Modulation Of Neural Oscillations Research Articles

Role of neural oscillations modulating long term potentiation to Alzheimer's Disease

Neural oscillations are key in forming long-term memory. Theta and gamma oscillations have particularly gained substantial interest over the year for their involvement in memory formation. Theta-Gamma Coupling (TGC) has proven to be critical in memory formation processes. However, the relationship between neural oscillations and molecular synaptic mechanisms, including Long Term Potentiation (LTP) and Long-Term Depression (LTD) has yet to be fully understood. Furthermore, the modulation of neural oscillations has emerged as a novel way of treating Alzheimers Disease (AD) and Mild Cognitive Impairments (MCI). Various methods have been exploited, including optogenetics and Deep Brain Stimulation (DBS). While offering promising results including enhanced memory performance and restored brain oscillations, such modulations applicability to clinical trials in human and potential side effects are still in doubt. In this review, we elucidated on the link between LTP and oscillations, assessed the various neuromodulation techniques introduced by recent studies and also provided insights into future research directions to optimize these present methods of neural modulation.

Weak-noise-induced transitions with inhibition and modulation of neural oscillations

We analyze the effect of weak-noise-induced transitions on the dynamics of the FitzHugh–Nagumo neuron model in a bistable state consisting of a stable fixed point and a stable unforced limit cycle. Bifurcation and slow-fast analysis give conditions on the parameter space for the establishment of this bi-stability. In the parametric zone of bi-stability, weak-noise amplitudes may strongly inhibit the neuron’s spiking activity. Surprisingly, increasing the noise strength leads to a minimum in the spiking activity, after which the activity starts to increase monotonically with an increase in noise strength. We investigate this inhibition and modulation of neural oscillations by weak-noise amplitudes by looking at the variation of the mean number of spikes per unit time with the noise intensity. We show that this phenomenon always occurs when the initial conditions lie in the basin of attraction of the stable limit cycle. For initial conditions in the basin of attraction of the stable fixed point, the phenomenon, however, disappears, unless the timescale separation parameter of the model is bounded within some interval. We provide a theoretical explanation of this phenomenon in terms of the stochastic sensitivity functions of the attractors and their minimum Mahalanobis distances from the separatrix isolating the basins of attraction.

Coherent neural oscillations induced by weak synaptic noise

We analyze the effect of synaptic noise on the dynamics of the FitzHugh–Nagumo (FHN) neuron model. In our deterministic parameter regime, a limit cycle solution cannot emerge through a singular Hopf bifurcation, but such a limit cycle can nevertheless arise as a stochastic effect, as a consequence of weak synaptic noise in a regime of strong timescale separation (varepsilon rightarrow 0) between the slow and fast variables of the model. We investigate the mechanism behind this phenomenon, known as self-induced stochastic resonance (SISR) (Muratov et al. in Physica D 210:227–240, 2005), by using multiple-time perturbation techniques and by analyzing the escape mechanism of the random trajectories from the stable manifolds of the model equation. Even though SISR occurs only in the limit as the singular parameter varepsilon rightarrow 0, decreasing varepsilon does not increase the coherence of the oscillations in the FHN model, but rather increases the interval of the noise amplitude sigma for which coherence occurs. This is in contrast to the dynamical system studied in Muratov et al. (2005). Moreover, the phenomenon is robust under parameter tuning. Numerical simulations exhibit the results predicted by the theoretical analysis. In fact, our analysis together with that in Yamakou and Jost (Weak noise-induced transitions with inhibition and modulation of neural oscillations, 2017) reveals that the FHN model can support different stochastic resonance phenomena. While it had been known (Pikovsky and Kurths in Phys Rev Lett 78:775–778, 1997) that coherence resonance can occur when the slow variable is subjected to noise, we show that, when noise is added to the fast variable, two other types, inverse stochastic resonance and SISR, may emerge in the same weak noise limit and that the transition between these phenomena can be induced by varying a simple parameter.

Noisy Galvanic Vestibular Stimulation Modulates the Amplitude of EEG Synchrony Patterns

Noisy galvanic vestibular stimulation has been associated with numerous cognitive and behavioural effects, such as enhancement of visual memory in healthy individuals, improvement of visual deficits in stroke patients, as well as possibly improvement of motor function in Parkinson’s disease; yet, the mechanism of action is unclear. Since Parkinson’s and other neuropsychiatric diseases are characterized by maladaptive dynamics of brain rhythms, we investigated whether noisy galvanic vestibular stimulation was associated with measurable changes in EEG oscillatory rhythms within theta (4–7.5 Hz), low alpha (8–10 Hz), high alpha (10.5–12 Hz), beta (13–30 Hz) and gamma (31–50 Hz) bands. We recorded the EEG while simultaneously delivering noisy bilateral, bipolar stimulation at varying intensities of imperceptible currents – at 10, 26, 42, 58, 74 and 90% of sensory threshold – to ten neurologically healthy subjects. Using standard spectral analysis, we investigated the transient aftereffects of noisy stimulation on rhythms. Subsequently, using robust artifact rejection techniques and the Least Absolute Shrinkage Selection Operator regression and cross-validation, we assessed the combinations of channels and power spectral features within each EEG frequency band that were linearly related with stimulus intensity. We show that noisy galvanic vestibular stimulation predominantly leads to a mild suppression of gamma power in lateral regions immediately after stimulation, followed by delayed increase in beta and gamma power in frontal regions approximately 20–25 s after stimulation ceased. Ongoing changes in the power of each oscillatory band throughout frontal, central/parietal, occipital and bilateral electrodes predicted the intensity of galvanic vestibular stimulation in a stimulus-dependent manner, demonstrating linear effects of stimulation on brain rhythms. We propose that modulation of neural oscillations is a potential mechanism for the previously-described cognitive and motor effects of vestibular stimulation, and noisy galvanic vestibular stimulation may provide an additional non-invasive means for neuromodulation of functional brain networks.

Frequency-domain EEG source analysis for acute tonic cold pain perception

ObjectiveTo investigate electrocortical responses to tonic cold pain by frequency-domain electroencephalogram (EEG) source analysis, and to identify potential electrocortical indices of acute tonic pain. MethodsScalp EEG data were recorded from 26 healthy subjects under tonic cold pain (CP) and no-pain control (NP) conditions. EEG power spectra and the standardized low-resolution brain electromagnetic tomography (sLORETA) localized EEG cortical sources were compared between the two conditions in five frequency bands: 1–4Hz, 4–8Hz, 8–12Hz, 12–18Hz and 18–30Hz. ResultsIn line with the EEG power spectral results, the source power significantly differed between the CP and NP conditions in 8–12Hz (CP<NP) and 18–30Hz (CP>NP) in extensive brain regions. Besides, there were also significantly different 4–8Hz and 12–18Hz source activities between the two conditions. Among the significant source activities, the left medial frontal and left superior frontal 4–8Hz activities, the anterior cingulate 8–12Hz activity and the posterior cingulate 12–18Hz activity showed significant negative correlations with subjective pain ratings. ConclusionsThe brain’s perception of tonic cold pain was characterized by cortical source power changes across different frequency bands in multiple brain regions. Oscillatory activities that significantly correlated with subjective pain ratings were found in the prefrontal and cingulate regions. SignificanceThese findings may offer useful measures for objective pain assessment and provide a basis for pain treatment by modulation of neural oscillations at specific frequencies in specific brain regions.

Cellular bases of neocortical activation: modulation of neural oscillations by the nucleus basalis and endogenous acetylcholine

In the mammalian neocortex, the EEG reflects the state of behavioral arousal. The EEG undergoes a transformation, known as activation, during the transition from sleep to waking. Abundant evidence indicates the involvement of the neurotransmitter acetylcholine (ACh) in EEG activation; however, the cellular basis of this involvement remains unclear. We have used electrophysiological techniques with in vivo and in vitro preparations to demonstrate actions of endogenous ACh on neurons in auditory neocortex. In vivo stimulation of the nucleus basalis (NB), a primary source of neocortical ACh, (1) elicited EEG activation via cortical muscarinic receptors, (2) depolarized cortical neurons, and (3) produced a change in subthreshold membrane potential fluctuations from large-amplitude, slow (1-5 Hz) oscillations to low-amplitude, fast (20-40 Hz) oscillations. The NB-mediated change in pattern of membrane potential fluctuations resulted in a shift of spike discharge pattern from phasic to tonic. Stimulation of afferents in the in vitro neocortex elicited cholinergic actions on putative layer 5 pyramidal neurons. Acting via muscarinic receptors, endogenous ACh (1) reduced slow, rhythmic burst discharge and facilitated higher-frequency, single-spike discharge in burst-generating neurons, and (2) facilitated the appearance and magnitude of intrinsic membrane potential oscillations. These in vivo and in vitro observations suggest that neocortical activation results from muscarinic modulation of intrinsic neural oscillations and firing modes. Rhythmic-bursting pyramidal neurons in layer 5 may act as cortical pacemakers; if so, then modifying their discharge characteristics could alter local cortical networks. Larger, intercortical networks could also be modified, due to the widespread projections of NB neurons. Thus, NB cholinergic neurons may play a critical role in producing different states of neocortical function.