scholarly journals Common coding of expected value and value uncertainty memories in the prefrontal cortex and basal ganglia output

2021 ◽  
Vol 7 (20) ◽  
pp. eabe0693
Author(s):  
Ali Ghazizadeh ◽  
Okihide Hikosaka
Keyword(s):  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Cortical Neurons ◽  
Expected Value ◽  
Common Coding ◽  
Repetition Suppression ◽  
Free Viewing ◽  
Gaze Bias ◽  
Single Unit Recordings ◽  
Value Preferences

Recent evidence implicates both basal ganglia and ventrolateral prefrontal cortex (vlPFC) in encoding value memories. However, comparative roles of cortical and basal nodes in value memory are not well understood. Here, single-unit recordings in vlPFC and substantia nigra reticulata (SNr), within macaque monkeys, revealed a larger value signal in SNr that was nevertheless correlated with and had a comparable onset to the vlPFC value signal. The value signal was maintained for many objects (>90) many weeks after reward learning and was resistant to extinction in both regions and to repetition suppression in vlPFC. Both regions showed comparable granularity in encoding expected value and value uncertainty, which was paralleled by enhanced gaze bias during free viewing. The value signal dynamics in SNr could be predicted by combining responses of vlPFC neurons according to their value preferences consistent with a scheme in which cortical neurons reached SNr via direct and indirect pathways.

Pathology, Phenomenology and the Dopamine Hypothesis of Schizophrenia

1987 ◽  
Vol 151 (3) ◽  
pp. 288-301 ◽  
Author(s):  
P. J. McKenna
Keyword(s):  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Functional Role ◽  
Ventral Striatum ◽  
Brain Structures ◽  
Schizophrenic Symptom ◽  
Dopamine Hypothesis ◽  
Dopamine Innervation

The dopamine hypothesis of schizophrenia implies that positive schizophrenic symptoms should be understandable by reference to brain structures receiving a dopamine innervation, or in terms of the functional role of dopamine itself. The basal ganglia, ventral striatum, septo-hippocampal system, and prefrontal cortex, sites of mesotelencephalic dopamine innervation, are examined and it is argued that their dysfunction could form the basis of particular schizophrenic symptom classes. The postulated involvement of dopamine in reinforcement processes might further assist such interpretations. This type of analysis can be extended to other categories of schizophrenic psychopathology.

scholarly journals The NKCC1 antagonist bumetanide mitigates interneuronopathy associated with ethanol exposure in utero

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Alexander GJ Skorput ◽  
Stephanie M Lee ◽  
Pamela WL Yeh ◽  
Hermes H Yeh
Keyword(s):  
Prefrontal Cortex ◽  
Cortical Neurons ◽  
Fetal Alcohol Spectrum Disorders ◽  
Behavioral Flexibility ◽  
Ethanol Exposure ◽  
Embryonic Mouse ◽  
Form And Function ◽  
Tangential Migration ◽  
And Function

Prenatal exposure to ethanol induces aberrant tangential migration of corticopetal GABAergic interneurons, and long-term alterations in the form and function of the prefrontal cortex. We have hypothesized that interneuronopathy contributes significantly to the pathoetiology of fetal alcohol spectrum disorders (FASD). Activity-dependent tangential migration of GABAergic cortical neurons is driven by depolarizing responses to ambient GABA present in the cortical enclave. We found that ethanol exposure potentiates the depolarizing action of GABA in GABAergic cortical interneurons of the embryonic mouse brain. Pharmacological antagonism of the cotransporter NKCC1 mitigated ethanol-induced potentiation of GABA depolarization and prevented aberrant patterns of tangential migration induced by ethanol in vitro. In a model of FASD, maternal bumetanide treatment prevented interneuronopathy in the prefrontal cortex of ethanol exposed offspring, including deficits in behavioral flexibility. These findings position interneuronopathy as a mechanism of FASD symptomatology, and posit NKCC1 as a pharmacological target for the management of FASD.

Towards a Neuropsychology of Schizophrenia

1988 ◽  
Vol 153 (4) ◽  
pp. 437-443 ◽  
Author(s):  
Christopher D. Frith ◽  
D. John Done
Keyword(s):  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Signs And Symptoms ◽  
Cingulate Cortex ◽  
Positive Symptoms ◽  
Psychological Processes ◽  
Parahippocampal Cortex ◽  
Spontaneous Action ◽  
Underlying Processes

A viable neuropsychology of schizophrenia requires, first, that signs and symptoms be understood in terms of underlying psychological processes and, second, that these underlying processes be related to brain systems. We propose that the negative signs of schizophrenia reflect a defect in the initiation of spontaneous action, while the positive symptoms reflect a defect in the internal monitoring of action. The spontaneous initiation of action depends upon brain systems linking the prefrontal cortex and the basal ganglia. Internal monitoring, carried out in the hippocampus, of spontaneous action, depends upon links between the prefrontal cortex and the hippocampus via the parahippocampal cortex and the cingulate cortex.

scholarly journals Spontaneous dynamics of neural networks in deep layers of prefrontal cortex

2017 ◽  
Vol 117 (4) ◽  
pp. 1581-1594 ◽  
Author(s):  
Andrew S. Blaeser ◽  
Barry W. Connors ◽  
Arto V. Nurmikko
Keyword(s):  
Prefrontal Cortex ◽  
Spontaneous Activity ◽  
Calcium Imaging ◽  
Cortical Neurons ◽  
Rhythmic Activity ◽  
Network Activity ◽  
Local Networks ◽  
Spatiotemporal Scale ◽  
Deep Layers ◽  
Delta Oscillations

Cortical systems maintain and process information through the sustained activation of recurrent local networks of neurons. Layer 5 is known to have a major role in generating the recurrent activation associated with these functions, but relatively little is known about its intrinsic dynamics at the mesoscopic level of large numbers of neighboring neurons. Using calcium imaging, we measured the spontaneous activity of networks of deep-layer medial prefrontal cortical neurons in an acute slice model. Inferring the simultaneous activity of tens of neighboring neurons, we found that while the majority showed only sporadic activity, a subset of neurons engaged in sustained delta frequency rhythmic activity. Spontaneous activity under baseline conditions was weakly correlated between pairs of neurons, and rhythmic neurons showed little coherence in their oscillations. However, we consistently observed brief bouts of highly synchronous activity that must be attributed to network activity. NMDA-mediated stimulation enhanced rhythmicity, synchrony, and correlation within these local networks. These results characterize spontaneous prefrontal activity at a previously unexplored spatiotemporal scale and suggest that medial prefrontal cortex can act as an intrinsic generator of delta oscillations. NEW & NOTEWORTHY Using calcium imaging and a novel analytic framework, we characterized the spontaneous and NMDA-evoked activity of layer 5 prefrontal cortex at a largely unexplored spatiotemporal scale. Our results suggest that the mPFC microcircuitry is capable of intrinsically generating delta oscillations and sustaining synchronized network activity that is potentially relevant for understanding its contribution to cognitive processes.

scholarly journals Relationships between the Prefrontal Cortex and the Basal Ganglia in the Rat: Physiology of the Cortico-Nigral Circuits

1999 ◽  
Vol 19 (11) ◽  
pp. 4674-4681 ◽  
Author(s):  
Nicolas Maurice ◽  
Jean-Michel Deniau ◽  
Jacques Glowinski ◽  
Anne-Marie Thierry
Keyword(s):  
Prefrontal Cortex ◽  
Basal Ganglia

scholarly journals Making Working Memory Work: A Computational Model of Learning in the Prefrontal Cortex and Basal Ganglia

2006 ◽  
Vol 18 (2) ◽  
pp. 283-328 ◽  
Author(s):  
Randall C. O'Reilly ◽  
Michael J. Frank
Keyword(s):  
Working Memory ◽  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Computational Model ◽  
Computational Models ◽  
Memory Task ◽  
Learning Mechanisms ◽  
Subcortical Structures ◽  
Credit Assignment ◽  
Gating Mechanism

The prefrontal cortex has long been thought to subserve both working memory (the holding of information online for processing) and executive functions (deciding how to manipulate working memory and perform processing). Although many computational models of working memory have been developed, the mechanistic basis of executive function remains elusive, often amounting to a homunculus. This article presents an attempt to deconstruct this homunculus through powerful learning mechanisms that allow a computational model of the prefrontal cortex to control both itself and other brain areas in a strategic, task-appropriate manner. These learning mechanisms are based on subcortical structures in the midbrain, basal ganglia, and amygdala, which together form an actor-critic architecture. The critic system learns which prefrontal representations are task relevant and trains the actor, which in turn provides a dynamic gating mechanism for controlling working memory updating. Computationally, the learning mechanism is designed to simultaneously solve the temporal and structural credit assignment problems. The model's performance compares favorably with standard backpropagation-based temporal learning mechanisms on the challenging 1-2-AX working memory task and other benchmark working memory tasks.

scholarly journals Human subthalamic nucleus activity during non-motor decision making

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Baltazar A Zavala ◽  
Anthony I Jang ◽  
Kareem A Zaghloul
Keyword(s):  
Decision Making ◽  
Working Memory ◽  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Subthalamic Nucleus ◽  
Motor Function ◽  
Beta Band ◽  
Daily Lives ◽  
Motor Actions ◽  
Shed Light

Recent studies have implicated the subthalamic nucleus (STN) in decisions that involve inhibiting movements. Many of the decisions that we make in our daily lives, however, do not involve any motor actions. We studied non-motor decision making by recording intraoperative STN and prefrontal cortex (PFC) electrophysiology as participants perform a novel task that required them to decide whether to encode items into working memory. During all encoding trials, beta band (15–30 Hz) activity decreased in the STN and PFC, and this decrease was progressively enhanced as more items were stored into working memory. Crucially, the STN and lateral PFC beta decrease was significantly attenuated during the trials in which participants were instructed not to encode the presented stimulus. These changes were associated with increase lateral PFC-STN coherence and altered STN neuronal spiking. Our results shed light on why states of altered basal ganglia activity disrupt both motor function and cognition.

scholarly journals The Role of Intact Frontostriatal Circuits in Error Processing

2006 ◽  
Vol 18 (4) ◽  
pp. 651-664 ◽  
Author(s):  
Markus Ullsperger ◽  
D. Yves von Cramon
Keyword(s):  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Anterior Cingulate Cortex ◽  
Performance Monitoring ◽  
Brain Plasticity ◽  
Cingulate Cortex ◽  
Anterior Cingulate ◽  
Cortical Circuits ◽  
Lateral Prefrontal Cortex ◽  
Error Related Negativity

The basal ganglia have been suggested to play a key role in performance monitoring and resulting behavioral adjustments. It is assumed that the integration of prefrontal and motor cortico—striato—thalamo—cortical circuits provides contextual information to the motor anterior cingulate cortex regions to enable their function in performance monitoring. So far, direct evidence is missing, however. We addressed the involvement of frontostriatal circuits in performance monitoring by collecting event-related brain potentials (ERPs) and behavioral data in nine patients with focal basal ganglia lesions and seven patients with lateral prefrontal cortex lesions while they performed a flanker task. In both patient groups, the amplitude of the error-related negativity was reduced, diminishing the difference to the ERPs on correct responses. Despite these electrophysiological abnormalities, most of the patients were able to correct errors. Only in lateral prefrontal cortex patients whose lesions extended into the frontal white matter, disrupting the connections to the motor anterior cingulate cortex and the striatum, were error corrections severely impaired. In sum, the fronto—striato—thalamo—cortical circuits seem necessary for the generation of error-related negativity, even when brain plasticity has resulted in behavioral compensation of the damage. Thus, error-related ERPs in patients provide a sensitive measure of the integrity of the performance monitoring network.

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