AMPA receptor antagonists reverse effects of extended habit training on signaled food approach responding in rats

Bespalov, Anton; Harich, Silke; Jongen-Rêlo, Ana-Lucia; Gaalen, Marcel M. van; Groß, Gerhard

doi:10.1007/s00213-007-0875-z

Cited by 8 publications

(9 citation statements)

References 24 publications

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“…Following similar suggestions in the literature (Ashby, Alfonso-Reese, Turken, & Waldron, 1998;Miller, 1981Miller, , 1988, Ashby et al (2007) proposed a model in which the development of automaticity is mediated by a transfer of control from the cortical-striatal pathways emphasized here to cortical-cortical pathways from the relevant areas of sensory cortex to the areas of premotor and motor cortices that mediate the selection and execution of the appropriate motor program. For example, several studies have reported evidence that with overtraining, skills of the type modeled here become independent of both dopamine and the striatum (e.g., Bespalov, Harich, Jongen-Rêlo, van Gaalen, & Gross, 2007;Choi, Balsam, & Horvitz, 2005;Turner, McCairn, Simmons, & Bar-Gad, 2005;Carelli et al, 1997). It would be straightforward to augment the present model with the cortical-cortical pathways proposed by Ashby et al (with cortical-cortical plasticity mediated by Hebbian learning).…”

Section: Limitationsmentioning

confidence: 72%

A Computational Model of How Cholinergic Interneurons Protect Striatal-dependent Learning

Ashby

Crossley²

2011

Journal of Cognitive Neuroscience

109

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An essential component of skill acquisition is learning the environmental conditions in which that skill is relevant. This article proposes and tests a neurobiologically detailed theory of how such learning is mediated. The theory assumes that a key component of this learning is provided by the cholinergic interneurons in the striatum known as tonically active neurons (TANs). The TANs are assumed to exert a tonic inhibitory influence over cortical inputs to the striatum that prevents the execution of any striatal-dependent actions. The TANs learn to pause in rewarding environments, and this pause releases the striatal output neurons from this inhibitory effect, thereby facilitating the learning and expression of striatal-dependent behaviors. When rewards are no longer available, the TANs cease to pause, which protects striatal learning from decay. A computational version of this theory accounts for a variety of single-cell recording data and some classic behavioral phenomena, including fast reacquisition after extinction.

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Section: Limitationsmentioning

confidence: 72%

A Computational Model of How Cholinergic Interneurons Protect Striatal-dependent Learning

Ashby

Crossley²

2011

Journal of Cognitive Neuroscience

109

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“…The goal-directed and habit systems are conceived of as competitors for the control of behavior – the system that is least uncertain about the appropriate behavior given the context may win that competition (Daw et al , 2005). Competition between them can be biased towards the habit system by extended behavioral training (Adams, 1981); boosting synaptic dopamine levels in the striatum (Nelson and Killcross, 2006), or modulating AMPA receptor function (Bespalov et al , 2007). Goal directedness can be rescued by restoring dopamine induced plasticity in the prefrontal cortex (Hitchcott et al , 2007).…”

Section: Explaining Delusion Contentmentioning

confidence: 99%

“…If delusions are learned habits, then pharmacological interventions that restore goal directedness should be effective therapeutically; for example, antagonizing AMPA receptors (Bespalov et al , 2007), boosting PFC dopamine levels (Hitchcott et al , 2007) and attenuating striatal dopamine (Nelson and Killcross, 2006) should favor plasticity and goal directedness. The dopamine partial agonist Aripiprazole combines both antagonism of elevated striatal dopamine and an elevation of attenuated prefrontal dopamine and may specifically target aberrant prediction error signaling in midbrain dopamine neurons (Hamamura and Harada, 2007).…”

Section: Testing the Hypothesismentioning

confidence: 99%

Toward a neurobiology of delusions

Corlett

Taylor

Wang³

et al. 2010

Progress in Neurobiology

352

380

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Delusions are the false and often incorrigible beliefs that can cause severe suffering in mental illness. We cannot yet explain them in terms of underlying neurobiological abnormalities. However, by drawing on recent advances in the biological, computational and psychological processes of reinforcement learning, memory, and perception it may be feasible to account for delusions in terms of cognition and brain function. The account focuses on a particular parameter, prediction error – the mismatch between expectation and experience – that provides a computational mechanism common to cortical hierarchies, frontostriatal circuits and the amygdala as well as parietal cortices. We suggest that delusions result from aberrations in how brain circuits specify hierarchical predictions, and how they compute and respond to prediction errors. Defects in these fundamental brain mechanisms can vitiate perception, memory, bodily agency and social learning such that individuals with delusions experience an internal and external world that healthy individuals would find difficult to comprehend. The present model attempts to provide a framework through which we can build a mechanistic and translational understanding of these puzzling symptoms.

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“…For example, some Parkinson's patients are able to emit an automatic motor response when presented with a familiar visual cue (e.g., kicking a ball), despite difficulties in initiating novel voluntary movements [45]. As another example, blockade of D1 receptors strongly disrupts rats' performance of a simple Pavlovian approach response to a sensory cue during early stages of training, but has little or no disruptive effect in rats that receive extended training prior to dopamine antagonist challenge [46–47]. …”

Section: Dopamine and Habit Expressionmentioning

confidence: 99%

Cortical and basal ganglia contributions to habit learning and automaticity

Ashby

Turner

Horvitz

2010

Trends in Cognitive Sciences

434

363

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The 20th century was dominated by the view that novel behaviors are mediated primarily in cortex and that the development of automaticity is a process of transferring control to subcortical structures. Much evidence suggests however, that subcortical structures, such as the striatum, make significant contributions to initial learning. More recently, evidence has been accumulating that neurons in the associative striatum are selectively activated during early learning, whereas those in the sensorimotor striatum are more active after automaticity has developed. At the same time, other recent reports suggest that automatic behaviors are striatum- and dopamine-independent, and may be mediated entirely within cortex. Resolving this apparent conflict should be a major goal of future research.

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AMPA receptor antagonists reverse effects of extended habit training on signaled food approach responding in rats

Abstract: These results indicate that AMPA receptor blockade restores sensitivity to appetitive behavior-disrupting effects of SCH-23390 in subjects exposed to extended training protocol.

Cited by 8 publications

References 24 publications

A Computational Model of How Cholinergic Interneurons Protect Striatal-dependent Learning

A Computational Model of How Cholinergic Interneurons Protect Striatal-dependent Learning

Toward a neurobiology of delusions

Cortical and basal ganglia contributions to habit learning and automaticity

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