Amplitude Of Gamma Oscillations Research Articles

Functional interaction of abnormal beta and gamma oscillations on bradykinesia in parkinsonian rats

Bradykinesia, a debilitating symptom characterized by impaired movement initiation and reduced speed in Parkinson’s disease (PD), is associated with abnormal oscillatory activity in the motor cortex-basal ganglia circuit. We investigated the interplay between abnormal beta and gamma oscillations in relation to bradykinesia in parkinsonian rats. Our findings showed reduced movement activities in parkinsonian rats, accompanied by enhanced high beta oscillations in the motor cortex, which are closely associated with movement transitional difficulties. Additionally, gamma oscillations correlated with movement velocity in control rats but not in parkinsonian rats. We observed selective coupling between high beta oscillation phase and gamma oscillation amplitude in PD, as well as cortical high beta-broadband gamma phase-amplitude coupling (PAC) negatively influencing locomotor activities in control and PD rats. These findings suggest a collaborative role of cortical beta and gamma oscillations in facilitating movement execution, with beta oscillations being linked to movement initiation and gamma oscillations associated with movement speed. Importantly, the aberrant alterations of these oscillations are closely related to the development of bradykinesia. Furthermore, PAC hold promise as a biomarker for comprehensive assessment of movement performance in PD.

Endogenous cannabinoids in the piriform cortex tune olfactory perception

Sensory perception depends on interactions between external inputs transduced by peripheral sensory organs and internal network dynamics generated by central neuronal circuits. In the sensory cortex, desynchronized network states associate with high signal-to-noise ratio stimulus-evoked responses and heightened perception. Cannabinoid-type-1-receptors (CB1Rs) - which influence network coordination in the hippocampus - are present in anterior piriform cortex (aPC), a sensory paleocortex supporting olfactory perception. Yet, how CB1Rs shape aPC network activity and affect odor perception is unknown. Using pharmacological manipulations coupled with multi-electrode recordings or fiber photometry in the aPC of freely moving male mice, we show that systemic CB1R blockade as well as local drug infusion increases the amplitude of gamma oscillations in aPC, while simultaneously reducing the occurrence of synchronized population events involving aPC excitatory neurons. In animals exposed to odor sources, blockade of CB1Rs reduces correlation among aPC excitatory units and lowers behavioral olfactory detection thresholds. These results suggest that endogenous endocannabinoid signaling promotes synchronized population events and dampen gamma oscillations in the aPC which results in a reduced sensitivity to external sensory inputs.

Estimating Time and Rhythm byPredicting External Stimuli.

In this chapter, we present recent findings from our group showing that elapsed time, interval timing, and rhythm maintenance might be achieved by the well-known ability of the brain to predict the future states of the world. The difference between predictions and actual sensory evidence is used to generate perceptual and behavioral adjustments that help subjects achieve desired behavioral goals. Concretely, we show that (1) accumulating prediction errors is a plausible strategy humans could use to determine whether a train of consecutive stimuli arrives at regular or irregular intervals. By analyzing the behavior of human and non-human primate subjects performing rhythm perception tasks, we demonstrate that (2) the ability to estimate elapsed time and internally maintain rhythms is shared across primates and humans. Neurophysiological recordings show that (3) the medial premotor cortex engages in rhythm entrainment and maintains oscillatory activity that reveals an internal metronome's spatial and temporal characteristics. Finally, we demonstrate that (4) the amplitude of gamma oscillations within this cortex increases proportionally to the total elapsed time. In conjunction with our most recent experiments, our results suggest that timing might be achieved by an internal simulation of the sensory stimuli and the motor commands that define the timing task that needs to be performed.

Abnormal gamma frequency phase‐amplitude coupling associated with network hyperexcitability in Alzheimer’s Disease

AbstractBackgroundAlzheimer’s disease (AD) carries an increased risk of seizures and subclinical epileptiform activity (Vossel et al. 2016). Network hyperexcitability which is the underlying phenomenon of epileptic manifestations is thought to contribute to AD pathophysiological processes. Recently we demonstrated that greater degree of neural synchronization deficits within 2‐8Hz range of frequency oscillations are sensitive indicators of network hyperexcitability (Ranasinghe et al. 2021). Here, we sought to examine the high frequency gamma band deficits associated with network hyperexcitability in AD patients.MethodsSpecifically, we quantified Phase Amplitude Coupling (PAC) between the amplitude of gamma oscillations (30‐40Hz); with the phase of 2‐8Hz oscillations) (Figure 1). We used 60s resting‐state magnetoencephalography (MEG) recordings from 48 AD patients (n = 22, with subclinical epileptiform activity, AD‐EPI+; n = 28 without subclinical epileptiform activity, AD‐EPI‐), and 35 age‐matched controls. We computed PAC for each of 68 cortical regions (Desikan et al. 2006) on source‐space reconstructed MEG signal using the mean vector length (Canolty et al. 2006).ResultsPermutation cluster test was performed for statistical comparisons between AD patients vs. age matched controls, and AD‐EPI+ vs. AD‐EPI‐. Patients with AD showed significantly higher theta (4‐8 Hz)‐gamma coupling in the left parahippocampal and right caudal‐middle frontal regions. Importantly, this increased left parahippocampal theta‐gamma coupling was significantly higher in AD‐EPI+ patients than in AD‐EPI‐. AD‐EPI+ also showed higher alpha (8‐12Hz)‐gamma coupling in the right parahippocampal region compared to AD‐EPI‐ (Figure 2).ConclusionThese results not only identify gamma band coupling deficits specifically localized to medial temporal regions which are the earliest affected regions in AD pathophysiology but also delineate the associated vulnerabilities of network hyperexcitability in AD.

High-power gamma-related delta phase alteration in schizophrenia patients at rest.

Information processing is supported by the cortico-cortical transmission of neural oscillations across brain regions. Recent studies have demonstrated that the rhythmic firing of neural populations is not random but is governed by interactions with other frequency bands. Specifically, the amplitude of gamma-band oscillations is associated with the phase of lower frequency oscillations in support of short and long-range communications among networks. This cross-frequency relation is thought to reflect the temporal coordination of neural communication. While schizophrenia patients show abnormal oscillatory responses across multiple frequencies at rest, it is unclear whether the functional relationships among frequency bands are intact. This study aimed to characterize the lower frequency (delta/theta, 1-8 Hz) phase and the amplitude of gamma oscillations in healthy subjects and schizophrenia patients at rest. Low frequency-phase (delta- and theta- band) angles and gamma-band amplitude relationships were assessed in 142 schizophrenia patients and 128 healthy subjects. Significant low-frequency phase alteration related to high-power gamma was detected across broadly distributed scalp regions in both healthy subjects and patients. In patients, delta phase synchronization related to high-power gamma was significantly decreased at the frontocentral, right middle temporal, and left temporoparietal electrodes but significantly increased at the left parietal electrode. High-power gamma-related delta phase alteration may reflect a core pathophysiologic abnormality in schizophrenia. Data-driven measures of functional relationships among frequency bands may prove useful in the development of novel therapeutics. Future studies are needed to determine whether these alterations are specific to schizophrenia or appear in other neuropsychiatric patient populations.

Neuronal biomarkers of Parkinson's disease are present in healthy aging

The prevalence of Parkinson's disease (PD) increases with aging and both processes share similar cellular mechanisms and alterations in the dopaminergic system. Yet it remains to be investigated whether aging can also demonstrate electrophysiological neuronal signatures typically associated with PD. Previous work has shown that phase-amplitude coupling (PAC) between the phase of beta oscillations and the amplitude of gamma oscillations as well as beta bursts features can serve as electrophysiological biomarkers for PD. Here we hypothesize that these metrics are also present in apparently healthy elderly subjects. Using resting state multichannel EEG measurements, we show that PAC between beta oscillation and broadband gamma activity (50–150 Hz) is elevated in a group of elderly (59–77 years) compared to young volunteers (20–35 years) without PD. Importantly, the increase of PAC is statistically significant even after ruling out confounds relating to changes in spectral power and non-sinusoidal shape of beta oscillation. Moreover, a trend for a higher percentage of longer beta bursts (> 0.2 s) along with the increase in their incidence rate is also observed for elderly subjects. Using inverse modeling, we further show that elevated PAC and longer beta bursts are most pronounced in the sensorimotor areas. Moreover, we show that PAC and longer beta bursts might reflect distinct mechanisms, since their spatial patterns only partially overlap and the correlation between them is weak. Taken together, our findings provide novel evidence that electrophysiological biomarkers of PD may already occur in apparently healthy elderly subjects. We hypothesize that PAC and beta bursts characteristics in aging might reflect a pre-clinical state of PD and suggest their predictive value to be tested in prospective longitudinal studies.

Neural indicators of perceptual variability of pain across species

Individuals exhibit considerable and unpredictable variability in painful percepts in response to the same nociceptive stimulus. Previous work has found neural responses that, while not necessarily responsible for the painful percepts themselves, can still correlate well with intensity of pain perception within a given individual. However, there is no reliable neural response reflecting the variability in pain perception across individuals. Here, we use an electrophysiological approach in humans and rodents to demonstrate that brain oscillations in the gamma band [gamma-band event-related synchronization (γ-ERS)] sampled by central electrodes reliably predict pain sensitivity across individuals. We observed a clear dissociation between the large number of neural measures that reflected subjective pain ratings at within-subject level but not across individuals, and γ-ERS, which reliably distinguished subjective ratings within the same individual but also coded pain sensitivity across different individuals. Importantly, the ability of γ-ERS to track pain sensitivity across individuals was selective because it did not track the between-subject reported intensity of nonpainful but equally salient auditory, visual, and nonnociceptive somatosensory stimuli. These results also demonstrate that graded neural activity related to within-subject variability should be minimized to accurately investigate the relationship between nociceptive-evoked neural activities and pain sensitivity across individuals.

Aberrant thalamocortical coherence in an animal model of tinnitus.

Electrophysiological and imaging studies from humans suggest that the phantom sound of tinnitus is associated with abnormal thalamocortical neural oscillations (dysrhythmia) and enhanced gamma band activity in the auditory cortex. However, these models have seldom been tested in animal models where it is possible to simultaneously assess the neural oscillatory activity within and between the thalamus and auditory cortex. To explore this issue, we used multichannel electrodes to examine the oscillatory behavior of local field potentials recorded in the rat medial geniculate body (MBG) and primary auditory cortex (A1) before and after administering a dose of sodium salicylate (SS) that reliably induces tinnitus. In the MGB, SS reduced theta, alpha, and beta oscillations and decreased coherence (synchrony) between electrode pairs in theta, alpha, and beta bands but increased coherence in the gamma band. Within A1, SS significantly increased gamma oscillations, decreased theta power, and decreased coherence between electrode pairs in theta and alpha bands but increased coherence in the gamma band. When coherence was measured between one electrode in the MGB and another in A1, SS decreased coherence in beta, alpha, and theta bands but increased coherence in the gamma band. SS also increased cross-frequency coupling between the phase of theta oscillations in the MGB and amplitude of gamma oscillations in A1. Altogether, our results suggest that SS treatment fundamentally alters the manner in which thalamocortical circuits communicate, leading to excessive cortical gamma power and synchronization, neurophysiological changes implicated in tinnitus. Our data provide support for elements of both the thalamocortical dysrhythmia (TD) and synchronization by loss of inhibition (SLIM) models of tinnitus, demonstrating that increased cortical gamma band activity is associated with both enhanced theta-gamma coupling as well as decreases alpha power/coherence between the MGB and A1. NEW & NOTEWORTHY There are no effective drugs to alleviate the phantom sound of tinnitus because the physiological mechanisms leading to its generation are poorly understood. Neural models of tinnitus suggest that it arises from abnormal thalamocortical oscillations, but these models have not been extensively tested. This article identifies abnormal thalamocortical oscillations in a drug-induced tinnitus model. Our findings open up new avenues of research to investigate whether cellular mechanisms underlying thalamocortical oscillations are causally linked to tinnitus.

Endogenously generated gamma-band oscillations in early visual cortex: A neurofeedback study.

Human subjects were trained with neurofeedback (NFB) to enhance the power of narrow-band gamma oscillations in circumscribed regions of early visual cortex. To select the region and the oscillation frequency for NFB training, gamma oscillations were induced with locally presented drifting gratings. The source and frequency of these induced oscillations were determined using beamforming methods. During NFB training the power of narrow band gamma oscillations was continuously extracted from this source with online beamforming and converted into the pitch of a tone signal. We found that seven out of ten subjects were able to selectively increase the amplitude of gamma oscillations in the absence of visual stimulation. One subject however failed completely and two subjects succeeded to manipulate the feedback signal by contraction of muscles. In all subjects the attempts to enhance visual gamma oscillations were associated with an increase of beta oscillations over precentral/frontal regions. Only successful subjects exhibited an additional marked increase of theta oscillations over precentral/prefrontal and temporal regions whereas unsuccessful subjects showed an increase of alpha band oscillations over occipital regions. We argue that spatially confined networks in early visual cortex can be entrained to engage in narrow band gamma oscillations not only by visual stimuli but also by top down signals. We interpret the concomitant increase in beta oscillations as indication for an engagement of the fronto-parietal attention network and the increase of theta oscillations as a correlate of imagery. Our finding support the application of NFB in disease conditions associated with impaired gamma synchronization.

Locus coeruleus phasic discharge is essential for stimulus-induced gamma oscillations in the prefrontal cortex.

The locus coeruleus (LC) noradrenergic (NE) neuromodulatory system is critically involved in regulation of neural excitability via its diffuse ascending projections. Tonic NE release in the forebrain is essential for maintenance of vigilant states and increases the signal-to-noise ratio of cortical sensory responses. The impact of phasic NE release on cortical activity and sensory processing is less explored. We previously reported that LC microstimulation caused a transient desynchronization of population activity in the medial prefrontal cortex (mPFC), similar to noxious somatosensory stimuli. The LC receives nociceptive information from the medulla and therefore may mediate sensory signaling to its forebrain targets. Here we performed extracellular recordings in LC and mPFC while presenting noxious stimuli in urethane-anesthetized rats. A brief train of foot shocks produced a robust phasic response in the LC and a transient change in the mPFC power spectrum, with the strongest modulation in the gamma (30-90 Hz) range. The LC phasic response preceded prefrontal gamma power increase, and cortical modulation was proportional to the LC excitation. We also quantitatively characterized distinct cortical states and showed that sensory responses in both LC and mPFC depend on the ongoing cortical state. Finally, cessation of the LC firing by bilateral local iontophoretic injection of clonidine, an α2-adrenoreceptor agonist, completely eliminated sensory responses in the mPFC without shifting cortex to a less excitable state. Together, our results suggest that the LC phasic response induces gamma power increase in the PFC and is essential for mediating sensory information along an ascending noxious pathway. NEW & NOTEWORTHY Our study shows linear relationships between locus coeruleus phasic excitation and the amplitude of gamma oscillations in the prefrontal cortex. Results suggest that the locus coeruleus phasic response is essential for mediating sensory information along an ascending noxious pathway.

Interaction between neuronal calcium sensor protein 1 and lithium in pedunculopontine neurons.

Bipolar disorder is characterized by sleep dysregulation, suggesting a role for the reticular activating system (RAS). Postmortem studies showed increased expression of neuronal calcium sensor protein 1 (NCS‐1) in the brains of some bipolar disorder patients, and reduced or aberrant gamma band activity is present in the same disorder. Lithium (Li+) has been shown to effectively treat the mood disturbances in bipolar disorder patients. We previously showed that NCS‐1 at low levels increased, and at high levels decreased, gamma oscillations in RAS pedunculopontine neurons (PPN), and that Li+ decreased these oscillations. We previously described the effects of each agent on oscillations, G‐protein mechanisms, and Ca2+ currents. However, we designed the present experiments to determine the nature of the interaction of NCS‐1 and Li+ at physiological concentrations that would have an effect within minutes of application. As expected, Li+ decreased gamma oscillation amplitude, while NCS‐1 increased the amplitude of gamma oscillations. We identified NCS‐1 at 2 μmol/L as a concentration that increased gamma oscillations within 5–10 min, and Li+ at 10 μmol/L as a concentration that decreased gamma oscillations within 5 min. The combined application of NCS‐1 and Li+ at these concentrations showed that Li+ reduced the effects of NCS‐1 on oscillation amplitude within 5–10 min. These results demonstrate that at physiological levels, Li+ acts to reduce the effects of NCS‐1 so that, given over expression of NCS‐1, Li+ would have salutary effects.

Movement-related dynamics of cortical oscillations in Parkinson's disease and essential tremor.

Recent electrocorticography data have demonstrated excessive coupling of beta-phase to gamma-amplitude in primary motor cortex and that deep brain stimulation facilitates motor improvement by decreasing baseline phase-amplitude coupling. However, both the dynamic modulation of phase-amplitude coupling during movement and the general cortical neurophysiology of other movement disorders, such as essential tremor, are relatively unexplored. To clarify the relationship of these interactions in cortical oscillatory activity to movement and disease state, we recorded local field potentials from hand sensorimotor cortex using subdural electrocorticography during a visually cued, incentivized handgrip task in subjects with Parkinson's disease (n = 11), with essential tremor (n = 9) and without a movement disorder (n = 6). We demonstrate that abnormal coupling of the phase of low frequency oscillations to the amplitude of gamma oscillations is not specific to Parkinson's disease, but also occurs in essential tremor, most prominently for the coupling of alpha to gamma oscillations. Movement kinematics were not significantly different between these groups, allowing us to show for the first time that robust alpha and beta desynchronization is a shared feature of sensorimotor cortical activity in Parkinson's disease and essential tremor, with the greatest high-beta desynchronization occurring in Parkinson's disease and the greatest alpha desynchronization occurring in essential tremor. We also show that the spatial extent of cortical phase-amplitude decoupling during movement is much greater in subjects with Parkinson's disease and essential tremor than in subjects without a movement disorder. These findings suggest that subjects with Parkinson's disease and essential tremor can produce movements that are kinematically similar to those of subjects without a movement disorder by reducing excess sensorimotor cortical phase-amplitude coupling that is characteristic of these diseases.

Changes of gamma-band oscillatory activity to tonic muscle pain

It is well know that phasic pain could induce suppression of alpha oscillations and enhancement of gamma oscillations. However, the cortical responses to tonic pain, especially tonic pain originating from deep tissue, which was proposed to better resemble the clinical pain, are not well understood. Here we aimed to investigate electroencephalographic (EEG) responses to tonic muscle pain. EEG signals and pain perceptions of three order-counterbalanced conditions: innocuous condition (A, infusion of isotonic saline), noxious conditions with low (B) and medium (C) intensities (infusion of hypertonic saline) were recorded from 43 subjects. We observed the enhancement of gamma oscillations in frontal-central region in condition C, as compared to either condition A or B. Positive relationship between the amplitude of gamma oscillations and pain intensity was also observed in frontal-central region. Therefore, we provide novel evidence for the encoding of frontal-central gamma oscillations in tonic pain processing.

Sensory-driven and spontaneous gamma oscillations engage distinct cortical circuitry.

Gamma oscillations are a robust component of sensory responses but are also part of the background spontaneous activity of the brain. To determine whether the properties of gamma oscillations in cortex are specific to their mechanism of generation, we compared in mouse visual cortex in vivo the laminar geometry and single-neuron rhythmicity of oscillations produced during sensory representation with those occurring spontaneously in the absence of stimulation. In mouse visual cortex under anesthesia (isoflurane and xylazine), visual stimulation triggered oscillations mainly between 20 and 50 Hz, which, because of their similar functional significance to gamma oscillations in higher mammals, we define here as gamma range. Sensory representation in visual cortex specifically increased gamma oscillation amplitude in the supragranular (L2/3) and granular (L4) layers and strongly entrained putative excitatory and inhibitory neurons in infragranular layers, while spontaneous gamma oscillations were distributed evenly through the cortical depth and primarily entrained putative inhibitory neurons in the infragranular (L5/6) cortical layers. The difference in laminar distribution of gamma oscillations during the two different conditions may result from differences in the source of excitatory input to the cortex. In addition, modulation of superficial gamma oscillation amplitude did not result in a corresponding change in deep-layer oscillations, suggesting that superficial and deep layers of cortex may utilize independent but related networks for gamma generation. These results demonstrate that stimulus-driven gamma oscillations engage cortical circuitry in a manner distinct from spontaneous oscillations and suggest multiple networks for the generation of gamma oscillations in cortex.

High-threshold Ca2+ channels behind gamma band activity in the pedunculopontine nucleus (PPN).

The pedunculopontine nucleus (PPN) is part of the Reticular Activating System, and active during waking and REM sleep. Previous results showed that all PPN cells plateau at gamma frequencies and intrinsic membrane oscillations in PPN neurons are mediated by high-threshold N- and P/Q-type Ca2+ channels. The present study was designed to determine whether some PPN cells have only N-, only P/Q-, or both N- and P/Q-type Ca2+ channels. We used patch-clamp recordings in PPN cells in slices from anesthetized rat pups in the presence of synaptic receptor blockers (SB) and Tetrodotoxin (TTX), and applied ramps to induce intrinsic membrane oscillations. We found that all PPN cell types showed gamma oscillations in the presence of SB+TTX when using current ramps. In 50% of cells, the N-type Ca2+ channel blocker ω-Conotoxin-GVIA (ω-CgTx) reduced gamma oscillation amplitude, while subsequent addition of the P/Q-type blocker ω-Agatoxin-IVA (ω-Aga) blocked the remaining oscillations. Another 20% manifested gamma oscillations that were not significantly affected by the addition of ω-CgTx, however, ω-Aga blocked the remaining oscillations. In 30% of cells, ω-Aga had no effect on gamma oscillations, while ω-CgTx blocked them. These novel results confirm the segregation of populations of PPN cells as a function of the calcium channels expressed, that is, the presence of cells in the PPN that manifest gamma band oscillations through only N-type, only P/Q-type, and both N-type and P/Q-type Ca2+ channels.

Abnormal cross-frequency coupling in the tinnitus network.

Neuroimaging studies have identified networks of brain areas and oscillations associated with tinnitus perception. However, how these regions relate to perceptual characteristics of tinnitus, and how oscillations in various frequency bands are associated with communications within the tinnitus network is still incompletely understood. Recent evidence suggests that apart from changes of the tinnitus severity the changes of tinnitus dominant pitch also have modulating effect on the underlying neuronal activity in a number of brain areas within the tinnitus network. Therefore, in a re-analysis of an existing dataset, we sought to determine how the oscillations in the tinnitus network in the various frequency bands interact. We also investigate how changes of tinnitus loudness, annoyance and pitch affect cross-frequency interaction both within and between nodes of the tinnitus network. Results of this study provide, to our knowledge, the first evidence that in tinnitus patients, aside from the previously described changes of oscillatory activity, there are also changes of cross-frequency coupling (CFC); phase-amplitude CFC was increased in tinnitus patients within the auditory cortex and the dorsolateral prefrontal regions between the phase of delta-theta and the amplitude of gamma oscillations (Modulation Index [MI] 0.17 in tinnitus patients vs. 0.08 in tinnitus free controls). Moreover, theta phase in the anterior cingulate region modulated gamma in the auditory (MI 0.1) and dorsolateral prefrontal regions (MI 0.19). Reduction of tinnitus severity after acoustic coordinated reset therapy led to a partial normalization of abnormal CFC. Also treatment induced changes in tinnitus pitch significantly modulated changes in CFC. Thus, tinnitus perception is associated with a more pronounced CFC within and between nodes of the tinnitus network. CFC can coordinate tinnitus-relevant activity in the tinnitus network providing a mechanism for effective communication between nodes of this network.

A brain–computer interface based on self-regulation of gamma-oscillations in the superior parietal cortex

Objective. Brain–computer interface (BCI) systems are often based on motor- and/or sensory processes that are known to be impaired in late stages of amyotrophic lateral sclerosis (ALS). We propose a novel BCI designed for patients in late stages of ALS that only requires high-level cognitive processes to transmit information from the user to the BCI. Approach. We trained subjects via EEG-based neurofeedback to self-regulate the amplitude of gamma-oscillations in the superior parietal cortex (SPC). We argue that parietal gamma-oscillations are likely to be associated with high-level attentional processes, thereby providing a communication channel that does not rely on the integrity of sensory- and/or motor-pathways impaired in late stages of ALS. Main results. Healthy subjects quickly learned to self-regulate gamma-power in the SPC by alternating between states of focused attention and relaxed wakefulness, resulting in an average decoding accuracy of 70.2%. One locked-in ALS patient (ALS-FRS-R score of zero) achieved an average decoding accuracy significantly above chance-level though insufficient for communication (55.8%). Significance. Self-regulation of gamma-power in the SPC is a feasible paradigm for brain–computer interfacing and may be preserved in late stages of ALS. This provides a novel approach to testing whether completely locked-in ALS patients retain the capacity for goal-directed thinking.

Layer-Specific GABAergic Control of Distinct Gamma Oscillations in the CA1 Hippocampus

The temporary interaction of distinct gamma oscillators effects binding, association, and information routing. How independent gamma oscillations are generated and maintained by pyramidal cells and interneurons within a cortical circuit remains unknown. We recorded the spike timing of identified parvalbumin-expressing basket cells in the CA1 hippocampus of anesthetized rats and simultaneously detected layer-specific gamma oscillations using current-source-density analysis. Spike timing of basket cells tuned the phase and amplitude of gamma oscillations generated around stratum pyramidale, where basket cells selectively innervate pyramidal cells with GABAergic synapses. Basket cells did not contribute to gamma oscillations generated at the apical tuft of pyramidal cells. This gamma oscillation was selectively modulated by a subset of local GABAergic interneurons and by medial entorhinal cortex layer 3 neurons. The generation of independent and layer-specific gamma oscillations, implemented onto hippocampal pyramidal cells along their somato-dendritic axis, can be explained by selective axonal targeting and precisely controlled temporal firing of GABAergic interneurons.

GABA level, gamma oscillation, and working memory performance in schizophrenia.

A relationship between working memory impairment, disordered neuronal oscillations, and abnormal prefrontal GABA function has been hypothesized in schizophrenia; however, in vivo GABA measurements and gamma band neural synchrony have not yet been compared in schizophrenia. This case–control pilot study (N = 24) compared baseline and working memory task-induced neuronal oscillations acquired with high-density electroencephalograms (EEGs) to GABA levels measured in vivo with magnetic resonance spectroscopy. Working memory performance, baseline GABA level in the left dorsolateral prefrontal cortex (DLPFC), and measures of gamma oscillations from EEGs at baseline and during a working memory task were obtained. A major limitation of this study is a relatively small sample size for several analyses due to the integration of diverse methodologies and participant compliance. Working memory performance was significantly lower for patients than for controls. During the working memory task, patients (n = 7) had significantly lower amplitudes in gamma oscillations than controls (n = 9). However, both at rest and across working memory stages, there were significant correlations between gamma oscillation amplitude and left DLPFC GABA level. Peak gamma frequency during the encoding stage of the working memory task (n = 16) significantly correlated with GABA level and working memory performance. Despite gamma band amplitude deficits in patients across working memory stages, both baseline and working memory-induced gamma oscillations showed strong dependence on baseline GABA levels in patients and controls. These findings suggest a critical role for GABA function in gamma band oscillations, even under conditions of system and cognitive impairments as seen in schizophrenia.

Chapter 9 - Circuit Oscillations in Odor Perception and Memory

Olfactory system neural oscillations as seen in the local field potential have been studied for many decades. Recent research has shown that there is a functional role for the most studied gamma oscillations (40-100Hz in rats and mice, and 20Hz in insects), without which fine odor discrimination is poor. When these oscillations are increased artificially, fine discrimination is increased, and when rats learn difficult and highly overlapping odor discriminations, gamma is increased in power. Because of the depth of study on this oscillation, it is possible to point to specific changes in neural firing patterns as represented by the increase in gamma oscillation amplitude. However, we know far less about the mechanisms governing beta oscillations (15-30Hz in rats and mice), which are best associated with associative learning of responses to odor stimuli. These oscillations engage every part of the olfactory system that has so far been tested, plus the hippocampus, and the beta oscillation frequency band is the one that is most reliably coherent with other regions during odor processing. Respiratory oscillations overlapping with the theta frequency band (2-12Hz) are associated with odor sniffing and normal breathing in rats. They also show coupling in some circumstances between olfactory areas and rare coupling between the hippocampus and olfactory bulb. The latter occur in specific learning conditions in which coherence strength is negatively or positively correlated with performance, depending on the task. There is still much to learn about the role of neural oscillations in learning and memory, but techniques that have been brought to bear on gamma oscillations (current source density, computational modeling, slice physiology, behavioral studies) should deliver much needed knowledge of these events.