Frontal Cortical Areas Research Articles

Human amygdala functional network development: A cross-sectional study from 3 months to 5 years of age

Although the amygdala’s role in shaping social behavior is especially important during early post-natal development, very little is known of amygdala functional development before childhood. To address this gap, this study uses resting-state fMRI to examine early amygdalar functional network development in a cross-sectional sample of 80 children from 3-months to 5-years of age. Whole brain functional connectivity with the amygdala, and its laterobasal and superficial sub-regions, were largely similar to those seen in older children and adults. Functional distinctions between sub-region networks were already established. These patterns suggest many amygdala functional circuits are intact from infancy, especially those that are part of motor, visual, auditory and subcortical networks. Developmental changes in connectivity were observed between the laterobasal nucleus and bilateral ventral temporal and motor cortex as well as between the superficial nuclei and medial thalamus, occipital cortex and a different region of motor cortex. These results show amygdala-subcortical and sensory-cortex connectivity begins refinement prior to childhood, though connectivity changes with associative and frontal cortical areas, seen after early childhood, were not evident in this age range. These findings represent early steps in understanding amygdala network dynamics across infancy through early childhood, an important period of emotional and cognitive development.

Effects of monoamines on the intrinsic excitability of lateral orbitofrontal cortex neurons in alcohol-dependent and non-dependent female mice

Changes in brain reward and control systems of frontal cortical areas including the orbitofrontal cortex (OFC) are associated with alcohol use disorders (AUD). The OFC is extensively innervated by monoamines, and drugs that target monoamine receptors have been used to treat a number of neuropsychiatric diseases, including AUDs. Recent findings from this laboratory demonstrate that D2, α2-adrenergic and 5HT1A receptors all decrease the intrinsic excitability of lateral OFC (lOFC) neurons in naïve male mice and that this effect is lost in mice exposed to repeated cycles of chronic intermittent ethanol (CIE) vapor. As biological sex differences may influence an individual's response to alcohol and contribute to the propensity to engage in addictive behaviors, we examined whether monoamines have similar effects on lOFC neurons in control and CIE exposed female mice. Dopamine, norepinephrine and serotonin all decreased spiking of lOFC neurons in naïve females via activation of Giα-coupled D2, α2-adrenergic and 5HT1A receptors, respectively. Firing was also inhibited by the direct GIRK channel activator ML297, while blocking these channels with barium eliminated the inhibitory actions of monoamines. Following CIE treatment, evoked spiking of lOFC neurons from female mice was significantly enhanced and monoamines and ML297 no longer inhibited firing. Unlike in male mice, the enhanced firing of neurons from CIE exposed female mice was not associated with changes in the after-hyperpolarization and the small-conductance potassium channel blocker apamin had no effect on current-evoked tail currents from either control or CIE exposed female mice. These results suggest that while CIE exposure alters monoamine regulation of OFC neuron firing similarly in males and female mice, there are sex-dependent differences in processes that regulate the intrinsic excitability of these neurons.

Using modern human cortical bone distribution to test the systemic robusticity hypothesis

The systemic robusticity hypothesis links the thickness of cortical bone in both the cranium and limb bones. This hypothesis posits that thick cortical bone is in part a systemic response to circulating hormones, such as growth hormone and thyroid hormone, possibly related to physical activity or cold climates. Although this hypothesis has gained popular traction, only rarely has robusticity of the cranium and postcranial skeleton been considered jointly. We acquired computed tomographic scans from associated crania, femora and humeri from single individuals representing 11 populations in Africa and North America (n = 228). Cortical thickness in the parietal, frontal and occipital bones and cortical bone area in limb bone diaphyses were analyzed using correlation, multiple regression and general linear models to test the hypothesis. Absolute thickness values from the crania were not correlated with cortical bone area of the femur or humerus, which is at odds with the systemic robusticity hypothesis. However, measures of cortical bone scaled by total vault thickness and limb cross-sectional area were positively correlated between the cranium and postcranium. When accounting for a range of potential confounding variables, including sex, age and body mass, variation in relative postcranial cortical bone area explained ∼20% of variation in the proportion of cortical cranial bone thickness. While these findings provide limited support for the systemic robusticity hypothesis, cranial cortical thickness did not track climate or physical activity across populations. Thus, some of the variation in cranial cortical bone thickness in modern humans is attributable to systemic effects, but the driving force behind this effect remains obscure. Moreover, neither absolute nor proportional measures of cranial cortical bone thickness are positively correlated with total cranial bone thickness, complicating the extrapolation of these findings to extinct species where only cranial vault thickness has been measured.

S177. FRONTAL CORTICAL PLASTICITY IN SCHIZOPHRENIA PATIENTS EXAMINED BY LTP-INDUCING ANODAL TDCS AND REPETITIVE EEG

BackgroundFrontal cortical deficits have repeatedly been shown to be relevant in the development of psychiatric disorders and are supposed to evoke characteristic psychiatric and cognitive symptoms in schizophrenia. It is assumed that plasticity and connectivity impairments following non-invasive brain stimulation, which are observed as common patterns in the motor system of schizophrenic patients, are as well present in frontal cortical areas and cause the mentioned dysfunctions. Until now experimental evidence is lacking substantiating that this hypothesis is correct and both cortical regions show similar patterns of deficits. Hence, this study aimed to assess the plasticity and connectivity in the frontal cortex of schizophrenia patients.MethodsWe applied anodal transcranial direct current stimulation (a-tDCS) to evoke long-term potentiation (LTP)-like plasticity in the dorsolateral prefrontal cortex (DLPFC). This non-invasive brain stimulation has been demonstrated to evoke plasticity in frontal cortical regions. As tDCS modulates cortical activity we employed electroencephalography (EEG) measurements to trace potential deficits in patients with schizophrenia compared to healthy participants. In total 20 schizophrenia patients and 20 age, gender and handedness matched healthy controls received 13Min of a-tDCS (1mA). EEG was measured before and after plasticity induction (up to 50 minutes) to record neuronal changes in excitability and plasticity.ResultsFirst analyses obtained a significant EEG alpha-activity change after LTP application in the frontal cortex of schizophrenia patients. This effect remained stable up to 50 minutes following a-tDCS stimulation.DiscussionWe were able to show for the first time that anodal tDCS is capable of inducing stable EEG alpha-activity changes in the frontal cortex of schizophrenia patients. Future analyses will focus on differences to healthy participants, which we hypothesize to show similar but stronger patterns of activity changes after a-tDCS stimulation.

Organization of afferents to the orbitofrontal cortex in the rat.

The prefrontal cortex (PFC) is usually defined as the frontal cortical area receiving a mediodorsal thalamic (MD) innervation. Certain areas in the medial wall of the rat frontal area receive a MD innervation. A second frontal area that is the target of MD projections is located dorsal to the rhinal sulcus and often referred to as the orbitofrontal cortex (OFC). Both the medial PFC and OFC are comprised of a large number of cytoarchitectonic regions. We assessed the afferent innervation of the different areas of the OFC, with a focus on projections arising from the mediodorsal thalamic nucleus, the basolateral nucleus of the amygdala, and the midbrain dopamine neurons. Although there are specific inputs to various OFC areas, a simplified organizational scheme could be defined, with the medial areas of the OFC receiving thalamic inputs, the lateral areas of the OFC being the recipient of amygdala afferents, and a central zone that was the target of midbrain dopamine neurons. Anterograde tracer data were consistent with this organization of afferents, and revealed that the OFC inputs from these three subcortical sites were largely spatially segregated. This spatial segregation suggests that the central portion of the OFC (pregenual agranular insular cortex) is the only OFC region that is a prefrontal cortical area, analogous to the prelimbic cortex in the medial prefrontal cortex. These findings highlight the heterogeneity of the OFC, and suggest possible functional attributes of the three different OFC areas.

Estrogen Interactions With Lipid Rafts Related to Neuroprotection. Impact of Brain Ageing and Menopause.

Estrogens (E2) exert a plethora of neuroprotective actions against aged-associated brain diseases, including Alzheimer's disease (AD). Part of these actions takes place through binding to estrogen receptors (ER) embedded in signalosomes, where numerous signaling proteins are clustered. Signalosomes are preferentially located in lipid rafts which are dynamic membrane microstructures characterized by a peculiar lipid composition enriched in gangliosides, saturated fatty acids, cholesterol, and sphingolipids. Rapid E2 interactions with ER-related signalosomes appear to trigger intracellular signaling ultimately leading to the activation of molecular mechanisms against AD. We have previously observed that the reduction of E2 blood levels occurring during menopause induced disruption of ER-signalosomes at frontal cortical brain areas. These molecular changes may reduce neuronal protection activities, as similar ER signalosome derangements were observed in AD brains. The molecular impairments may be associated with changes in the lipid composition of lipid rafts observed in neurons during menopause and AD. These evidences indicate that the changes in lipid raft structure during aging may be at the basis of alterations in the activity of ER and other neuroprotective proteins integrated in these membrane microstructures. Moreover, E2 is a homeostatic modulator of lipid rafts. Recent work has pointed to this relevant aspect of E2 activity to preserve brain integrity, through mechanisms affecting lipid uptake and local biosynthesis in the brain. Some evidences have demonstrated that estrogens and the docosahexaenoic acid (DHA) exert synergistic effects to stabilize brain lipid matrix. DHA is essential to enhance molecular fluidity at the plasma membrane, promoting functional macromolecular interactions in signaling platforms. In support of this, DHA detriment in neuronal lipid rafts has been associated with the most common age-associated neuropathologies, namely AD and Parkinson disease. Altogether, these findings indicate that E2 may participate in brain preservation through a dual membrane-related mechanism. On the one hand, E2 interacting with ER related signalosomes may protect against neurotoxic insults. On the other hand, E2 may exert lipostatic actions to preserve lipid balance in neuronal membrane microdomains. The different aspects of the emerging multifunctional role of estrogens in membrane-related signalosomes will be discussed in this review.

Cortical Measures of Phoneme-Level Speech Encoding Correlate with the Perceived Clarity of Natural Speech.

In real-world environments, humans comprehend speech by actively integrating prior knowledge (P) and expectations with sensory input. Recent studies have revealed effects of prior information in temporal and frontal cortical areas and have suggested that these effects are underpinned by enhanced encoding of speech-specific features, rather than a broad enhancement or suppression of cortical activity. However, in terms of the specific hierarchical stages of processing involved in speech comprehension, the effects of integrating bottom-up sensory responses and top-down predictions are still unclear. In addition, it is unclear whether the predictability that comes with prior information may differentially affect speech encoding relative to the perceptual enhancement that comes with that prediction. One way to investigate these issues is through examining the impact of P on indices of cortical tracking of continuous speech features. Here, we did this by presenting participants with degraded speech sentences that either were or were not preceded by a clear recording of the same sentences while recording non-invasive electroencephalography (EEG). We assessed the impact of prior information on an isolated index of cortical tracking that reflected phoneme-level processing. Our findings suggest the possibility that prior information affects the early encoding of natural speech in a dual manner. Firstly, the availability of prior information, as hypothesized, enhanced the perceived clarity of degraded speech, which was positively correlated with changes in phoneme-level encoding across subjects. In addition, P induced an overall reduction of this cortical measure, which we interpret as resulting from the increase in predictability.

Coactivation of cognitive control networks during task switching.

The ability to flexibly switch between tasks is considered an important component of cognitive control that involves frontal and parietal cortical areas. The present study was designed to characterize network dynamics across multiple brain regions during task switching. Functional magnetic resonance images (fMRI) were captured during a standard rule-switching task to identify switching-related brain regions. Multiregional psychophysiological interaction (PPI) analysis was used to examine effective connectivity between these regions. During switching trials, behavioral performance declined and activation of a generic cognitive control network increased. Concurrently, task-related connectivity increased within and between cingulo-opercular and fronto-parietal cognitive control networks. Notably, the left inferior frontal junction (IFJ) was most consistently coactivated with the 2 cognitive control networks. Furthermore, switching-dependent effective connectivity was negatively correlated with behavioral switch costs. The strength of effective connectivity between left IFJ and other regions in the networks predicted individual differences in switch costs. Task switching was supported by coactivated connections within cognitive control networks, with left IFJ potentially acting as a key hub between the fronto-parietal and cingulo-opercular networks. (PsycINFO Database Record

EEG Source Imaging Indices of Cognitive Control Show Associations with Dopamine System Genes

Cognitive or executive control is a critical mental ability, an important marker of mental illness, and among the most heritable of neurocognitive traits. Two candidate genes, catechol-O-methyltransferase (COMT) and DRD4, which both have a roles in the regulation of cortical dopamine, have been consistently associated with cognitive control. Here, we predicted that individuals with the COMT Met/Met allele would show improved response execution and inhibition as indexed by event-related potentials in a Go/NoGo task, while individuals with the DRD4 7-repeat allele would show impaired brain activity. We used independent component analysis (ICA) to separate brain source processes contributing to high-density EEG scalp signals recorded during the task. As expected, individuals with the DRD4 7-repeat polymorphism had reduced parietal P3 source and scalp responses to response (Go) compared to those without the 7-repeat. Contrary to our expectation, the COMT homozygous Met allele was associated with a smaller frontal P3 source and scalp response to response-inhibition (NoGo) stimuli, suggesting that while more dopamine in frontal cortical areas has advantages in some tasks, it may also compromise response inhibition function. An interaction effect emerged for P3 source responses to Go stimuli. These were reduced in those with both the 7-repeat DRD4 allele and either the COMT Val/Val or the Met/Met homozygous polymorphisms but not in those with the heterozygous Val/Met polymorphism. This epistatic interaction between DRD4 and COMT replicates findings that too little or too much dopamine impairs cognitive control. The anatomic and functional separated maximally independent cortical EEG sources proved more informative than scalp channel measures for genetic studies of brain function and thus better elucidate the complex mechanisms in psychiatric illness.

Disruption and rescue of interareal theta phase coupling and adaptive behavior

Rescuing executive functions in people with neurological and neuropsychiatric disorders has been a major goal of psychology and neuroscience for decades. Innovative computer-training regimes for executive functions have made tremendous inroads, yet the positive effects of training have not always translated into improved cognitive functioning and often take many days to emerge. In the present study, we asked whether it was possible to immediately change components of executive function by directly manipulating neural activity using a stimulation technology called high-definition transcranial alternating current stimulation (HD-tACS). Twenty minutes of inphase stimulation over medial frontal cortex (MFC) and right lateral prefrontal cortex (lPFC) synchronized theta (∼6 Hz) rhythms between these regions in a frequency and spatially specific manner and rapidly improved adaptive behavior with effects lasting longer than 40 min. In contrast, antiphase stimulation in the same individuals desynchronized MFC-lPFC theta phase coupling and impaired adaptive behavior. Surprisingly, the exogenously driven impairments in performance could be instantly rescued by reversing the phase angle of alternating current. The results suggest executive functions can be rapidly up- or down-regulated by modulating theta phase coupling of distant frontal cortical areas and can contribute to the development of tools for potentially normalizing executive dysfunction in patient populations.

Pyramidal Cell Subtypes and Their Synaptic Connections in Layer 5 of Rat Frontal Cortex.

The frontal cortical areas make a coordinated response that generates appropriate behavior commands, using individual local circuits with corticostriatal and corticocortical connections in longer time scales than sensory areas. In secondary motor cortex (M2), situated between the prefrontal and primary motor areas, major subtypes of layer 5 corticostriatal cells are crossed-corticostriatal (CCS) cells innervating both sides of striatum, and corticopontine (CPn) cells projecting to the ipsilateral striatum and pontine nuclei. CCS cells innervate CPn cells unidirectionally: the former are therefore hierarchically higher than the latter among L5 corticostriatal cells. CCS cells project directly to both frontal and nonfrontal areas. On the other hand, CPn cells innervate the thalamus and layer 1a of frontal areas, where thalamic fibers relaying basal ganglia outputs are distributed. Thus, CCS cells can make activities of frontal areas in concert with those of nonfrontal area using corticocortical loops, whereas CPn cells are more involved in closed corticostriatal loops than CCS cells. Since reciprocal connections between CPn cells with facilitatory synapses may be related to persistent activity, CPn cells play a key role of longer time constant processes in corticostriatal as well as in corticocortical loops between the frontal areas.

Behavioral and brain oscillatory correlates of affective processing in subclinical depression

ABSTRACTNamed among the most dangerous diseases of the modern era, depression is characterized primarily by distortions in the affective sphere. Despite extensive investigations of underlying the neural background, mechanisms of the distortion still remain unknown. The current study analyzed brain oscillatory dynamics in different frequencies during resting state and presentation of affective stimuli in nonclinical individuals with high Beck Depression Inventory–II (BDI–II) scores (HB) versus controls. Both behavioral and electrocortical “markers” of clinical depression were apparent at subclinical level. A resting-state electroencephalogram (EEG) of HB revealed increased power in low frequencies, predominantly in the frontal cortical areas, that is in accordance with a “spatio-temporal dysfunction” model of depression. Related to that, transition from an eyes-closed to eyes-open condition was associated with diminished alpha blockade in HB, suggesting difficulties with the relocation of attention focus from inner processes toward environmental stimuli. Subsequently, independently of a sign of emotion, five out of six discrete emotions were evaluated as less valenced and four out of six as less intense by HB than by controls, corroborating the view of emotion context insensitivity (ECI) associated with depression. Underlying brain oscillatory dynamics revealed that depression was associated with deficits in the early, implicit, processing stages of emotional stimuli. Later processing stages were characterized by prominent power surges in low and alpha frequencies, presumably indicating emotion upregulation processes and increased engagement of cognitive mechanisms in affective tasks. The study provides brain oscillatory-based mechanisms of emotion processing distortions associated with depression.

A PITX3-EGFP Reporter Line Reveals Connectivity of Dopamine and Non-dopamine Neuronal Subtypes in Grafts Generated from Human Embryonic Stem Cells.

SummaryDevelopment of safe and effective stem cell-based therapies for brain repair requires an in-depth understanding of the in vivo properties of neural grafts generated from human stem cells. Replacing dopamine neurons in Parkinson's disease remains one of the most anticipated applications. Here, we have used a human PITX3-EGFP embryonic stem cell line to characterize the connectivity of stem cell-derived midbrain dopamine neurons in the dopamine-depleted host brain with an unprecedented level of specificity. The results show that the major A9 and A10 subclasses of implanted dopamine neurons innervate multiple, developmentally appropriate host targets but also that the majority of graft-derived connectivity is non-dopaminergic. These findings highlight the promise of stem cell-based procedures for anatomically correct reconstruction of specific neuronal pathways but also emphasize the scope for further refinement in order to limit the inclusion of uncharacterized and potentially unwanted cell types.

The rat retrosplenial cortex as a link for frontal functions: A lesion analysis

Cohorts of rats with excitotoxic retrosplenial cortex lesions were tested on four behavioural tasks sensitive to dysfunctions in prelimbic cortex, anterior cingulate cortex, or both. In this way the study tested whether retrosplenial cortex has nonspatial functions that reflect its anatomical interactions with these frontal cortical areas. In Experiment 1, retrosplenial cortex lesions had no apparent effect on a set-shifting digging task that taxed intradimensional and extradimensional attention, as well as reversal learning. Likewise, retrosplenial cortex lesions did not impair a strategy shift task in an automated chamber, which involved switching from visual-based to response-based discriminations and, again, included a reversal (Experiment 2). Indeed, there was evidence that the retrosplenial lesions aided the initial switch to response-based selection. No lesion deficit was found on an automated cost-benefit task that pitted size of reward against effort to achieve that reward (Experiment 3). Finally, while retrosplenial cortex lesions affected matching-to-place task in a T-maze, the profile of deficits differed from that associated with prelimbic cortex damage (Experiment 4). When the task was switched to a nonmatching design, retrosplenial cortex lesions had no apparent effect on performance. The results from the four experiments show that many frontal tasks do not require the retrosplenial cortex, highlighting the specificity of their functional interactions. The results show how retrosplenial cortex lesions spare those learning tasks in which there is no mismatch between the internal and external representations used to guide behavioural choice. In addition, these experiments further highlight the importance of the retrosplenial cortex in solving tasks with a spatial component.

Effect of tobacco smoking on frontal cortical thickness development: A longitudinal study in a mixed cohort of ADHD-affected and -unaffected youth

Smoking rates are particularly high during adolescence and young adulthood, when the brain is still undergoing significant developmental changes. Cross-sectional studies have revealed altered brain structure in smokers, such as thinner frontal cortical areas. Attention-deficit/hyperactivity disorder (ADHD) increases the risk of becoming nicotine-dependent, and has also been associated with abnormalities in frontal gray matter structure. The present study examines the relationships between smoking, cortical thickness and ADHD symptoms in a longitudinal design that compares adolescent and young adult smokers (n=44; 35 ADHD-affected) and non-smokers (n=45; 32 ADHD-affected) on frontal cortical thickness. Average frontal cortical thickness was estimated through structural magnetic resonance imaging (MRI) at two time points (mean ages 17.7 and 21.1 years), on average 3.4 years apart. Smokers had a 2.6% thinner frontal cortex than non-smokers and this difference was not explained by ADHD or other confounding factors. The rate of cortical thinning across the 3.4-year MRI measurement interval was similar in the total group of smokers compared to non-smokers. However, speeded thinning did occur in smokers who had started regular smoking more recently, in between the two measurements. These novel regular smokers did not differ significantly from the non-smokers at baseline. This suggests that the thinner frontal cortex was not a predisposing factor but rather a consequence of smoking. Although smokers had more ADHD symptoms overall, smoking did not influence the developmental course of ADHD symptoms.

What can Cortical Development in Attention-Deficit/Hyperactivity Disorder Teach us About the Early Developmental Mechanisms Involved?

Studies of Attention-Deficit/Hyperactivity Disorder (ADHD) have shown developmental changes in the cortical mantle. Different dimensions of cortical morphology, such as surface area and thickness, relate to different neurodevelopmental mechanisms. As such, studying multiple dimensions may inform us about the developmental origins of ADHD. Furthermore, results from existing longitudinal samples await replication. Therefore, we conducted a longitudinal study of multiple cortical dimensions in a sizable, independent ADHD sample. We analyzed 297 anatomical MRI scans from two matched groups of 94 subjects with ADHD and 94 controls, aged 6-28 years. We estimated the developmental trajectories of cortical volume, surface, thickness and gyrification for 68 regions using mixed-effects regression analysis. Subjects with ADHD had smaller overall cortical volume, predominantly driven by decreases in frontal lobe volume that were associated with reduced surface area and gyrification. Nearly all decreases were stable across development. Only a few decreases survived stringent Bonferroni correction for multiple comparisons, with the smallest detectable Cohen's d |0.43|. There were no between-group differences in cortical thickness, or in subcortical volumes. Our results suggest that ADHD is associated with developmentally persistent reductions in frontal cortical volume, surface area, and gyrification. This may implicate early neurodevelopmental mechanisms regulating cortical expansion and convolution in ADHD.

Brain activity patterns induced by interrupting the cognitive processes with online advertising

As a result of the increasing role of online advertising and strong competition among advertisers, intrusive techniques are commonly used to attract web users’ attention. Moreover, since marketing content is usually delivered to the target audience when they are performing typical online tasks, like searching for information or reading online content, its delivery interrupts the web user’s current cognitive process. The question posed by many researchers in the field of online advertising is: how should we measure the influence of interruption of cognitive processes on human behavior and emotional state? Much research has been conducted in this field; however, most of this research has focused on monitoring activity in the simulated environment, or processing declarative responses given by users in prepared questionnaires. In this paper, a more direct real-time approach is taken, and the effect of the interruption on a web user is analyzed directly by studying the activity of his brain. This paper presents the results of an experiment that was conducted to find the brain activity patterns associated with interruptions of the cognitive process by showing internet advertisements during a text-reading task. Three specific aspects were addressed in the experiment: individual patterns, the consistency of these patterns across trials, and the intra-subject correlation of the individual patterns. Two main effects were observed for most subjects: a drop in activity in the frontal and prefrontal cortical areas across all frequency bands, and significant changes in the frontal/prefrontal asymmetry index.

Decoding of intended saccade direction in an oculomotor brain–computer interface

Objective. To date, invasive brain–computer interface (BCI) research has largely focused on replacing lost limb functions using signals from the hand/arm areas of motor cortex. However, the oculomotor system may be better suited to BCI applications involving rapid serial selection from spatial targets, such as choosing from a set of possible words displayed on a computer screen in an augmentative and alternative communication (AAC) application. Here we aimed to demonstrate the feasibility of a BCI utilizing the oculomotor system. Approach. We developed a chronic intracortical BCI in monkeys to decode intended saccadic eye movement direction using activity from multiple frontal cortical areas. Main results. Intended saccade direction could be decoded in real time with high accuracy, particularly at contralateral locations. Accurate decoding was evident even at the beginning of the BCI session; no extensive BCI experience was necessary. High-frequency (80–500 Hz) local field potential magnitude provided the best performance, even over spiking activity, thus simplifying future BCI applications. Most of the information came from the frontal and supplementary eye fields, with relatively little contribution from dorsolateral prefrontal cortex. Significance. Our results support the feasibility of high-accuracy intracortical oculomotor BCIs that require little or no practice to operate and may be ideally suited for ‘point and click’ computer operation as used in most current AAC systems.

Psychopathology of Brain Frontal Lobe Tumors: When the Neurosurgery Meets Psychiatry

Brain tumors occur when abnormal cells form within the brain.There are two main types of tumors: malignant and benign tumors. Then, tumors can be divided into primary that start within the brain, and secondary tumors that have spread from somewhere else, known as brain metastasis tumors. Secondary brain tumors occur in approximately 15 % of cancer patients with about half of metastases coming from lung cancer. Primary brain tumors occur in around 250,000 people a year globally, making up less than 2% of whole body tumors. According to American Brain Tumor Association the most common types of primary tumors are gliomas, representing 74,6 % of all malignant tumors and meningiomas ( 36,6% ) while more affected region is frontal lobe, about 22 % . Particularly, prefrontal cortex ( PFC ), the anterior part of the frontal lobe that is highly developed in humans plays a role in the regulation of personality, emotional, and behavioral functioning, leading to serious cognitive impairments 1. These are the psychological signs of frontal lobe tumors, in addition to other functions such as the expressive language of Broca's area or those relating to voluntary movement, linked to frontal cortical motor areas. It relates to the so-called higher nervous functions, concerning the life of relationship and communication. The PFC physiology explains the psychological mechanisms of its associated functions: connections with the limbic cortex, thalamus, hypothalamus, basal ganglia and other subcortical areas.The regions of the PFC at the base of the psychophysiological mechanisms involved are basically the dorso-lateral, the ventro-medial, the orbito-frontal establishing contacts primarily with limbic structures, such as the cingulate gyrus, hippocampus, amygdala.

Distinct Sources of Deterministic and Stochastic Components of Action Timing Decisions in Rodent Frontal Cortex

The selection and timing of actions are subject to determinate influences such as sensory cues and internal state as well as to effectively stochastic variability. Although stochastic choice mechanisms are assumed by many theoretical models, their origin and mechanisms remain poorly understood. Here we investigated this issue by studying how neural circuits in the frontal cortex determine action timing in rats performing a waiting task. Electrophysiological recordings from two regions necessary for this behavior, medial prefrontal cortex (mPFC) and secondary motor cortex (M2), revealed an unexpected functional dissociation. Both areas encoded deterministic biases in action timing, but only M2 neurons reflected stochastic trial-by-trial fluctuations. This differential coding was reflected in distinct timescales of neural dynamics in the two frontal cortical areas. These results suggest a two-stage model in which stochastic components of action timing decisions are injected by circuits downstream of those carrying deterministic bias signals.