Frontiers in Systems Neuroscience最新文献

The role of the cerebellum in emotional control has gained increasing interest, with studies showing it is involved in fear learning and memory in both humans and rodents. This review will focus on the contributions of the cerebellum to the extinction of learned fear responses. Extinction of fearful memories is critical for adaptive behaviour, and is clinically relevant to anxiety disorders such as post-traumatic stress disorder, in which deficits in extinction processes are thought to occur. We present evidence that supports cerebellar involvement in fear extinction, from rodent studies that investigate molecular mechanisms and functional connectivity with other brain regions of the known fear extinction network, to fMRI studies in humans. This evidence is considered in relation to the theoretical framework that the cerebellum is involved in the formation and updating of internal models of the inner and outer world by detecting errors between predicted and actual outcomes. In the case of fear conditioning, these internal models are thought to predict the occurrence of an aversive unconditioned stimulus (US), and when the aversive US is unexpectedly omitted during extinction learning the cerebellum uses prediction errors to update the internal model. Differences between human and rodent studies are highlighted to help inform future work.

When we interact with the environment around us, we are sometimes active participants, making directed physical motor movements and other times only mentally engaging with our environment, taking in sensory information and internally planning our next move without directed physical movement. Traditionally, cortical motor regions and key subcortical structures such as the cerebellum have been tightly linked to motor initiation, coordination, and directed motor behavior. However, recent neuroimaging studies have noted the activation of the cerebellum and wider cortical networks specifically during various forms of motor processing, including the observations of actions and mental rehearsal of movements through motor imagery. This phenomenon of cognitive engagement of traditional motor networks raises the question of how these brain regions are involved in the initiation of movement without physical motor output. Here, we will review evidence for distributed brain network activation during motor execution, observation, and imagery in human neuroimaging studies as well as the potential for cerebellar involvement specifically in motor-related cognition. Converging evidence suggests that a common global brain network is involved in both movement execution and motor observation or imagery, with specific task-dependent shifts in these global activation patterns. We will further discuss underlying cross-species anatomical support for these cognitive motor-related functions as well as the role of cerebrocerebellar communication during action observation and motor imagery.

There is general agreement that cerebrocerebellar interactions via cerebellothalamocortical pathways are essential for a cerebellar cognitive and motor functions. Cerebellothalamic projections were long believed target mainly the ventral lateral (VL) and part of the ventral anterior (VA) nuclei, which project to cortical motor and premotor areas. Here we review new insights from detailed tracing studies, which show that projections from the cerebellum to the thalamus are widespread and reach almost every thalamic subnucleus, including nuclei involved in cognitive functions. These new insights into cerebellothalamic pathways beyond the motor thalamus are consistent with the increasing evidence of cerebellar cognitive function. However, the function of cerebellothalamic pathways and how they are involved in the various motor and cognitive functions of the cerebellum is still unknown. We briefly review literature on the role of the thalamus in coordinating the coherence of neuronal oscillations in the neocortex. The coherence of oscillations, which measures the stability of the phase relationship between two oscillations of the same frequency, is considered an indicator of increased functional connectivity between two structures showing coherent oscillations. Through thalamocortical interactions coherence patterns dynamically create and dissolve functional cerebral cortical networks in a task dependent manner. Finally, we review evidence for an involvement of the cerebellum in coordinating coherence of oscillations between cerebral cortical structures. We conclude that cerebellothalamic pathways provide the necessary anatomical substrate for a proposed role of the cerebellum in coordinating neuronal communication between cerebral cortical areas by coordinating the coherence of oscillations.

There is a growing appreciation for the cerebellum beyond its role in motor function and accumulating evidence that the cerebellum and hippocampus interact across a range of brain states and behaviors. Acute and chronic manipulations, simultaneous recordings, and imaging studies together indicate coordinated coactivation and a bidirectional functional connectivity relevant for various physiological functions, including spatiotemporal processing. This bidirectional functional connectivity is likely supported by multiple circuit paths. It is also important in temporal lobe epilepsy: the cerebellum is impacted by seizures and epilepsy, and modulation of cerebellar circuitry can be an effective strategy to inhibit hippocampal seizures. This review highlights some of the recent key hippobellum literature.

Evidence shows that females have increased supra-threshold peripheral auditory processing compared to males. This is indicated by larger auditory brainstem responses (ABR) wave I amplitude, which measures afferent spiral ganglion neuron (SGN)-auditory nerve synchrony. However, the underlying molecular mechanisms of this sex difference are mostly unknown. We sought to elucidate sex differences in ABR wave I amplitude by examining molecular markers known to affect synaptic transmission kinetics. Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) mediate fast excitatory transmission in mature SGN afferent synapses. Each AMPAR channel is a tetramer composed of GluA2, 3, and 4 subunits (Gria2, 3, and 4 genes), and those lacking GluA2 subunits have larger currents, are calcium-permeable, and have faster gating kinetics. Moreover, alternatively spliced flip and flop isoforms of each AMPAR subunit affect channel kinetics, having faster kinetics those AMPARs containing Gria3 and Gria4 flop isoforms. We hypothesized that SGNs of females have more fast-gating AMPAR subunit mRNA than males, which could contribute to more temporally precise synaptic transmission and increased SGN synchrony. Our data show that the index of Gria3 relative to Gria2 transcripts on SGN was higher in females than males (females: 48%; males: 43%), suggesting that females have more SGNs with higher Gria3 mRNA relative to Gria2. Analysis of the relative abundance of the flip and flop alternatively spliced isoforms showed that females have a 2-fold increase in fast-gating Gria3 flop mRNA, while males have more slow-gating (2.5-fold) of the flip. We propose that Gria3 may in part mediate greater SGN synchrony in females. Significance Statement: Females of multiple vertebrate species, including fish and mammals, have been reported to have enhanced sound-evoked synchrony of afferents in the auditory nerve. However, the underlying molecular mediators of this physiologic sex difference are unknown. Elucidating potential molecular mechanisms related to sex differences in auditory processing is important for maintaining healthy ears and developing potential treatments for hearing loss in both sexes. This study found that females have a 2-fold increase in Gria3 flop mRNA, a fast-gating AMPA-type glutamate receptor subunit. This difference may contribute to greater neural synchrony in the auditory nerve of female mice compared to males, and this sex difference may be conserved in all vertebrates.

Introduction: Can we apply graph representation learning algorithms to identify autism spectrum disorder (ASD) patients within a large brain imaging dataset? ASD is mainly identified by brain functional connectivity patterns. Attempts to unveil the common neural patterns emerged in ASD are the essence of ASD classification. We claim that graph representation learning methods can appropriately extract the connectivity patterns of the brain, in such a way that the method can be generalized to every recording condition, and phenotypical information of subjects. These methods can capture the whole structure of the brain, both local and global properties.

Methods: The investigation is done for the worldwide brain imaging multi-site database known as ABIDE I and II (Autism Brain Imaging Data Exchange). Among different graph representation techniques, we used AWE, Node2vec, Struct2vec, multi node2vec, and Graph2Img. The best approach was Graph2Img, in which after extracting the feature vectors representative of the brain nodes, the PCA algorithm is applied to the matrix of feature vectors. The classifier adapted to the features embedded in graphs is an LeNet deep neural network.

Results and discussion: Although we could not outperform the previous accuracy of 10-fold cross-validation in the identification of ASD versus control patients in this dataset, for leave-one-site-out cross-validation, we could obtain better results (our accuracy: 80%). The result is that graph embedding methods can prepare the connectivity matrix more suitable for applying to a deep network.

Higher mammals are able to simultaneously learn and perform a wide array of complex behaviors, which raises questions about how the neural representations of multiple tasks coexist within the same neural network. Do neurons play invariant roles across different tasks? Alternatively, do the same neurons play different roles in different tasks? To address these questions, we examined neuronal activity in the posterior medial prefrontal cortex of primates while they were performing two versions of arm-reaching tasks that required the selection of multiple behavioral tactics (i.e., the internal protocol of action selection), a critical requirement for the activation of this area. During the performance of these tasks, neurons in the pmPFC exhibited selective activity for the tactics, visuospatial information, action, or their combination. Surprisingly, in 82% of the tactics-selective neurons, the selective activity appeared in a particular task but not in both. Such task-specific neuronal representation appeared in 72% of the action-selective neurons. In addition, 95% of the neurons representing visuospatial information showed such activity exclusively in one task but not in both. Our findings indicate that the same neurons can play different roles across different tasks even though the tasks require common information, supporting the latter hypothesis.

A working hypothesis is put forward in this article that the contralateral organization of the human nervous system appears to function like a quantum unfolded holographic apparatus by appearing to invert and reverse quantum unfolded visual and non-visual spatial information. As such, the three-dimensional contralateral organization would be an artifactual representation of the underlying dynamics of a fundamentally two-dimensional universe. According to the holographic principle, nothing that is experienced as three-dimensional could have been processed in a three-dimensional brain. Everything we would experience at a two-dimensional level would appear as a three-dimensional holographic representation, including the architecture of our brains. Various research observations reported elsewhere are reviewed and interpreted here as they may be related in a process that is fundamental to the underlying two-dimensional dynamics of the contralateral organization. The classic holographic method and characteristics of image formation contained by a holograph are described as they relate to the working hypothesis. The double-slit experiment is described and its relevance to the working hypothesis.

This study aimed to clarify whether short-term neurofeedback training during the acute stroke phase led to prefrontal activity self-regulation, providing positive efficacy to working memory. A total of 30 patients with acute stroke performed functional near-infrared spectroscopy-based neurofeedback training for a day to increase their prefrontal activity. A randomized, Sham-controlled, double-blind study protocol was used comparing working memory ability before and after neurofeedback training. Working memory was evaluated using a target-searching task requiring spatial information retention. A decline in spatial working memory performance post-intervention was prevented in patients who displayed a higher task-related right prefrontal activity during neurofeedback training compared with the baseline. Neurofeedback training efficacy was not associated with the patient's clinical background such as Fugl-Meyer Assessment score and time since stroke. These findings demonstrated that even short-term neurofeedback training can strengthen prefrontal activity and help maintain cognitive ability in acute stroke patients, at least immediately after training. However, further studies investigating the influence of individual patient clinical background, especially cognitive impairment, on neurofeedback training is needed. Current findings provide an encouraging option for clinicians to design neurorehabilitation programs, including neurofeedback protocols, for acute stroke patients.