scholarly journals Motor system dysfunction in the schizophrenia diathesis: Neural systems to neurotransmitters

2017 ◽  
Vol 44 ◽  
pp. 125-133 ◽  
Author(s):  
R. Abboud ◽  
C. Noronha ◽  
V.A. Diwadkar
Keyword(s):  
Motor Control ◽  
Prefrontal Cortex ◽  
Basal Ganglia ◽  
Motor System ◽  
Primary Motor Cortex ◽  
Multiple Scales ◽  
Motor Dysfunction ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex

AbstractMotor control is a ubiquitous aspect of human function, and from its earliest origins, abnormal motor control has been proposed as being central to schizophrenia. The neurobiological architecture of the motor system is well understood in primates and involves cortical and sub-cortical components including the primary motor cortex, supplementary motor area, dorsal anterior cingulate cortex, the prefrontal cortex, the basal ganglia, and cerebellum. Notably all of these regions are associated in some manner to the pathophysiology of schizophrenia. At the molecular scale, both dopamine and γ-Aminobutyric Acid (GABA) abnormalities have been associated with working memory dysfunction, but particularly relating to the basal ganglia and the prefrontal cortex respectively. As evidence from multiple scales (behavioral, regional and molecular) converges, here we provide a synthesis of the bio-behavioral relevance of motor dysfunction in schizophrenia, and its consistency across scales. We believe that the selective compendium we provide can supplement calls arguing for renewed interest in studying the motor system in schizophrenia. We believe that in addition to being a highly relevant target for the study of schizophrenia related pathways in the brain, such focus provides tractable behavioral probes for in vivo imaging studies in the illness. Our assessment is that the motor system is a highly valuable research domain for the study of schizophrenia.

scholarly journals In vivo electrophysiology of nigral and thalamic neurons in alpha-synuclein-overexpressing mice highlights differences from toxin-based models of parkinsonism

2013 ◽  
Vol 110 (12) ◽  
pp. 2792-2805 ◽  
Author(s):  
C. J. Lobb ◽  
A. K. Zaheer ◽  
Y. Smith ◽  
D. Jaeger
Keyword(s):  
Primary Motor Cortex ◽  
Alpha Synuclein ◽  
Motor Dysfunction ◽  
Motor Deficits ◽  
Dopamine Depletion ◽  
Wild Type ◽  
Beta Oscillations ◽  
Nigrostriatal Dopamine ◽  
6 Hydroxydopamine

Numerous studies have suggested that alpha-synuclein plays a prominent role in both familial and idiopathic Parkinson's disease (PD). Mice in which human alpha-synuclein is overexpressed (ASO) display progressive motor deficits and many nonmotor features of PD. However, it is unclear what in vivo pathophysiological mechanisms drive these motor deficits. It is also unknown whether previously proposed pathophysiological features (i.e., increased beta oscillations, bursting, and synchronization) described in toxin-based, nigrostriatal dopamine-depletion models are also present in ASO mice. To address these issues, we first confirmed that 5- to 6-mo-old ASO mice have robust motor dysfunction, despite the absence of significant nigrostriatal dopamine degeneration. In the same animals, we then recorded simultaneous single units and local field potentials (LFPs) in the substantia nigra pars reticulata (SNpr), the main basal ganglia output nucleus, and one of its main thalamic targets, the ventromedial nucleus, as well as LFPs in the primary motor cortex in anesthetized ASO mice and their age-matched, wild-type littermates. Neural activity was examined during slow wave activity and desynchronized cortical states, as previously described in 6-hydroxydopamine-lesioned rats. In contrast to toxin-based models, we found a small decrease, rather than an increase, in beta oscillations in the desynchronized state. Similarly, synchronized burst firing of nigral neurons observed in toxin-based models was not observed in ASO mice. Instead, we found more subtle changes in pauses of SNpr firing compared with wild-type control mice. Our results suggest that the pathophysiology underlying motor dysfunction in ASO mice is distinctly different from striatal dopamine-depletion models of parkinsonism.

scholarly journals Dissociable roles of cortical excitation-inhibition balance during patch-leaving versus value-guided decisions

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Luca F. Kaiser ◽  
Theo O. J. Gruendler ◽  
Oliver Speck ◽  
Lennart Luettgau ◽  
Gerhard Jocham
Keyword(s):  
Decision Making ◽  
Prefrontal Cortex ◽  
Neuronal Activity ◽  
Ventromedial Prefrontal Cortex ◽  
Anterior Cingulate ◽  
Mutual Inhibition ◽  
Dorsal Anterior Cingulate Cortex ◽  
Cortical Excitation ◽  
The Cost

AbstractIn a dynamic world, it is essential to decide when to leave an exploited resource. Such patch-leaving decisions involve balancing the cost of moving against the gain expected from the alternative patch. This contrasts with value-guided decisions that typically involve maximizing reward by selecting the current best option. Patterns of neuronal activity pertaining to patch-leaving decisions have been reported in dorsal anterior cingulate cortex (dACC), whereas competition via mutual inhibition in ventromedial prefrontal cortex (vmPFC) is thought to underlie value-guided choice. Here, we show that the balance between cortical excitation and inhibition (E/I balance), measured by the ratio of GABA and glutamate concentrations, plays a dissociable role for the two kinds of decisions. Patch-leaving decision behaviour relates to E/I balance in dACC. In contrast, value-guided decision-making relates to E/I balance in vmPFC. These results support mechanistic accounts of value-guided choice and provide evidence for a role of dACC E/I balance in patch-leaving decisions.

scholarly journals FDG-PET patterns associated with underlying pathology in corticobasal syndrome

Neurology ◽  
2019 ◽  
Vol 92 (10) ◽  
pp. e1121-e1135 ◽  
Author(s):  
Matteo Pardini ◽  
Edward D. Huey ◽  
Salvatore Spina ◽  
William C. Kreisl ◽  
Silvia Morbelli ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Fdg Pet ◽  
Primary Motor Cortex ◽  
Rating Scale ◽  
Corticobasal Degeneration ◽  
Anterior Cingulate ◽  
Corticobasal Syndrome ◽  
Control Group ◽  
Pathologic Diagnosis ◽  
Pet Scans

ObjectiveTo evaluate brain 18Fluorodeoxyglucose PET (FDG-PET) differences among patients with a clinical diagnosis of corticobasal syndrome (CBS) and distinct underling primary pathologies.MethodsWe studied 29 patients with a diagnosis of CBS who underwent FDG-PET scan and postmortem neuropathologic examination. Patients were divided into subgroups on the basis of primary pathologic diagnosis: CBS-corticobasal degeneration (CBS-CBD) (14 patients), CBS-Alzheimer disease (CBS-AD) (10 patients), and CBS–progressive supranuclear palsy (CBS-PSP) (5 patients). Thirteen age-matched healthy patients who underwent FDG-PET were the control group (HC). FDG-PET scans were compared between the subgroups and the HC using SPM-12, with a threshold of pFWE < 0.05.ResultsThere were no differences in Mattis Dementia Rating Scale or finger tapping scores between CBS groups. Compared to HC, the patients with CBS presented significant hypometabolism in frontoparietal regions, including the perirolandic area, basal ganglia, and thalamus of the clinically more affected hemisphere. Patients with CBS-CBD showed a similar pattern with a more marked, bilateral involvement of the basal ganglia. Patients with CBS-AD presented with posterior, asymmetric hypometabolism, including the lateral parietal and temporal lobes and the posterior cingulate. Finally, patients with CBS-PSP disclosed a more anterior hypometabolic pattern, including the medial frontal regions and the anterior cingulate. A conjunction analysis revealed that the primary motor cortex was the only common area of hypometabolism in all groups, irrespective of pathologic diagnosis.Discussion and conclusionsIn patients with CBS, different underling pathologies are associated with different patterns of hypometabolism. Our data suggest that FDG-PET scans could help in the etiologic diagnosis of CBS.

Role of the Human Rostral Supplementary Motor Area and the Basal Ganglia in Motor Sequence Control: Investigations With H2 15O PET

1998 ◽  
Vol 79 (2) ◽  
pp. 1070-1080 ◽  
Author(s):  
H. Boecker ◽  
A. Dagher ◽  
A. O. Ceballos-Baumann ◽  
R. E. Passingham ◽  
M. Samuel ◽  
...  
Keyword(s):  
Basal Ganglia ◽  
Primary Motor Cortex ◽  
Supplementary Motor Area ◽  
Motor Area ◽  
Anterior Cingulate ◽  
Central Control ◽  
Motor Sequence ◽  
Finger Movements ◽  
Sequence Complexity

Boecker, H., A. Dagher, A. O. Ceballos-Baumann, R. E. Passingham, M. Samuel, K. J. Friston, J.-B. Poline, C. Dettmers, B. Conrad, and D. J. Brooks. Role of the human rostral supplementary motor area and the basal ganglia in motor sequence control: investigations with H2 15O PET. J. Neurophysiol. 79: 1070–1080, 1998. The aim of this study was to investigate the functional anatomy of distributed cortical and subcortical motor areas in the human brain that participate in the central control of overlearned complex sequential unimanual finger movements. On the basis of previous research in nonhuman primates, a principal involvement of basal ganglia (medial premotor loops) was predicted for central control of finger sequences performed automatically. In pertinent areas, a correlation of activation levels with the complexity of a motor sequence was hypothesized. H2 15O positron emission tomography (PET) was used in a group of seven healthy male volunteers [mean age 32.0 ± 10.4 yr] to determine brain regions where levels of regional cerebral blood flow (rCBF) correlated with graded complexity levels of five different key-press sequences. All sequences were overlearned before PET and involved key-presses of fingers II–V of the right hand. Movements of individual fingers were kept constant throughout all five conditions by external pacing at 1-Hz intervals. Positive correlations of rCBF with increasing sequence complexity were identified in the contralateral rostral supplementary motor area (pre-SMA) and the associated pallido-thalamic loop, as well as in right parietal area 7 and ipsilateral primary motor cortex (M1). In contrast, while rCBF in contralateral M1 and and extensive parts of caudal SMA was increased compared with rest during task performance, significant correlated increases of rCBF with sequence complexity were not observed. Inverse correlations of rCBF with increasing sequence complexity were identified in mesial prefrontal-, medial temporal-, and anterior cingulate areas. The findings provide further evidence in humans supporting the notion of a segregation of SMA into functionally distinct subcomponents: although pre-SMA was differentially activated depending on the complexity of a sequence of learned finger movements, such modulation was not detectable in caudal SMA (except the most antero-superior part), implicating a motor executive role. Our observations of complexity-correlated rCBF increases in anterior globus palllidus suggest a specific role for the basal ganglia in the process of sequence facilitation and control. They may act to filter and focus input from motor cortical areas as patterns of action become increasingly complex.

scholarly journals Parallel Information Processing in Motor Systems: Intracerebral Recordings of Readiness Potential and CNV in Human Subjects

2000 ◽  
Vol 7 (1-2) ◽  
pp. 65-72 ◽  
Author(s):  
Ivan Rektor
Keyword(s):  
Basal Ganglia ◽  
Motor Cortex ◽  
Primary Motor Cortex ◽  
Human Subjects ◽  
Anterior Cingulate ◽  
Readiness Potential ◽  
Task Context ◽  
Subcortical Structures ◽  
Depth Electrodes ◽  
Simultaneous Activation

We performed intracerebral recordings of Readiness Potential (RP) and Contingent Negative Variation (CNV) with simple repetitive distal limb movement in candidates for epilepsy surgery. In 26 patients (in Paris), depth electrodes were located in various cortical structures; in eight patients (in Brno), in the basal ganglia and the cortex. RPs were displayed in the conteral primary motor cortex, conteral somato-sensory cortex, and bilaterally in the SMA and the caudal part of the anterior cingulate cortices. CNVs were recorded in the same cortical regiom as the RP, as well as in the ipsilateral primary motor cortex, and bilaterally in the premotor fronto-lateral, parietal superior, and middle temporal regions. In the basal ganglia, the RP was recorded in the putamen in six of seven patients, and in the head of the caudate nucleus and the pallidum in the only patient with electrodes in these recording sites. We suggest that our results are consistent with a long-lasting, simultaneous activation of cortical and subcortical structures, before and during self-paced and stimulus-triggered movements. The particular regiom that are simultaneously active may be determined by the task context.

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.

scholarly journals Distinguishing neural correlates of context-dependent advantageous- and disadvantageous-inequity aversion

2018 ◽  
Vol 115 (33) ◽  
pp. E7680-E7689 ◽  
Author(s):  
Xiaoxue Gao ◽  
Hongbo Yu ◽  
Ignacio Sáez ◽  
Philip R. Blue ◽  
Lusha Zhu ◽  
...  
Keyword(s):  
Decision Making ◽  
Prefrontal Cortex ◽  
Computational Models ◽  
Social Contexts ◽  
Inequity Aversion ◽  
Context Dependency ◽  
Anterior Cingulate ◽  
Dorsal Anterior Cingulate Cortex ◽  
Decision Making Processes ◽  
Context Dependent

Humans can integrate social contextual information into decision-making processes to adjust their responses toward inequity. This context dependency emerges when individuals receive more (i.e., advantageous inequity) or less (i.e., disadvantageous inequity) than others. However, it is not clear whether context-dependent processing of advantageous and disadvantageous inequity involves differential neurocognitive mechanisms. Here, we used fMRI to address this question by combining an interactive game that modulates social contexts (e.g., interpersonal guilt) with computational models that enable us to characterize individual weights on inequity aversion. In each round, the participant played a dot estimation task with an anonymous coplayer. The coplayer would receive pain stimulation with 50% probability when either of them responded incorrectly. At the end of each round, the participant completed a variant of dictator game, which determined payoffs for him/herself and the coplayer. Computational modeling demonstrated the context dependency of inequity aversion: when causing pain to the coplayer (i.e., guilt context), participants cared more about the advantageous inequity and became more tolerant of the disadvantageous inequity, compared with other conditions. Consistently, neuroimaging results suggested the two types of inequity were associated with differential neurocognitive substrates. While the context-dependent processing of advantageous inequity was associated with social- and mentalizing-related processes, involving left anterior insula, right dorsolateral prefrontal cortex, and dorsomedial prefrontal cortex, the context-dependent processing of disadvantageous inequity was primarily associated with emotion- and conflict-related processes, involving left posterior insula, right amygdala, and dorsal anterior cingulate cortex. These results extend our understanding of decision-making processes related to inequity aversion.

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