Reduced Theta Power Research Articles

Cross-strata co-occurrence of ripples with theta-frequency oscillations in the hippocampus of foraging rats.

Brain rhythms have been postulated to play central roles in animal cognition. A prominently reported dichotomy of hippocampal rhythms links theta-frequency oscillations (4-12Hz) and ripples (120-250Hz) exclusively to preparatory and consummatory behaviours, respectively. However, because of the differential power expression of these two signals across hippocampal strata, such exclusivity requires validation through analyses of simultaneous multi-strata recordings. We assessed co-occurrence of theta-frequency oscillations with ripples in multi-channel recordings of extracellular potentials across hippocampal strata from foraging rats. We detected all ripple events from an identified stratum pyramidale (SP) channel. We then defined theta epochs based on theta oscillations detected from the stratum lacunosum-moleculare (SLM) or the stratum radiatum (SR). We found ∼20% of ripple events (in SP) to co-occur with theta epochs identified from SR/SLM channels, defined here as theta ripples. Strikingly, when theta epochs were instead identified from the SP channel, such co-occurrences were significantly reduced because of a progressive reduction in theta power along the SLM-SR-SP axis. Behaviourally, we found most theta ripples to occur during immobile periods, with comparable theta power during exploratory and immobile theta epochs. Furthermore, the progressive reduction in theta power along the SLM-SR-SP axis was common to exploratory and immobile periods. Finally, we found a strong theta-phase preference of theta ripples within the fourth quadrant [3π/2-2π] of the associated theta oscillation. The prevalence of theta ripples expands the potential roles of ripple-frequency oscillations to span the continuum of encoding, retrieval and consolidation, achieved through interactions with theta oscillations. KEY POINTS: The brain manifests oscillations in recorded electrical potentials, with different frequencies of oscillation associated with distinct behavioural states. A prominently reported dichotomy assigns theta-frequency oscillations (4-12Hz) and ripples (120-250Hz) recorded in the hippocampus to be exclusively associated with preparatory and consummatory behaviours, respectively. Our multi-strata recordings from the rodent hippocampus coupled with cross-strata analyses provide direct quantitative evidence for the occurrence of ripple events nested within theta oscillations. These results highlight the need for an analysis pipeline that explicitly accounts for the specific strata where individual oscillatory power is high, in analysing simultaneously recorded data from multiple strata. Our observations open avenues for investigations involving cross-strata interactions between theta oscillations and ripples across different behavioural states.

Optogenetic Stimulation of CA1 Pyramidal Neurons at Theta Enhances Recognition Memory in Brain Injured Animals.

Abstract The hippocampus plays a prominent role in learning and memory formation. The functional integrity of this structure is often compromised after traumatic brain injury (TBI), resulting in lasting cognitive dysfunction. The activity of hippocampal neurons, particularly place cells, is coordinated by local theta oscillations. Previous studies aimed at examining hippocampal theta oscillations after experimental TBI have reported disparate findings. Using a diffuse brain injury model, the lateral fluid percussion injury (FPI; 2.0 atm), we report a significant reduction in hippocampal theta power that persists for at least three weeks after injury. We questioned whether the behavioral deficit associated with this reduction of theta power can be overcome by optogenetically stimulating CA1 neurons at theta in brain injured rats. Our results show that memory impairments in brain injured animals could be reversed by optogenetically stimulating CA1 pyramidal neurons expressing channelrhodopsin (ChR2) during learning. In contrast, injured animals receiving a control virus (lacking ChR2) did not benefit from optostimulation. These results suggest that direct stimulation of CA1 pyramidal neurons at theta may be a viable option for enhancing memory after TBI.

Reductions in regional theta power and fronto-parietal theta-gamma phase-amplitude coupling during gaze processing in bipolar disorder

Impaired social cognition is common in bipolar disorder (BD) and predicts poor functional outcomes. A critical determinant of social cognition is the ability to discriminate others’ gaze direction, and its alteration may contribute to functional impairment in BD. However, the neural mechanisms underlying gaze processing in BD are unclear. Because neural oscillations are crucial neurobiological mechanisms supporting cognition, we aimed to understand their role in gaze processing in BD. Using electroencephalography (EEG) data recorded during a gaze discrimination task for 38 BD and 34 controls (HC), we examined: theta and gamma power over bilateral posterior and midline anterior locations associated with early face processing and higher-level cognitive processing, and theta-gamma phase-amplitude coupling (PAC) between locations. Compared to HC, BD showed reduced midline-anterior and left-posterior theta power, and diminished bottom-up/top-down theta-gamma PAC between anterior/posterior sites. Reduced theta power and theta-gamma PAC related to slower response times. These findings suggest that altered theta oscillations and anterior-posterior cross-frequency coupling between areas associated with higher-level cognition and early face processing may underlie impaired gaze processing in BD. This is a crucial step towards translational research that may inform novel social cognitive interventions (e.g., neuromodulation to target specific oscillatory dynamics) to improve functioning in BD.

The Average Reward Rate Modulates Behavioral and Neural Indices of Effortful Control Allocation.

People tend to avoid exerting cognitive effort, and findings from recent behavioral studies suggest that effort allocation is in part determined by the opportunity cost of slothful responding-operationalized as the average reward rate per unit time. When the average rate of reward is high, individuals make more errors in cognitive control tasks, presumably owing to a withdrawal of costly cognitive processing. An open question remains whether the presumed modulations of cognitively effortful control processes are observable at the neural level. Here, we measured EEG while participants completed the Simon task, a well-known response conflict task, while the experienced average reward rate fluctuated across trials. We examined neural activity associated with the opportunity cost of time by applying generalized eigendecomposition, a hypothesis-driven source separation technique, to identify a midfrontal component associated with the average reward rate. Fluctuations in average reward rate modulated not only component amplitude but also, most importantly, component theta power (4-8 Hz). Higher average reward rate was associated with reduced theta power, suggesting that the opportunity of time modulates effort allocation. These neural results provide evidence for the idea that people strategically modulate the amount of cognitive effort they exert based on the opportunity cost of time.

The Effect of Traumatic Brain Injury on Sleep Architecture and Circadian Rhythms in Mice-A Comparison of High-Frequency Head Impact and Controlled Cortical Injury.

Simple SummaryTraumatic brain injury (TBI) is a significant risk factor for the development of sleep and circadian rhythm impairments. In order to understand if TBI models with different injury mechanism, severity and pathology have different sleep and circadian rhythm disruptions, we performed a detailed sleep and circadian analysis of the high-frequency head impact TBI model (a mouse model that mimics sports-related head impacts) and the controlled cortical impact TBI model (a mouse model that mimics severe brain trauma). We found that both TBI models disrupt the ability of brain cells to maintain circadian rhythms; however, both injury groups could still maintain circadian behavior patterns. Both the mild head impact model and the severe brain injury model had normal amount of sleep at 7 d after injury; however, the severe brain injury mice had disrupted brain wave patterns during sleep. We conclude that different types of TBI have different patterns of sleep disruptions.Traumatic brain injury (TBI) is a significant risk factor for the development of sleep and circadian rhythm impairments. In this study we compare the circadian rhythms and sleep patterns in the high-frequency head impact (HFHI) and controlled cortical impact (CCI) mouse models of TBI. These mouse models have different injury mechanisms key differences of pathology in brain regions controlling circadian rhythms and EEG wave generation. We found that both HFHI and CCI caused dysregulation in the diurnal expression of core circadian genes (Bmal1, Clock, Per1,2, Cry1,2) at 24 h post-TBI. CCI mice had reduced locomotor activity on running wheels in the first 7 d post-TBI; however, both CCI and HFHI mice were able to maintain circadian behavior cycles even in the absence of light cues. We used implantable EEG to measure sleep cycles and brain activity and found that there were no differences in the time spent awake, in NREM or REM sleep in either TBI model. However, in the sleep states, CCI mice have reduced delta power in NREM sleep and reduced theta power in REM sleep at 7 d post-TBI. Our data reveal that different types of brain trauma can result in distinct patterns of circadian and sleep disruptions and can be used to better understand the etiology of sleep disorders after TBI.

EEG time–frequency analysis reveals blunted tendency to approach and increased processing of unpleasant stimuli in dysphoria

To date, affective and cognitive processing of emotional information in individuals with depressive symptoms have been examined through peripheral psychophysiological measures, event-related potentials, and time–frequency analysis of oscillatory activity. However, electrocortical correlates of emotional and cognitive processing of affective content in depression have not been fully understood. Time–frequency analysis of electroencephalographic activity allows disentangling the brain's parallel processing of information. The present study employed a time–frequency approach to simultaneously examine affective disposition and cognitive processing during the viewing of emotional stimuli in dysphoria. Time–frequency event-related changes were examined during the viewing of pleasant, neutral and unpleasant pictures in 24 individuals with dysphoria and 24 controls. Affective disposition was indexed by delta and alpha power, while theta power was employed as a correlate of cognitive elaboration of the stimuli. Cluster-based statistics revealed a centro-parietal reduction in delta power for pleasant stimuli in individuals with dysphoria relative to controls. Also, dysphoria was characterized by an early fronto-central increase in theta power for unpleasant stimuli relative to neutral and pleasant ones. Comparatively, controls were characterized by a late fronto-central and occipital reduction in theta power for unpleasant stimuli relative to neutral and pleasant. The present study granted novel insights on the interrelated facets of affective elaboration in dysphoria, mainly characterized by a hypoactivation of the approach-related motivational system and a sustained facilitated cognitive processing of unpleasant stimuli.

The Antidepressant-Like and Analgesic Effects of Kratom Alkaloids are accompanied by Changes in Low Frequency Oscillations but not ΔFosB Accumulation.

Mitragyna speciosa (“kratom”), employed as a traditional medicine to improve mood and relieve pain, has shown increased use in Europe and North America. Here, the dose-dependent effects of a purified alkaloid kratom extract on neuronal oscillatory systems function, analgesia, and antidepressant-like behaviour were evaluated and kratom-induced changes in ΔFosB expression determined. Male rats were administered a low or high dose of kratom (containing 0.5 or 1 mg/kg of mitragynine, respectively) for seven days. Acute or repeated low dose kratom suppressed ventral tegmental area (VTA) theta oscillatory power whereas acute or repeated high dose kratom increased delta power, and reduced theta power, in the nucleus accumbens (NAc), prefrontal cortex (PFC), cingulate cortex (Cg) and VTA. The repeated administration of low dose kratom additionally elevated delta power in PFC, decreased theta power in NAc and PFC, and suppressed beta and low gamma power in Cg. Suppressed high gamma power in NAc and PFC was seen selectively following repeated high dose kratom. Both doses of kratom elevated NAc-PFC, VTA-NAc, and VTA-Cg coherence. Low dose kratom had antidepressant-like properties whereas both doses produced analgesia. No kratom-induced changes in ΔFosB expression were evident. These results support a role for kratom as having both antidepressant and analgesic properties that are accompanied by specific changes in neuronal circuit function. However, the absence of drug-induced changes in ΔFosB expression suggest that the drug may circumvent this cellular signaling pathway, a pathway known for its significant role in addiction.

P 37. The cognitive course in Parkinson's disease patients treated with Deep Brain Stimulation of subthalamic nucleus – Correlations with qEEG

Objective. Deep brain stimulation of the subthalamic nucleus (STN-DBS) improve motor functioning in Parkinson“s disease patients– Additionally it can also influence cognitive functioning. In most patients, a decline of verbal fluency test performance after STN-DBS is often reported. The purpose of this study was to determine whether preoperative quantitative electroencephalography (qEEG) may be useful in the preoperative assessment predicting cognitive changes in PD patients treated with STN-DBS. Methods. We compared the cognitive performance of 16 PD patients who underwent bilateral STN-DBS and 15 PD controls (matched for age, sex and education) at baseline as well as after 24 months. Cognitive scores were calculated for all patients across 5 cognitive domains covered by different cognitive tests (attention, executive function, episodic & working memory, verbal fluency, visuo-construction). A preoperative 256-channels EEG was recorded of each patient at rest and global relative power spectra were computed. Correlation and linear regression models were used to assess the association of preoperative EEG measures with postoperative cognitive scores in stimulated PD patients compared to PD controls. Results. The decline of verbal fluency performance after two years in the PD group treated with STN-DBS was significant in comparison to the PD controls ( p < 0.001). All other cognitive domains declined in the same manner as in the PD controls or remained stable over the 24-months period. EEG frequency analyses revealed increased global theta power (4-8 Hz) at baseline to be associated with reduced postoperative verbal fluency performance ( r = 0.50, p < 0.05) at follow-up. Conclusion. Consistent with the results of former studies, STN stimulation deteriorates verbal fluency in the course of two years. Accordingly, we observed significant decline in tests measuring verbal fluency in the group of PD patients treated with STN-DBS compared to a control group of PD patients. The decline of verbal fluency performance could be predicted by a reduced theta power at baseline. No other significant differences in cognitive alterations between patients in the STN-DBS group and the PD control group occur over two years.

Electrocorticography Analysis in Patients With Dual Neurostimulators Supports Desynchronization as a Mechanism of Action for Acute Vagal Nerve Stimulator Stimulation.

Both vagal nerve stimulation (VNS) and responsive neurostimulation (RNS System) are treatment options for medically refractory focal epilepsy. The mechanism of action of both devices remains poorly understood. Limited prior evidence suggests that acute VNS stimulation may reduce epileptiform activity and cause EEG desynchronization on electrocorticography (ECoG). Our study aims to isolate effects of VNS on ECoG as recorded by RNS System in patients who have both devices, by comparing ECoG samples with and without acute VNS stimulation. Ten 60-second ECoGs each from 22 individuals at 3 epilepsy centers were obtained-5 ECoGs with VNS "off" and 5 ECoGs with VNS "on." Electrocorticograps containing seizures or loss of telemetry connection artifact were excluded from analysis (total of 169 ECoGs were included). Electrocorticographs were analyzed for differences in spectral content by generating average spectrograms for "on" and "off" states and using a linear mixed-effects model to isolate effects of VNS stimulation. Acute VNS stimulation reduced average power in the theta band by 4.9%, beta band by 3.8%, and alpha band by 2.5%. The reduction in theta power reached statistical significance with a P value of <0.05. Our results provide evidence that acute VNS stimulation results in desynchronization of specific frequency bands (salient decrease in theta and beta bands, smaller decrease in alpha band) in ECoGs recorded by the RNS device in patients with dual (VNS and RNS) neurostimulators. This finding offers support for desynchronization as a theorized mechanism of action of VNS. Further research may lead to future improved neurostimulator efficacy by informing optimal stimulation programming parameters.

Sex differences in innate and adaptive neural oscillatory patterns link resilience and susceptibility to chronic stress in rats.

BackgroundMajor depressive disorder is a chronic illness with a higher incidence in women. Dysregulated neural oscillatory activity is an emerging mechanism thought to underlie major depressive disorder, but whether sex differences in these rhythms contribute to the development of symptoms is unknown.MethodsWe exposed male and female rats to chronic unpredictable stress and characterized them as stress-resilient or stress-susceptible based on behavioural output in the forced swim test and the sucrose preference test. To identify sex-specific neural oscillatory patterns associated with stress response, we recorded local field potentials from the prefrontal cortex, cingulate cortex, nucleus accumbens and dorsal hippocampus throughout stress exposure.ResultsAt baseline, female stress-resilient rats innately exhibited higher theta coherence in hippocampal connections compared with stress-susceptible female rats. Following stress exposure, additional oscillatory changes manifested: stress-resilient females were characterized by increased dorsal hippocampal theta power and cortical gamma power, and stress-resilient males were characterized by a widespread increase in high gamma coherence. In stress-susceptible animals, we observed a pattern of increased delta and reduced theta power; the changes were restricted to the cingulate cortex and dorsal hippocampus in males but occurred globally in females. Finally, stress exposure was accompanied by the time-dependent recruitment of specific neural pathways, which culminated in system-wide changes that temporally coincided with the onset of depression-like behaviour.LimitationsWe could not establish causality between the electrophysiological changes and behaviours with the methodology we employed.ConclusionSex-specific neurophysiological patterns can function as early markers for stress vulnerability and the onset of depression-like behaviours in rats.

The unsolved mystery of hippocampal cholinergic neurostimulating peptide: A potent cholinergic regulator

Cholinergic efferent networks located from the medial septal nucleus to the hippocampus play a pivotal role in learning and memory outcomes by generating regular theta rhythms that enhance information retention. Hippocampal cholinergic neurostimulating peptide (HCNP), derived from the N-terminus of HCNP precursor protein (HCNP-pp), promotes the synthesis of acetylcholine in the medial septal nuclei. HCNP-pp deletion significantly reduced theta power in CA1 possibly due to lower levels of choline acetyltransferase-positive axons in CA1 stratum oriens, suggesting cholinergic disruptions in the septo-hippocampal system. This review also explores HCNP as a potent cholinergic regulator in the septo-hippocampal network while also examining the limitations of our understanding of the neurostimulating peptide.

The Dynamic Properties of a Brain Network During Spatial Working Memory Tasks in College Students With ADHD Traits.

This study investigated deficits of spatial working memory in college students with attention-deficit/hyperactivity disorder (ADHD) traits using event-related potentials (ERPs) and the spatial 2-back task. We also computed sensory-level activity using EEG data and investigated theta and alpha neural oscillations, phase-locking values (PLV), and brain networks. Based on the scores from the Adult ADHD Self-Report Scale (ASRS) and Conners’ Adult ADHD Rating Scales (CAARS), an ADHD-trait group (n = 40) and a normal control group (n = 41) were selected. Participants were required to respond to whether the presented stimulus was at the same location as that presented two trials earlier. The ADHD-trait group showed significantly slower response times than the control group in the spatial 2-back task. In terms of spectrum, the ADHD-trait group showed significantly reduced theta power than the control group. In contrast, the ADHD-trait group exhibited an increased alpha power compared to the control group with the 250–1000 ms interval after stimulus onset. In terms of the PLV, the ADHD-trait group showed significantly weaker theta phase synchrony and fewer connection numbers in frontal-occipital areas than the control group. In terms of the theta brain network, the ADHD-trait group showed a significantly lower clustering coefficient and longer characteristic path length than the control group for the theta band. The present results indicate that college students with ADHD traits have deficits in spatial working memory and that these abnormal activities in neural oscillation, functional connectivity, and the network may contribute to spatial working memory deficits.

Acute mitragynine administration suppresses cortical oscillatory power and systems theta coherence in rats.

Mitragynine is the major alkaloid of Mitragyna speciosa (kratom) with potential as a therapeutic in pain management and in depression. There has been debate over the potential side effects of the drug including addiction risk and cognitive decline. To evaluate the effects of mitragynine on neurophysiological systems function in the prefrontal cortex (PFC), cingulate cortex (Cg), orbitofrontal cortex, nucleus accumbens (NAc), hippocampus (HIP), thalamus (THAL), basolateral amygdala (BLA) and ventral tegmental area of rats. Local field potential recordings were taken from animals at baseline and for 45 min following mitragynine administration (10 mg/kg, intraperitoneally). Drug-induced changes in spectral power and coherence between regions at specific frequencies were evaluated. Mitragynine-induced changes in c-fos expression were also analyzed. Mitragynine increased delta power and reduced theta power in all three cortical regions that were accompanied by increased c-fos expression. A transient suppression of gamma power in PFC and Cg was also evident. There were no effects of mitragynine on spectral power in any of the other regions. Mitragynine induced a widespread reduction in theta coherence (7-9 Hz) that involved disruptions in cortical and NAc connectivity with the BLA, HIP and THAL. These findings show that mitragynine induces frequency-specific changes in cortical neural oscillatory activity that could potentially impact cognitive functioning. However, the absence of drug effects within regions of the mesolimbic pathway may suggest either a lack of addiction potential, or an underlying mechanism of addiction that is distinct from other opioid analgesic agents.

Reduced Theta Power During Memory Retrieval in Depressed Adults

BackgroundMajor depressive disorder (MDD) is associated with poor recollection, but the neural mechanisms responsible for this deficit are unclear. Recollection is supported by interactions between the hippocampus and cortex that appear to be mediated by oscillatory activity in the theta band (4-7 Hz) and that are elicited during source memory retrieval. Therefore, we tested the hypothesis that evoked theta power during source memory retrieval would be reduced in MDD, as this would provide a physiological basis for deficient recollection in adults with depression. MethodsMorlet wavelets were applied to event-related potentials collected from 24 unmedicated adults with MDD and 24 healthy control adults during the retrieval of source and semantic memories. Whole-scalp analyses focused on group differences in evoked theta power. ResultsThere were no group differences in behavior. Nevertheless, from 400 to 799 ms, theta power was broadly reduced in adults with depression versus healthy adults. This reduction was observed during source and semantic retrieval. Parietal midline electrodes showed significantly reduced theta power during source—but not semantic—retrieval in adults with depression versus healthy adults in this interval. Furthermore, theta power over parietal midline sites from 400 to 799 ms was more strongly related to source memory accuracy in healthy adults versus adults with depression. ConclusionsRelative to healthy control adults, adults with depression showed reduced theta power during memory retrieval and a weaker relationship between parietal midline theta power and source memory accuracy. These findings indicate that abnormal theta signals may contribute to memory deficits in adults with MDD.

Brain Oscillatory Correlates of Visual Short-Term Memory Errors.

Brain dynamics of memory formation were explored during encoding and retention intervals of a visual working memory task. EEG data were acquired while subjects were exposed to grayscale images of widely known object categories (e.g., “luggage,” “chair,” and “car”). Following a short delay, two probes were shown to test memory accuracy. Oscillatory portraits of successful and erroneous memories were contrasted. Where significant differences were identified, oscillatory traits of false memories (i.e., when a novel probe item of the same category is recognized as familiar) were compared with those of successful and erroneous memories. Spectral analysis revealed theta (6–8 Hz) power over occipital channels for encoding of successful and false memories that was smaller when compared to other types of memory errors. The reduced theta power indicates successful encoding and reflects the efficient activation of the underlying neural assemblies. Prominent alpha-beta (10–26 Hz) activity belonging to the right parieto-occipital channels was identified during the retention interval. It was found to be larger for false memories and errors than that of correctly answered trials. High levels of alpha-beta oscillatory activity for errors correspond to poor maintenance leading to inefficient allocation of WM resources. In case of false memories, this would imply necessary cognitive effort to manage the extra semantic and perceptual load induced by the encoded stimuli.

Bi-Directional Theta Modulation between the Septo-Hippocampal System and the Mammillary Area in Free-Moving Rats

Hippocampal (HPC) theta oscillations have long been linked to various functions of the brain. Many cortical and subcortical areas that also exhibit theta oscillations have been linked to functional circuits with the hippocampus on the basis of coupled activities at theta frequencies. We examine, in freely moving rats, the characteristics of diencephalic theta local field potentials (LFPs) recorded in the supramammillary/mammillary (SuM/MM) areas that are bi-directionally connected to the HPC through the septal complex. Using partial directed coherence (PDC), we find support for previous suggestions that SuM modulates HPC theta at higher frequencies. We find weak separation of SuM and MM by dominant theta frequency recorded locally. Contrary to oscillatory cell activities under anesthesia where SuM is insensitive, but MM is sensitive to medial septal (MS) inactivation, theta LFPs persisted and became indistinguishable after MS-inactivation. However, MS-inactivation attenuated SuM/MM theta power, while increasing the frequency of SuM/MM theta. MS-inactivation also reduced root mean squared power in both HPC and SuM/MM equally, but reduced theta power differentially in the time domain. We provide converging evidence that SuM is preferentially involved in coding HPC theta at higher frequencies, and that the MS-HPC circuit normally imposes a frequency-limiting modulation over the SuM/MM area as suggested by cell-based recordings in anesthetized animals. In addition, we provide evidence that the postulated SuM-MS-HPC-MM circuit is under complex bi-directional control, rather than SuM and MM having roles as unidirectional relays in the network.

Transient reduction in theta power caused by interictal spikes in human temporal lobe epilepsy.

The inhibitory impacts of spikes on LFP theta rhythms(4-8Hz) are investigated around sporadic spikes(SSs) based on intracerebral EEG of 4 REM sleep patients with temporal lobe epilepsy(TLE) under the pre-surgical monitoring. Sequential interictal spikes in both genesis area and extended propagation pathway are collected, that, SSs genesis only in anterior hippocampus(aH)(possible propagation pathway in Entorhinal cortex(EC)), only in EC(possible propagation pathway in aH), and in both aH and EC synchronously. Instantaneous theta power was estimated by using Gabor wavelet transform, and theta power level was estimated by averaged over time and frequency before SSs(350ms pre-spike) and after SSs(350ms post-spike). The inhibitory effect around spikes was evaluated by the ratio of theta power level difference between pre-spike and post-spike to pre-spike theta power level. The findings were that theta power level was reduced across SSs, and the effects were more sever in the case of SSs in both aH and EC synchronously than either SSs only in EC or SSs only in aH. It is concluded that interictal spikes impair LFP theta rhythms transiently and directly. The work suggests that the reduction of theta power after the interictal spike might be an evaluation indicator of damage of epilepsy to human cognitive rhythms.

记忆遗忘的电生理机制

记忆中不可避免的会存储一些令人厌恶或不愉快的信息，这些信息会对人们的社会适应和心理状态产生诸多消极影响。因此，人们通常会被动或主动的对不想要的记忆进行限制，这种限制可能体现在编码阶段，也可能体现在线索诱发提取阶段。本研究对遗忘过程中的脑电成分和节律活动特征进行概括，旨在找到遗忘的特异性电生理标志。我们发现，遗忘过程主要体现在N2振幅的增加，alpha能量的增强，晚正成分(LPC)减少，theta能量和同步性下降，以及alpha/beta频带间同步性下降，并且以上变化可以预测后续遗忘的成功发生。因此，遗忘可以通过特定的电生理机制来反映，进一步也可能从电生理现象反推遗忘对应的认知过程。 Not all memories are equally welcome in awareness. It is inevitably that human memory would store some disgusting or unwanted information; the information may have negative effects on people’s social adaptability and psychological states. People usually limit the time they spend on thinking about unwanted experiences, a process that begins during encoding, but continues when later reminded by some cues. This study summarizes the electrophysiological components and rhythmic characteristics during the process of motivated forgetting, aiming to reveal the specific electrophysiological indicators of forgetting. And we find that the process of forgetting mainly embodied some changes such as the increase of N2 amplitude, the enhanced power of alpha band, the reduction of theta power and its synchronicity, and the decline of synchronicity between alpha and beta band. While those changes can further successfully predict the occurrence of motivated forgetting. Therefore, the forgetting can be reflected by specific electrophysiological mechanism. And the following researchers may speculate the corresponding cognitive process through the electrophysiological phenomenon.

Infant social attention: an endophenotype of ASD-related traits?

As a neurodevelopmental disorder, symptoms of ASD likely emerge from a complex interaction between preexisting genetic vulnerabilities and the child's environment. One way to understand causal paths to ASD is to identify dimensional ASD-related traits that vary in the general population and that predispose individuals with other risk factors toward ASD. Moving beyond behavioral traits to explore underlying neurocognitive processes may further constrain the underlying genetics. Endophenotypes are quantitative, heritable, trait-related differences that are generally assessed with laboratory-based methods, can be identified in the general population, and may be more closely tied to particular causal chains that have a more restricted set of genetic roots. The most fruitful endophenotypes may be those observed in infancy, prior to the emergence of behavioral symptoms that they are hypothesized to cause. Social motivation is an ASD-related trait that is highly heritable. In this study, we investigate whether infant endophenotypes of social attention relate to familial risk for lower social motivation in the general population. We examined whether infant social attention (measured using habituation, EEG power, and event-related potential tasks previously used in infants/toddlers with ASD) varies quantitatively with parental social motivation in 117 six-month-old and 106 twelve-month-old typically developing infants assessed cross-sectionally. To assess heritable aspects of social motivation, primary caregiver biological parents completed two self-report measures of social avoidance and discomfort that have shown high heritability in previous work. Parents with higher social discomfort and avoidance had infants who showed shorter looks to faces but not objects; reduced theta power during naturalistic social attention; and smaller P400 responses to faces versus objects. Early reductions in social attention are continuously related to lower parental social motivation. Alterations in social attention may be infant endophenotypes of social motivation traits related to ASD.

Functional Reduction in Cannabinoid-Sensitive Heterotypic Inhibition of Dentate Basket Cells in Epilepsy: Impact on Network Rhythms.

Strong perisomatic inhibition by fast-spiking basket cells (FS-BCs) regulates dentate throughput. Homotypic FS-BC interconnections that support gamma oscillations, and heterotypic inputs from diverse groups of interneurons that receive extensive neurochemical regulation, together, shape FS-BC activity patterns. However, whether seizures precipitate functional changes in inhibitory networks and contribute to abnormal network activity in epilepsy is not known. In the first recordings from dentate interneuronal pairs in a model of temporal lobe epilepsy, we demonstrate that status epilepticus (SE) selectively compromises GABA release at synapses from dentate accommodating interneurons (AC-INs) to FS-BCs, while efficacy of homotypic FS-BC synapses is unaltered. The functional decrease in heterotypic cannabinoid receptor type 1 (CB1R)-sensitive inhibition of FS-BCs resulted from enhanced baseline GABAB-mediated suppression of synaptic release after SE. The frequency of CB1R-sensitive inhibitory synaptic events in FS-BCs was depressed early after SE induction and remained reduced in epileptic rats. In biologically based simulations of heterogeneous inhibitory networks and excitatory-inhibitory cell networks, experimentally identified decrease in reliability of AC-IN to FS-BCs synaptic release reduced theta power and theta-gamma coupling and enhanced gamma coherence. Thus, the experimentally identified functional reduction in heterotypic inhibition of FS-BCs can contribute to compromised network oscillations in epilepsy and could precipitate memory and cognitive co-morbidities.