Corticostriatal Interactions during Learning, Memory Processing, and Decision Making

Pennartz, Cyriel M. A.; Berke, Joshua D.; Graybiel, Ann M.; Ito, Rutsuko; Lansink, Carien S.; Meer, Matthijs A. A. van der; Redish, A. David; Smith, Karen; Voorn, Pieter

doi:10.1523/jneurosci.3177-09.2009

Cited by 192 publications

(135 citation statements)

References 111 publications

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“…This dissociation is similar to what is observed in the hippocampus (40). However, differently from the hippocampus, VS manipulations also impair responding to cues in auto-shaping, in Pavlovian-instrumental transfer, or in the early stages of instrumental conditioning, coherently with the high number of reward-responding neurons in this structure but not in the hippocampus (41).…”

Section: Discussionsupporting

confidence: 79%

Ventral striatal plasticity and spatial memory

Ferretti

Roullet

Sargolini

et al. 2010

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

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Spatial memory formation is a dynamic process requiring a series of cellular and molecular steps, such as gene expression and protein translation, leading to morphological changes that have been envisaged as the structural bases for the engram. Despite the role suggested for medial temporal lobe plasticity in spatial memory, recent behavioral observations implicate specific components of the striatal complex in spatial information processing. However, the potential occurrence of neural plasticity within this structure after spatial learning has never been investigated. In this study we demonstrate that blockade of cAMP response element binding protein-induced transcription or inhibition of protein synthesis or extracellular proteolytic activity in the ventral striatum impairs longterm spatial memory. These findings demonstrate that, in the ventral striatum, similarly to what happens in the hippocampus, several key molecular events crucial for the expression of neural plasticity are required in the early stages of spatial memory formation. T he formation of long-term memories is believed to involve a dynamic process by which a labile memory is progressively converted into a more stable and potentially permanent trace. Evidence for such a time-dependent process comes from studies demonstrating that electroconvulsive shock produces amnesia only if delivered shortly after learning, whereas the same treatment is ineffective when delivered several hours later (1). Long-term memory is accompanied by changes in neuronal morphology and connectivity, and these alterations are thought to be essential for the stabile encoding of new information (2). This transformation has been suggested to depend upon plastic changes that involve a sequence of specific and coordinated cellular processes. These begin with neurotransmitter receptor activation that induces shortterm changes in synaptic efficacy based on receptor phosphorylation and trafficking (3, 4). Subsequently, alterations in gene expression and protein synthesis occur that are the basis for longterm structural modifications (5, 6).A key issue in the study of memory in vertebrates is the brain site at which these processes occur. Clinical evidence in humans suggests that structures within the medial temporal lobe (MTL) play a prominent role in long-term memories. MTL lesions induce profound deficits in the formation of long-lasting declarative memories while sparing the acquisition of nondeclarative memories such as visual-motor skills (7,8). Such findings suggest that the hippocampus might be an essential site where plasticity occurs in the initial steps of declarative memory stabilization. Accordingly, those molecular events thought to be crucial for the long-term encoding of memories such as regulation of gene expression and protein synthesis, as well as structural changes, have been described in the hippocampus after spatial learning (6, 9, 10).Recent experimental evidence, however, demonstrates that structures different from the hippocampus might also be involved in ...

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Section: Discussionsupporting

confidence: 79%

Ventral striatal plasticity and spatial memory

Ferretti

Roullet

Sargolini

et al. 2010

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

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“…In reward memory formation, dopamine, in addition to enabling late-LTP, contributes to offline consolidation processes that continue after a stimulus-stimulus or stimulus-response learning and help better remember the learned association (Shohamy and Adcock, 2010;Wimber et al, 2011). Rodent research revealed that rewarded memories may be spontaneously reactivated during sleep, with a coordinated replay of neuronal activity in the hippocampus and in the striatum during slow-wave sleep Pennartz et al, 2009). Moreover, generation of outcome predictions is proposed to rely on synaptic plasticity mechanisms boosted during slow-wave sleep (SWS) ).…”

Section: Box 2: Role Of Sleep In the Consolidation And Generalizationmentioning

confidence: 99%

Influence of reward motivation on human declarative memory

Miendlarzewska

Bavelier

Schwartz

2016

Neuroscience & Biobehavioral Reviews

146

134

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a b s t r a c tMotivational relevance can prioritize information for memory encoding and consolidation based on reward value. In this review, we pinpoint the possible psychological and neural mechanisms by which reward promotes learning, from guiding attention to enhancing memory consolidation. We then discuss how reward value can spill-over from one conditioned stimulus to a non-conditioned stimulus. Such generalization can occur across perceptually similar items or through more complex relations, such as associative or logical inferences. Existing evidence suggests that the neurotransmitter dopamine boosts the formation of declarative memory for rewarded information and may also control the generalization of reward values. In particular, temporally-correlated activity in the hippocampus and in regions of the dopaminergic circuit may mediate value-based decisions and facilitate cross-item integration. Given the importance of generalization in learning, our review points to the need to study not only how reward affects later memory but how learned reward values may generalize to related representations and ultimately alter memory structure.

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“…Striatal dopamine release also plays a role in procedural and reinforcement learning [e.g., [104][105][106][107][108], owing to synaptic plasticity and remodeling. In terms of procedural learning, the Bassociative^portions of the caudate nucleus appear to be involved in early phases of learning, while the Bmotor^puta-men is more prominently engaged when animals execute previously learned movement sequences [109][110][111][112][113][114][115][116][117][118].…”

Section: Functional/anatomic Considerations Of the Basal Ganglia Circmentioning

confidence: 99%

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

2016

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Deep brain stimulation (DBS) is highly effective for both hypo-and hyperkinetic movement disorders of basal ganglia origin. The clinical use of DBS is, in part, empiric, based on the experience with prior surgical ablative therapies for these disorders, and, in part, driven by scientific discoveries made decades ago. In this review, we consider anatomical and functional concepts of the basal ganglia relevant to our understanding of DBS mechanisms, as well as our current understanding of the pathophysiology of two of the most commonly DBS-treated conditions, Parkinson's disease and dystonia. Finally, we discuss the proposed mechanism(s) of action of DBS in restoring function in patients with movement disorders. The signs and symptoms of the various disorders appear to result from signature disordered activity in the basal ganglia output, which disrupts the activity in thalamocortical and brainstem networks. The available evidence suggests that the effects of DBS are strongly dependent on targeting sensorimotor portions of specific nodes of the basal gangliathalamocortical motor circuit, that is, the subthalamic nucleus and the internal segment of the globus pallidus. There is little evidence to suggest that DBS in patients with movement disorders restores normal basal ganglia functions (e.g., their role in movement or reinforcement learning). Instead, it appears that high-frequency DBS replaces the abnormal basal ganglia output with a more tolerable pattern, which helps to restore the functionality of downstream networks.

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Corticostriatal Interactions during Learning, Memory Processing, and Decision Making

Cited by 192 publications

References 111 publications

Ventral striatal plasticity and spatial memory

Ventral striatal plasticity and spatial memory

Influence of reward motivation on human declarative memory

Deep Brain Stimulation for Movement Disorders of Basal Ganglia Origin: Restoring Function or Functionality?

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