Synchronized Gamma Oscillations Research Articles

Neural Oscillations and Multisensory Processing.

Neural oscillations play a role in sensory processing by coordinating synchronized neuronal activity. Synchronization of gamma oscillations is engaged in local computation of feedforward signals and synchronization of alpha-beta oscillations is engaged in feedback processing over long-range areas. These spatially and spectrally segregated bi-directional signals may be integrated by a mechanism of cross-frequency coupling. Synchronization of neural oscillations has also been proposed as a mechanism for information integration across multiple sensory modalities. A transient stimulus or rhythmic stimulus from one modality may lead to phase alignment of ongoing neural oscillations in multiple sensory cortices, through a mechanism of cross-modal phase reset or cross-modal neural entrainment. Synchronized activities in multiple sensory cortices are more likely to boost stronger activities in downstream areas. Compared to synchronized oscillations, asynchronized oscillations may impede signal processing, and may contribute to sensory selection by setting the oscillations in the target-related cortex and the oscillations in the distractor-related cortex to opposite phases.

Auditory Gamma Entrainment Leads to Theta Oscillations Asymmetric behavior in both Alzheimer’s Disease and Healthy Participants

AbstractBackgroundBrain oscillations known for handling various information across brain. The gamma rhythms observed in high‐level cognitive process (Fries et al., Trends in neurosciences 2018) and theta cycle observed to process sensory information and interact with gamma oscillations (Amemiya et al., Cell Reports 2018). Disruption in synchronization of gamma oscillations have been observed in Alzheimer’s disease patients (Uhlhaas et al., Neuron 2006). Gamma stimulation had been shown to reduce the mentioned dysfunction and reported to have therapeutic results (Martorell et al., Cell 2019; Suk et al. Alzheimer’s and Dementia 2020). This study examines the effect of gamma band activity induced by auditory chirp stimulation as a driver for other frequency sources. The chirp signal is designed to entrain 40Hz which had been shown to have therapeutics effects.Method33 participants were included in this study including 17 mild AD, 6 MCI and 10 healthy elderlies. A session consists of interleaved periods of forty second stimulation and twenty second silence. The stimulation is a 5kHz tone modulated by a 40Hz chirp at 0.1 duty cycle. EEG data were collected by a 10/20 system. Relative magnitude of the 40Hz oscillations with respect to neighbors’ magnitude during the stimulation was measured as an indicator of the entrained gamma oscillations. Total participants are categorized into entrained and not‐entrained group based on the indicator. Phase locking Value (PLV) is then calculated in theta frequency band.Result40Hz entrainment have been observed in healthy participants and also some Alzheimer’s disease patients. Based on the power spectral density (PSD) at forty hertz 23 entrained and 10 not‐entrained participants are separated and PLV analysis have been calculated for the two groups. Theta oscillatory asymmetry have been observed in posterior temporal cortex during auditory stimulation.ConclusionEntraining gamma oscillations using auditory stimulation results in cross frequency variation. Phase‐amplitude or phase‐phase coupling measures the simultaneous correlation between specific oscillations. This study suggests that despite the concurrent association of theta‐gamma frequencies, some brain network changes occur in response to gamma oscillation which should be more discussed in related researches.

Neurophysiological assessment of cortical activity in DEPDC5- and NPRL3-related epileptic mTORopathies

BackgroundMutations in the GATOR1 complex genes, DEPDC5 and NPRL3, play a major role in the development of lesional and non-lesional focal epilepsy through increased mTORC1 signalling. We aimed to assess the effects of mTORC1 hyperactivation on GABAergic inhibitory circuits, in 3 and 5 individuals carrying DEPDC5 and NPRL3 mutations respectively using a multimodal approach including transcranial magnetic stimulation (TMS), magnetic resonance spectroscopy (MRS), and electroencephalography (EEG).ResultsInhibitory functions probed by TMS and MRS showed no effect of mutations on cortical GABAergic receptor-mediated inhibition and GABA concentration, in both cortical and subcortical regions. However, stronger EEG theta oscillations and stronger and more synchronous gamma oscillations were observed in DEPDC5 and NPRL3 mutations carriers.ConclusionsThese results suggest that DEPDC5 and NPRL3-related epileptic mTORopathies may not directly modulate GABAergic functions but are nonetheless characterized by a stronger neural entrainment that may be reflective of a cortical hyperexcitability mediated by increased mTORC1 signaling.

Association between abnormal brain oscillations and cognitive performance in patients with bipolar disorder: Molecular mechanisms and clinical evidence.

Brain oscillations have gained great attention in neuroscience during recent decades as functional building blocks of cognitive-sensory processes. Research has shown that oscillations in "alpha," "beta," "gamma," "delta," and "theta" frequency windows are highly modified in brain pathology, including in patients with cognitive impairment like bipolar disorder (BD). The study of changes in brain oscillations can provide fundamental knowledge for exploring neurophysiological biomarkers in cognitive impairment. The present article reviews findings from the role and molecular basis of abnormal neural oscillation and synchronization in the symptoms of patients with BD. An overview of the results clearly demonstrates that, in cognitive-sensory processes, resting and evoked/event-related electroencephalogram (EEG) spectra in the delta, theta, alpha, beta, and gamma bands are abnormally changed in patients with BD showing psychotic features. Abnormal oscillations have been found to be associated with several neural dysfunctions and abnormalities contributing to BD, including abnormal GABAergic neurotransmission signaling, hippocampal cell discharge, abnormal hippocampal neurogenesis, impaired cadherin and synaptic contact-based cell adhesion processes, extended lateral ventricles, decreased prefrontal cortical gray matter, and decreased hippocampal volume. Mechanistically, impairment in calcium voltage-gated channel subunit alpha1 I, neurotrophic tyrosine receptor kinase proteins, genes involved in brain neurogenesis and synaptogenesis like WNT3 and ACTG2, genes involved in the cell adhesion process like CDH12 and DISC1, and gamma-aminobutyric acid (GABA) signaling have been reported as the main molecular contributors to the abnormalities in resting-state low-frequency oscillations in BD patients. Findings also showed the association of impaired synaptic connections and disrupted membrane potential with abnormal beta/gamma oscillatory activity in patients with BD. Of note, the synaptic GABA neurotransmitter has been found to be a fundamental requirement for the occurrence of long-distance synchronous gamma oscillations necessary for coordinating the activity of neural networks between various brain regions.

Controlling synchronization of gamma oscillations by astrocytic modulation in a model hippocampal neural network

Recent in vitro and in vivo experiments demonstrate that astrocytes participate in the maintenance of cortical gamma oscillations and recognition memory. However, the mathematical understanding of the underlying dynamical mechanisms remains largely incomplete. Here we investigate how the interplay of slow modulatory astrocytic signaling with fast synaptic transmission controls coherent oscillations in the network of hippocampal interneurons that receive inputs from pyramidal cells. We show that the astrocytic regulation of signal transmission between neurons improves the firing synchrony and extends the region of coherent oscillations in the biologically relevant values of synaptic conductance. Astrocyte-mediated potentiation of inhibitory synaptic transmission markedly enhances the coherence of network oscillations over a broad range of model parameters. Astrocytic regulation of excitatory synaptic input improves the robustness of interneuron network gamma oscillations induced by physiologically relevant excitatory model drive. These findings suggest a mechanism, by which the astrocytes become involved in cognitive function and information processing through modulating fast neural network dynamics.

Transforming Discoveries About Cortical Microcircuits and Gamma Oscillations Into New Treatments for Cognitive Deficits in Schizophrenia.

The major cause of disability in schizophrenia is cognitive impairment, which remains largely refractory to existing treatments. This reflects the fact that antipsychotics and other therapies have not been designed to address specific brain abnormalities that cause cognitive impairment. This overview proposes that understanding how specific cellular and synaptic loci within cortical microcircuits contribute to cortical gamma oscillations may reveal treatments for cognitive impairment. Gamma oscillations are rhythmic patterns of high frequency (∼30-100 Hz) neuronal activity that are synchronized within and across brain regions, generated by a class of inhibitory interneurons that express parvalbumin, and recruited during a variety of cognitive tasks. In schizophrenia, both parvalbumin interneuron function and task-evoked gamma oscillations are deficient. While it has long been controversial whether gamma oscillations are merely a biomarker of circuit function or actually contribute to information processing by neuronal networks, recent neurobiological studies in mice have shown that disrupting or enhancing synchronized gamma oscillations can reproduce or ameliorate cognitive deficits resembling those seen in schizophrenia. In fact, transiently enhancing the synchrony of parvalbumin interneuron-generated gamma oscillations can lead to long-lasting improvements in cognition in mice that model aspects of schizophrenia. Gamma oscillations emerge from specific patterns of connections between a variety of cell types within cortical microcircuits. Thus, a critical next step is to understand how specific cell types and synapses generate gamma oscillations, mediate the effects of gamma oscillations on information processing, and/or undergo plasticity following the induction of gamma oscillations. Modulating these circuit loci, potentially in combination with other approaches such as cognitive training and brain stimulation, may yield potent and selective interventions for enhancing cognition in schizophrenia.

Activity Stabilization in a Population Model of Working Memory by Sinusoidal and Noisy Inputs.

According to mechanistic theories of working memory (WM), information is retained as stimulus-dependent persistent spiking activity of cortical neural networks. Yet, how this activity is related to changes in the oscillatory profile observed during WM tasks remains a largely open issue. We explore joint effects of input gamma-band oscillations and noise on the dynamics of several firing rate models of WM. The considered models have a metastable active regime, i.e., they demonstrate long-lasting transient post-stimulus firing rate elevation. We start from a single excitatory-inhibitory circuit and demonstrate that either gamma-band or noise input could stabilize the active regime, thus supporting WM retention. We then consider a system of two circuits with excitatory intercoupling. We find that fast coupling allows for better stabilization by common noise compared to independent noise and stronger amplification of this effect by in-phase gamma inputs compared to anti-phase inputs. Finally, we consider a multi-circuit system comprised of two clusters, each containing a group of circuits receiving a common noise input and a group of circuits receiving independent noise. Each cluster is associated with its own local gamma generator, so all its circuits receive gamma-band input in the same phase. We find that gamma-band input differentially stabilizes the activity of the “common-noise” groups compared to the “independent-noise” groups. If the inter-cluster connections are fast, this effect is more pronounced when the gamma-band input is delivered to the clusters in the same phase rather than in the anti-phase. Assuming that the common noise comes from a large-scale distributed WM representation, our results demonstrate that local gamma oscillations can stabilize the activity of the corresponding parts of this representation, with stronger effect for fast long-range connections and synchronized gamma oscillations.

Cross-Hemispheric Circuit Dysfunction Impairs Novelty Discrimination in Alzheimer's Disease Mice

SUMMARYA clinical hallmark of Alzheimer’s disease is significant reductions in the white matter connecting the two cerebral hemispheres, as well as in the correlated activity between anatomically corresponding bilateral brain areas. However, the underlying circuit mechanisms and the cognitive relevance of cross-hemispheric communication remain poorly studied. Here, we show that novelty discrimination behavior activated cross-hemispheric neurons and enhanced homotopic synchronized gamma oscillations in the visual cortex. Cross-hemispheric neurons provide excitatory drive required for synchronous gamma oscillations between hemispheres and unilateral inhibition of the cross-hemispheric circuit is sufficient to impair behavior. In the 5XFAD mouse model of Alzheimer’s disease, cross-hemispheric communication is compromised and novelty discrimination is impaired; a deficit rescued by gamma sensory stimulation. These data establish a causal link between a cross-hemispheric circuit and behavior and highlight its impairment in Alzheimer’s disease mice.

Lactate Attenuates Synaptic Transmission and Affects Brain Rhythms Featuring High Energy Expenditure.

SummaryLactate shuttled from blood, astrocytes, and/or oligodendrocytes may serve as the major glucose alternative in brain energy metabolism. However, its effectiveness in fueling neuronal information processing underlying complex cortex functions like perception and memory is unclear. We show that sole lactate disturbs electrical gamma and theta-gamma oscillations in hippocampal networks by either attenuation or neural bursts. Bursting is suppressed by elevating the glucose fraction in substrate supply. By contrast, lactate does not affect electrical sharp wave-ripple activity featuring lower energy use. Lactate increases the oxygen consumption during the network states, reflecting enhanced oxidative ATP synthesis in mitochondria. Finally, lactate attenuates synaptic transmission in excitatory pyramidal cells and fast-spiking, inhibitory interneurons by reduced neurotransmitter release from presynaptic terminals, whereas action potential generation in the axon is regular. In conclusion, sole lactate is less effective and potentially harmful during gamma-band rhythms by omitting obligatory ATP delivery through fast glycolysis at the synapse.

Dynamic Recovery from Depression Enables Rate Encoding in Inhibitory Synapses.

SummaryParvalbumin-expressing fast-spiking interneurons (PV-INs) control network firing and the gain of cortical response to sensory stimulation. Crucial for these functions, PV-INs can sustain high-frequency firing with no accommodation. However, PV-INs also exhibit short-term depression (STD) during sustained activation, largely due to the depletion of synaptic resources (vesicles). In most synapses the rate of replenishment of depleted vesicles is constant, determining an inverse relationship between depression levels and the activation rate, which theoretically, severely limits rate-coding capabilities. We examined STD of the PV-IN to pyramidal cell synapse in the mouse visual cortex and found that in these synapses the recovery from depression is not constant but increases linearly with the frequency of use. By combining modeling, dynamic clamp, and optogenetics, we demonstrated that this recovery enables PV-INs to reduce pyramidal cell firing in a linear manner, which theoretically is crucial for controlling the gain of cortical visual responses.

Disruption of gamma-delta relationship related to working memory deficits in first-episode psychosis.

Working memory (WM) deficits constitute a core symptom of schizophrenia. Inadequacy of WM maintenance in schizophrenia has been reported to reflect abnormalities in the excitation/inhibition (E/I) balance between pyramidal neurons and parvalbumin basket cells, which may explain alterations of the dynamics of gamma and delta oscillations. To address this issue, we assessed event-related gamma (35-45Hz) and delta (0.5-4Hz) oscillatory responses in a visual n-back WM task in patients with first-episode psychosis (FEP) and healthy controls (HC). Periodicity analyses of oscillations were computed to explore the relationship between the psychiatric status and the WM load-related processes reflected by each frequency range. The correspondence between nested delta-gamma oscillations was estimated to assess the strength of the frontal E/I balance. In HC, gamma oscillations were synchronized by the stimulus in a 50-150ms time range for all tasks, and periodicity of the delta cycle was comparable between the tasks. In addition, synchronization of gamma oscillations in HC occurred at the maximal descending phase of the delta cycle half-period, supporting the coexistence of delta-nested gamma oscillations. Compared with controls, FEP patients showed a lack of gamma synchronization independently of the nature of the task, and the period of delta oscillation increased significantly with the difficulty of the WM task. We thus demonstrated in FEP an inability to encode multiple items in short-term memory associated with abnormalities in the relationship between oscillations related to the difficulty of the WM task. These results argue in favor of a dysfunction of the E/I balance in psychosis.

Dependency of gamma oscillations in E/I neuronal network on illumination contrast of external stimulus

Synchronous gamma oscillations are believed to play a prominent role in the information processing of biological neural systems. Experimental observations have found that the frequency and power of gamma oscillations in the primary visual cortex (V1 zone) are regulated by the illumination contrast of visual stimulus. However, the underlying mechanism of how the synchronous oscillations depend on the illumination contrast has not been well explained. We propose a local excitatory/inhibitory (E/I) neuronal network of integrate-and-fire (IAF) neurons with the difference-of-Gaussians (DOG) receptive field to unveil this mechanism. Simulation results demonstrate that the higher the illumination contrast, the higher the frequency of gamma oscillations. The power of gamma oscillations also increases with the increase of illumination contrast. These results are consistent with the experimental findings.

Aberrant Sensory Gating of the Primary Somatosensory Cortex Contributes to the Motor Circuit Dysfunction in Paroxysmal Kinesigenic Dyskinesia.

Paroxysmal kinesigenic dyskinesia (PKD) is conventionally regarded as a movement disorder (MD) and characterized by episodic hyperkinesia by sudden movements. However, patients of PKD often have sensory aura and respond excellently to antiepileptic agents. PRRT2 mutations, the most common genetic etiology of PKD, could cause epilepsy syndromes as well. Standing in the twilight zone between MDs and epilepsy, the pathogenesis of PKD is unclear. Gamma oscillations arise from the inhibitory interneurons which are crucial in the thalamocortical circuits. The role of synchronized gamma oscillations in sensory gating is an important mechanism of automatic cortical inhibition. The patterns of gamma oscillations have been used to characterize neurophysiological features of many neurological diseases, including epilepsy and MDs. This study was aimed to investigate the features of gamma synchronizations in PKD. In the paired-pulse electrical-stimulation task, we recorded the magnetoencephalographic data with distributed source modeling and time-frequency analysis in 19 patients of newly-diagnosed PKD without receiving pharmacotherapy and 18 healthy controls. In combination with the magnetic resonance imaging, the source of gamma oscillations was localized in the primary somatosensory cortex. Somatosensory evoked fields of PKD patients had a reduced peak frequency (p < 0.001 for the first and the second response) and a prolonged peak latency (the first response p = 0.02, the second response p = 0.002), indicating the synchronization of gamma oscillation is significantly attenuated. The power ratio between two responses was much higher in the PKD group (p = 0.013), indicating the incompetence of activity suppression. Aberrant gamma synchronizations revealed the defective sensory gating of the somatosensory area contributes the pathogenesis of PKD. Our findings documented disinhibited cortical function is a pathomechanism common to PKD and epilepsy, thus rationalized the clinical overlaps of these two diseases and the therapeutic effect of antiepileptic agents for PKD. There is a greater reduction of the peak gamma frequency in PRRT2-related PKD than the non-PRRT PKD group (p = 0.028 for the first response, p = 0.004 for the second response). Loss-of-function PRRT2 mutations could lead to synaptic dysfunction. The disinhibiton change on neurophysiology reflected the impacts of PRRT2 mutations on human neurophysiology.

Ketamine induced converged synchronous gamma oscillations in the cortico-basal ganglia network of nonhuman primates.

N-methyl-d-aspartate (NMDA) antagonists are widely used in anesthesia, pain management, and schizophrenia animal model studies, and recently as potential antidepressants. However, the mechanisms underlying their anesthetic, psychotic, cognitive, and emotional effects are still elusive. The basal ganglia (BG) integrate input from different cortical domains through their dopamine-modulated connections to achieve optimal behavior control. NMDA antagonists have been shown to induce gamma oscillations in human EEG recordings and in rodent cortical and BG networks. However, network relations and implications to the primate brain are still unclear. We recorded local field potentials (LFPs) simultaneously from the primary motor cortex (M1) and the external globus pallidus (GPe) of four vervet monkeys (26 sessions, 97 and 76 cortical and pallidal LFPs, respectively) before and after administration of ketamine (NMDA antagonist, 10 mg/kg im). Ketamine induced robust, spontaneous gamma (30-50 Hz) oscillations in M1 and GPe. These oscillations were initially modulated by ultraslow oscillations (~0.3 Hz) and were highly synchronized within and between M1 and the GPe (mean coherence magnitude = 0.76, 0.88, and 0.41 for M1-M1, GPe-GPe, and M1-GPe pairs). Phase differences were distributed evenly around zero with broad and very narrow distribution for the M1-M1 and GPe-GPe pairs (-3.5 ± 31.8° and -0.4 ± 6.0°), respectively. The distribution of M1-GPe phase shift was skewed to the left with a mean of -18.4 ± 20.9°. The increased gamma coherence between M1 and GPe, two central stages in the cortico-BG loops, suggests a global abnormal network phenomenon with a unique spectral signature, which is enabled by the BG funneling architecture.NEW & NOTEWORTHY This study is the first to show spontaneous gamma oscillations under NMDA antagonist in nonhuman primates. These oscillations appear in synchrony in the cortex and the basal ganglia. Phase analysis refutes the confounding effects of volume conduction and supports the funneling and amplifying architecture of the cortico-basal ganglia loops. These results suggest an abnormal network phenomenon with a unique spectral signature that could account for pathological mental and neurological states.

Electroconductive polymer-coated silk fiber electrodes for neural recording and stimulation in vivo

We fabricated a silk-based low-impedance flexible electrode by coating a silk thread with the electroconductive polymer poly(3,4-ethylenedioxythiophene) doped with p-toluenesulfonate (PEDOT:pTS). This electrode had a lower impedance (about 1.8 kΩ/cm) than the silk electrode coated with PEDOT doped with poly(styrene sulfonate) (PEDOT:PSS) (about 1.3 MΩ/cm) reported previously. Using this electrode, a novel gamma-band oscillatory activity was recorded in the electrocorticogram from the embryonic chick brain with a high signal-to-noise ratio. Electrical stimulation was also possible with the silk electrode. We also fabricated an all-silk electrode array and recorded synchronized gamma oscillations. These results demonstrate that the silk electrode can be used for electrophysiological recording and local stimulation in vivo. The silk electrode has the potential to be used for diagnostic and therapeutic purposes and as a brain–machine interface.

Aβ1-42-induced dysfunction in synchronized gamma oscillation during working memory

Amyloid-β peptide (Aβ) is recognized as a causative factor for the cognitive impairments in Alzheimer’s disease (AD). The studies on the effects of Aβ to cognitive impairments are beneficial for lifting the veil of the pathophysiology in AD. Neuronal oscillations are proposed to play an important role in cognition and its ensuing behavior. Specially, the synchronized gamma oscillations are essential for the successful execution of working memory. However, whether the Aβ will induce the abnormal neuronal oscillations and working memory deficits has remained largely unexplored. In the present study, rats (control and Aβ-injected groups) were trained to perform a delay-alternation task on Y-maze while spikes and local field potentials (LFPs) were recorded from multi-electrodes implanted in the medial prefrontal cortex (mPFC), an area that is strongly modulated by working memory. Synchronized neuronal oscillations were assessed by phase locking between spike trains and LFPs. We found the significant working memory impairment in the Aβ-injected group. Moreover, in the control group, during the memory retention period, a transient burst of gamma synchronization preceded an animal’s correct choice, but not an animal’s error choice. In the Aβ-injected group, however, gamma synchronization experience no change in neither correct nor error trials. Our results indicate that the Aβ1-42-induced dysfunction in gamma synchronization may provide a potential mechanism for working memory deficits.

A biophysical neural network model for visual working memory that accounts for memory binding errors

Binding errors, also called swap errors, occur in working memory tasks when the participant fails to report the feature of a previously presented target but the response is accurate relative to a non-target stimulus (for instance, s/he reports the of the green item when the red item's was to be reported). Psychophysical experiments have shown the importance of these errors in working memory tasks [1-3], and they reflect the failure of the system to maintain bundled through memory the conjunction of features that define one object. How the brain is able to integrate and maintain integrated several features of an item in one single memory is still an open question. Conjunctive selectivity, where single units are selective to combination of stimuli, has been suggested as a possible solution [4]. However, with the increase of features to encode the number of necessary neurons escalates exponentially. A hypothesis formulated for this problem in visual perception states that synchrony of different neural assemblies coding each of them a single feature of an item plays the main role [5]. This is an attractive hypothesis, because of its parsimonious and flexible neural representation: a particular neuron can participate in the coding of different objects at different times. Because under this hypothesis there is no hardwired selectivity for each group of features, it allows ex novo representations to emerge. Current neurophysiological data provides partial support for this idea but the specific neural mechanism remains unknown [5,6]. In order to understand this phenomenon and to test this synchrony hypothesis, we built a biophysical neural network model for the storage of items orks for working memory (ring models, as in [7]), one representing colors and the other one locations of equal eccentricity. These two networks are then connected via weak cortico-cortical excitation through AMPA synapses. With this model we are able to maintain persistent activity through recurrent synaptic interactions in memory [8] that encode colors and locations. AMPA synapses in recurrent excitation within each network induce gamma oscillations during bump activity through the interplay of fast excitation and slower feedback inhibition [7]. We found that when multiple are maintained within one ring model, the corresponding bump attractors oscillate out of synchrony with each other. In this model, the binding between and is effectively accomplished through the synchronization of gamma oscillations between individual in the two networks as a result of weak cortico-cortical excitation. As previously proposed [9-10], in our network model different memories are held at different phases of a low-frequency oscillation. In some simulations swap errors arise: color bumps abruptly change their phase and thus change their synchrony relationship with location bumps. This leads to a wrong association between and that may underlie memory binding errors reported in working memory tasks.

Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.

SummaryLoss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are among the most common genetic abnormalities associated with autism spectrum disorders, but little is known about the function of Neuroligin-4 and the consequences of its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout mice, focusing on the hippocampus as a model brain region with a critical role in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects of the protein composition and function of GABAergic synapses in the hippocampal CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced perturbations of γ-oscillatory network activity, which has been implicated in cognitive function and is altered in multiple psychiatric and neurodevelopmental disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent GABAergic synapses may contribute to autism phenotypes and indicate new strategies for therapeutic approaches.

Conscious auditory perception related to long-range synchrony of gamma oscillations

While the role of synchronized oscillatory activity in the gamma-band frequency range for conscious perception is well established in the visual domain, there is limited evidence concerning neurophysiological mechanisms in conscious auditory perception. In the current study, we addressed this issue with 64-channel EEG and a dichotic listening (DL) task in twenty-five healthy participants. The typical finding of DL is a more frequent conscious perception of the speech syllable presented to the right ear (RE), which is attributed to the supremacy of the contralateral pathways running from the RE to the speech-dominant left hemisphere. In contrast, the left ear (LE) input initially accesses the right hemisphere and needs additional transfer via interhemispheric pathways before it is processed in the left hemisphere. Using lagged phase synchronization (LPS) analysis and eLORETA source estimation we examined the functional connectivity between right and left primary and secondary auditory cortices in the main frequency bands (delta, theta, alpha, beta, gamma) during RE/LE-reports. Interhemispheric LPS between right and left primary and secondary auditory cortices was specifically increased in the gamma-band range, when participants consciously perceived the syllable presented to the LE. Our results suggest that synchronous gamma oscillations are involved in interhemispheric transfer of auditory information.

Structured Connectivity in Cerebellar Inhibitory Networks

SummaryDefining the rules governing synaptic connectivity is key to formulating theories of neural circuit function. Interneurons can be connected by both electrical and chemical synapses, but the organization and interaction of these two complementary microcircuits is unknown. By recording from multiple molecular layer interneurons in the cerebellar cortex, we reveal specific, nonrandom connectivity patterns in both GABAergic chemical and electrical interneuron networks. Both networks contain clustered motifs and show specific overlap between them. Chemical connections exhibit a preference for transitive patterns, such as feedforward triplet motifs. This structured connectivity is supported by a characteristic spatial organization: transitivity of chemical connectivity is directed vertically in the sagittal plane, and electrical synapses appear strictly confined to the sagittal plane. The specific, highly structured connectivity rules suggest that these motifs are essential for the function of the cerebellar network.