications

(1,737 citation statements)

References 99 publications

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“…As in animals (Lisman and Grace, 2005), also the human SN/VTA responds to stimulus novelty even in the absence of reward (Bunzeck and Duzel, 2006). These data provide evidence in favor of a recent model suggesting a functional hippocampal-SN/VTA loop of novelty processing and encoding (Lisman and Grace, 2005). Prefrontal dopaminergic neuromodulation is also held to be critical for attention (Robbins and Roberts, 2007) and for the ability to maintain and manipulate stimulus information online in working memory (Wang et al, 2004;Williams and Goldman-Rakic, 1995).…”

Section: Introductionmentioning

confidence: 72%

“…There is converging evidence that dopamine plays a role not only in reinforcement learning but also in hippocampus-dependent declarative memory formation (Adcock et al, 2006;Lisman and Grace, 2005;Schott et al, 2006;Wittmann et al, 2005). As in animals (Lisman and Grace, 2005), also the human SN/VTA responds to stimulus novelty even in the absence of reward (Bunzeck and Duzel, 2006).…”

Section: Introductionmentioning

confidence: 99%

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Basal forebrain integrity and cognitive memory profile in healthy aging

Düzel¹,

Münte²,

Lindenberger³

et al. 2010

Brain Research

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Age-related dysfunctions in cholinergic and dopaminergic neuromodulation are assumed to contribute to age-associated impairment of explicit memory. Both neurotransmitters also modulate attention, working memory, and processing speed. To date, in vivo evidence linking structural age-related changes in these neuromodulatory systems to dysfunction within or across these cognitive domains remains scarce. Using a factor analytical approach in a cross-sectional study including 86 healthy older (aged 55 to 83 years) and 24 young (aged 18 to 30 years) adults, we assessed the relationship between structural integrity-as measured by magnetization transfer ratio (MTR)-of the substantia nigra/ventral tegmental area (SN/VTA), main origin of dopaminergic projections, basal forebrain (major origin of cortical cholinergic projections), frontal white matter (FWM), and hippocampus to neuropsychological and psychosocial scores. Basal forebrain MTR and FWM changes correlated with a factor combining verbal learning and memory and working memory and, as indicated by measures of diffusion, were most likely due to vascular pathology. These findings suggest that frontal white matter integrity and cholinergic neuromodulation provide clues as to why age-related cognitive decline is often correlated across cognitive domains. IntroductionAge-related decline in learning and memory, often termed age-associated memory impairment (AAMI) (Crook et al., 1986), is a well-documented finding in healthy older adults (Balota et al., 2000;Cabeza et al., 2000;Craik, 1994;Salthouse, 2003), but the neurobiological correlates of this decline are still under debate. A consistent pattern of AAMI is a decrement in declarative memory (Tulving, 1985) most clearly apparent in impaired free recall and recollection (Buckner, 2004;Craik, 2006;Hedden and Gabrieli, 2004;Nilsson, 2003). Evidence from lesion studies in humans and animals indicates that

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Section: Introductionmentioning

confidence: 72%

Section: Introductionmentioning

confidence: 99%

Basal forebrain integrity and cognitive memory profile in healthy aging

Düzel¹,

Münte²,

Lindenberger³

et al. 2010

Brain Research

View full text Add to dashboard Cite

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“…Even though we demonstrated that hippocampaldependent spatial navigation is clearly preserved in DAT-KO mice, impaired DA transmission in the hippocampus could be involved in their initial delayed acquisition. The potential implication of the hippocampus in the observed deficits is further supported by a growing body of evidence demonstrating that both striatal and hippocampal systems interact intimately in various cognitive functions (Poldrack and Packard, 2003;Voermans et al, 2004), and that the hippocampus and the midbrain form a DA-dependent loop that contributes to the role of the hippocampus in novelty detection (Lisman and Grace, 2005). However, further molecular characterization of DA homeostasis within the hippocampal region of DAT-KO mice remains to be carried out.…”

Section: Discussionmentioning

confidence: 95%

Parallel Loss of Hippocampal LTD and Cognitive Flexibility in a Genetic Model of Hyperdopaminergia

Morice

Billard

Denis

et al. 2007

Neuropsychopharmacol

101

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Dopamine-mediated neurotransmission has been implicated in the modulation of synaptic plasticity and in the mechanisms underlying learning and memory. In the present study, we tested different forms of activity-dependent neuronal and behavioral plasticity in knockout mice for the dopamine transporter (DAT-KO), which constitute a unique genetic model of constitutive hyperdopaminergia. We report that DAT-KO mice exhibit slightly increased long-term potentiation and severely decreased long-term depression at hippocampal CA3-CA1 excitatory synapses. Mutant mice also show impaired adaptation to environmental changes in the Morris watermaze. Both the electrophysiological and behavioral phenotypes are reversed by the dopamine antagonist haloperidol, suggesting that hyperdopaminergia is involved in these deficits. These findings support the modulation by dopamine of synaptic plasticity and cognitive flexibility. The behavioral deficits seen in DAT-KO mice are reminiscent of the deficits in executive functions observed in dopamine-related neuropsychiatric disorders, suggesting that the study of DAT-KO mice can contribute to the understanding of the molecular basis of these disorders.

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“…A large number of animal studies indicates that memory performance is impaired when dopamine (DA) receptors are blocked and enhanced when DA agonists are injected in hippocampus (for review, see Lisman and Grace, 2005). DA prolongs long-term potentiation (LTP; Frey et al, 1990Frey et al, , 1993Huang and Kandel, 1995), a cellular mechanism necessary for successful memory formation and consolidation (for review, see Cooke and Bliss, 2006).…”

Section: Dopaminergic Modulation Of Episodic Memorymentioning

confidence: 99%

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

Papenberg¹,

Li²,

Nagel³

et al. 2014

Neurobiology of Aging

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a b s t r a c tBoth the dopaminergic and glutamatergic systems modulate episodic memory consolidation. Evidence from animal studies suggests that these two neurotransmitters may interact in influencing memory performance. Given that individual differences in episodic memory are heritable, we investigated whether variations of the dopamine D2 receptor gene (rs6277, C957T) and the N-methyl-D-aspartate 3A (NR3A) gene, coding for the N-methyl-D-aspartate 3A subunit of the glutamate N-methyl-D-aspartate receptor (rs10989591, Val362Met), interactively modulate episodic memory in large samples of younger (20e31 years; n ¼ 670) and older (59e71 years; n ¼ 832) adults. We found a reliable gene-gene interaction, which was observed in older adults only: older individuals carrying genotypes associated with greater D2 and N-methyl-D-aspartate receptor efficacy showed better episodic performance. These results are in line with findings showing magnification of genetic effects on memory in old age, presumably as a consequence of reduced brain resources. Our findings underscore the need for investigating interactive effects of multiple genes to understand individual difference in episodic memory.

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The Hippocampal-VTA Loop: Controlling the Entry of Information into Long-Term Memory

Cited by 1,681 publications

References 99 publications

Basal forebrain integrity and cognitive memory profile in healthy aging

Basal forebrain integrity and cognitive memory profile in healthy aging

Parallel Loss of Hippocampal LTD and Cognitive Flexibility in a Genetic Model of Hyperdopaminergia

Dopamine and glutamate receptor genes interactively influence episodic memory in old age

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