Faculty Opinions recommendation of Neurophysiology of rule switching in the corticostriatal circuit.

Abstract Probabilistic reward learning reflects the ability to adapt choices based on probabilistic feedback. The dopaminergically innervated corticostriatal circuit in the brain plays an important role in supporting successful probabilistic reward learning. Several components of the corticostriatal circuit deteriorate with age, as it does probabilistic reward learning. We showed previously that D1 receptor availability in NAcc predicts the strength of anticipatory value signaling in vmPFC, a neural correlate of probabilistic learning that is attenuated in older participants and predicts probabilistic reward learning performance. We investigated how white matter integrity in the pathway between nucleus accumbens (NAcc) and ventromedial prefrontal cortex (vmPFC) relates to the strength of anticipatory value signaling in vmPFC in younger and older participants. We found that in a sample of 22 old and 23 young participants, fractional anisotropy in the pathway between NAcc and vmPFC predicted the strength of value signaling in vmPFC independently from D1 receptor availability in NAcc. These findings provide tentative evidence that integrity in the dopaminergic and white matter pathways of corticostriatal circuitry supports the expression of value signaling in vmPFC which supports reward learning, however, the limited sample size calls for independent replication. These and future findings could add to the improved understanding of how corticostriatal integrity contributes to reward learning ability.

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A plastic corticostriatal circuit model of adaptation in perceptual decision making

Frontiers in Computational Neuroscience ◽

10.3389/fncom.2013.00178 ◽

2013 ◽

Vol 7 ◽

Cited By ~ 4

Author(s):

Pao-Yueh Hsiao

Keyword(s):

Decision Making ◽

Circuit Model ◽

Perceptual Decision Making ◽

Perceptual Decision ◽

Corticostriatal Circuit

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Corticostriatal circuit dysfunction in Huntington’s disease: intersection of glutamate, dopamine and calcium

Future Neurology ◽

10.2217/fnl.10.41 ◽

2010 ◽

Vol 5 (5) ◽

pp. 735-756 ◽

Cited By ~ 40

Author(s):

Benjamin Ray Miller ◽

Ilya Bezprozvanny

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Corticostriatal Circuit

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Erratum: Corticostriatal circuit defects in Hoxb8 mutant mice

Molecular Psychiatry ◽

10.1038/mp.2017.251 ◽

2017 ◽

Cited By ~ 3

Author(s):

N Nagarajan ◽

B W Jones ◽

P J West ◽

R E Marc ◽

M R Capecchi

Keyword(s):

Mutant Mice ◽

Circuit Defects ◽

Corticostriatal Circuit

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Type III Neuregulin-1 Is Required for Normal Sensorimotor Gating, Memory-Related Behaviors, and Corticostriatal Circuit Components

Journal of Neuroscience ◽

10.1523/jneurosci.1815-08.2008 ◽

2008 ◽

Vol 28 (27) ◽

pp. 6872-6883 ◽

Cited By ~ 141

Author(s):

Y.-J. J. Chen ◽

M. A. Johnson ◽

M. D. Lieberman ◽

R. E. Goodchild ◽

S. Schobel ◽

...

Keyword(s):

Sensorimotor Gating ◽

Neuregulin 1 ◽

Type Iii ◽

Circuit Components ◽

Corticostriatal Circuit

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TRiC subunits enhance BDNF axonal transport and rescue striatal atrophy in Huntington’s disease

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1603020113 ◽

2016 ◽

Vol 113 (38) ◽

pp. E5655-E5664 ◽

Cited By ~ 37

Author(s):

Xiaobei Zhao ◽

Xu-Qiao Chen ◽

Eugene Han ◽

Yue Hu ◽

Paul Paik ◽

...

Keyword(s):

Huntington's Disease ◽

Huntington’S Disease ◽

Cortical Neurons ◽

Striatal Neurons ◽

Anterograde Transport ◽

T Complex ◽

Ring Complex ◽

Microfluidic Chambers ◽

Tyrosine Receptor Kinase ◽

Corticostriatal Circuit

Corticostriatal atrophy is a cardinal manifestation of Huntington’s disease (HD). However, the mechanism(s) by which mutant huntingtin (mHTT) protein contributes to the degeneration of the corticostriatal circuit is not well understood. We recreated the corticostriatal circuit in microfluidic chambers, pairing cortical and striatal neurons from the BACHD model of HD and its WT control. There were reduced synaptic connectivity and atrophy of striatal neurons in cultures in which BACHD cortical and striatal neurons were paired. However, these changes were prevented if WT cortical neurons were paired with BACHD striatal neurons; synthesis and release of brain-derived neurotrophic factor (BDNF) from WT cortical axons were responsible. Consistent with these findings, there was a marked reduction in anterograde transport of BDNF in BACHD cortical neurons. Subunits of the cytosolic chaperonin T-complex 1 (TCP-1) ring complex (TRiC or CCT for chaperonin containing TCP-1) have been shown to reduce mHTT levels. Both CCT3 and the apical domain of CCT1 (ApiCCT1) decreased the level of mHTT in BACHD cortical neurons. In cortical axons, they normalized anterograde BDNF transport, restored retrograde BDNF transport, and normalized lysosomal transport. Importantly, treating BACHD cortical neurons with ApiCCT1 prevented BACHD striatal neuronal atrophy by enhancing release of BDNF that subsequently acts through tyrosine receptor kinase B (TrkB) receptor on striatal neurons. Our findings are evidence that TRiC reagent-mediated reductions in mHTT enhanced BDNF delivery to restore the trophic status of BACHD striatal neurons.

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Corticostriatal oscillations predict high vs. low drinkers in a preclinical model of limited access alcohol consumption

10.1101/293597 ◽

2018 ◽

Author(s):

Angela M. Henricks ◽

Lucas L. Dwiel ◽

Nicholas H. Deveau ◽

Amanda A. Simon ◽

Metztli J. Ruiz-Jaquez ◽

...

Keyword(s):

Alcohol Consumption ◽

Alcohol Dependence ◽

Drinking Behavior ◽

Clinical Population ◽

Preclinical Model ◽

Sprague Dawley ◽

Nucleus Accumbens Shell ◽

Limited Access ◽

The Impact ◽

Corticostriatal Circuit

AbstractIndividuals differ in their vulnerability to develop alcohol dependence that are determined by innate and environmental factors. The corticostriatal circuit is heavily involved in the development of alcohol dependence and may contain neural information regarding vulnerability to drink excessively. In the current experiment, we hypothesized that we could characterize high and low alcohol-drinking rats (HD and LD, respectively) based on corticostriatal oscillations, and that these subgroups would differentially respond to corticostriatal brain stimulation. Rats were trained to drink 10% alcohol in a limited access paradigm. In separate sessions, local field potentials (LFPs) were recorded from the nucleus accumbens shell (NAcSh) and medial prefrontal cortex (mPFC) of male Sprague-Dawley rats (n=13). Based on training alcohol consumption levels, we classified rats using a median split as HD or LD. Then, using machine-learning, we built predictive models to classify rats as HD or LD by corticostriatal LFPs and compared the model performance from real data to the performance of models built on data permutations. Additionally, we explored the impact of NAcSh or mPFC stimulation on alcohol consumption in HD vs. LD. Corticostriatal LFPs were able predict HD vs. LD group classification with greater accuracy than expected by chance (>80% accuracy). Additionally, NAcSh stimulation significantly reduced alcohol consumption in HD, but not LD (p<0.05), while mPFC stimulation did not alter drinking behavior in either HD or LD (p>0.05). These data collectively show that the corticostriatal circuit is differentially involved in regulating alcohol intake in HD vs. LD rats, and suggests that corticostriatal activity may have the potential to predict a vulnerability to develop alcohol dependence in a clinical population.

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