scholarly journals Amygdala Low-Frequency Stimulation Reduces Pathological Phase-Amplitude Coupling in the Pilocarpine Model of Epilepsy

2020 ◽  
Vol 10 (11) ◽  
pp. 856
Author(s):  
István Mihály ◽  
Károly Orbán-Kis ◽  
Zsolt Gáll ◽  
Ádám-József Berki ◽  
Réka-Barbara Bod ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Low Frequency ◽  
Brain Regions ◽  
Theta Power ◽  
Interictal Epileptiform Discharge ◽  
Seizure Rate ◽  
Male Wistar Rats ◽  
Pilocarpine Model ◽  
Drug Resistant Epilepsy ◽  
Phase Amplitude

Temporal-lobe epilepsy (TLE) is the most common type of drug-resistant epilepsy and warrants the development of new therapies, such as deep-brain stimulation (DBS). DBS was applied to different brain regions for patients with epilepsy; however, the mechanisms of action are not fully understood. Therefore, we tried to characterize the effect of amygdala DBS on hippocampal electrical activity in the lithium-pilocarpine model in male Wistar rats. After status epilepticus (SE) induction, seizure patterns were determined based on continuous video recordings. Recording electrodes were inserted in the left and right hippocampus and a stimulating electrode in the left basolateral amygdala of both Pilo and age-matched control rats 10 weeks after SE. Daily stimulation protocol consisted of 4 × 50 s stimulation trains (4-Hz, regular interpulse interval) for 10 days. The hippocampal electroencephalogram was analyzed offline: interictal epileptiform discharge (IED) frequency, spectral analysis, and phase-amplitude coupling (PAC) between delta band and higher frequencies were measured. We found that the seizure rate and duration decreased (by 23% and 26.5%) and the decrease in seizure rate correlated negatively with the IED frequency. PAC was elevated in epileptic animals and DBS reduced the pathologically increased PAC and increased the average theta power (25.9% ± 1.1 vs. 30.3% ± 1.1; p < 0.01). Increasing theta power and reducing the PAC could be two possible mechanisms by which DBS may exhibit its antiepileptic effect in TLE; moreover, they could be used to monitor effectiveness of stimulation.

scholarly journals Short-Term Amygdala Low-Frequency Stimulation Does not Influence Hippocampal Interneuron Changes Observed in the Pilocarpine Model of Epilepsy

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 520
Author(s):  
István Mihály ◽  
Tímea Molnár ◽  
Ádám-József Berki ◽  
Réka-Barbara Bod ◽  
Károly Orbán-Kis ◽  
...  
Keyword(s):  
Cell Density ◽  
Basolateral Amygdala ◽  
Low Frequency ◽  
Low Frequency Stimulation ◽  
Male Wistar Rats ◽  
Pilocarpine Model ◽  
Frequency Stimulation ◽  
Stimulation Period ◽  
Oxide Synthase ◽  
Deep Brain

Temporal lobe epilepsy (TLE) is characterized by changes in interneuron numbers in the hippocampus. Deep brain stimulation (DBS) is an emerging tool to treat TLE seizures, although its mechanisms are not fully deciphered. We aimed to depict the effect of amygdala DBS on the density of the most common interneuron types in the CA1 hippocampal subfield in the lithium-pilocarpine model of epilepsy. Status epilepticus was induced in male Wistar rats. Eight weeks later, a stimulation electrode was implanted to the left basolateral amygdala of both pilocarpine-treated (Pilo, n = 14) and age-matched control rats (n = 12). Ten Pilo and 4 control animals received for 10 days 4 daily packages of 50 s 4 Hz regular stimulation trains. At the end of the stimulation period, interneurons were identified by immunolabeling for parvalbumin (PV), neuropeptide Y (NPY), and neuronal nitric oxide synthase (nNOS). Cell density was determined in the CA1 subfield of the hippocampus using confocal microscopy. We found that PV+ cell density was preserved in pilocarpine-treated rats, while the NPY+/nNOS+ cell density decreased significantly. The amygdala DBS did not significantly change the cell density in healthy or in epileptic animals. We conclude that DBS with low frequency applied for 10 days does not influence interneuron cell density changes in the hippocampus of epileptic rats.

scholarly journals Spectral fingerprints or spectral tilt? Evidence for distinct oscillatory signatures of memory formation

2018 ◽  
Author(s):  
Marie-Christin Fellner ◽  
Stephanie Gollwitzer ◽  
Stefan Rampp ◽  
Gernot Kreiselmeyr ◽  
Daniel Bush ◽  
...  
Keyword(s):  
Power Spectrum ◽  
High Frequency ◽  
Low Frequency ◽  
Brain Regions ◽  
Memory Formation ◽  
Memory Encoding ◽  
Frequency Bands ◽  
Theta Power ◽  
Gamma Power ◽  
Frequency Power

AbstractDecreases in low frequency power (2-30 Hz) alongside high frequency power increases (>40 Hz) have been demonstrated to predict successful memory formation. Parsimoniously this change in the frequency spectrum can be explained by one factor, a change in the tilt of the power spectrum (from steep to flat) indicating engaged brain regions. A competing view is that the change in the power spectrum contains several distinct brain oscillatory fingerprints, each serving different computations. Here, we contrast these two theories in a parallel MEG-intracranial EEG study where healthy participants and epilepsy patients, respectively, studied either familiar verbal material, or unfamiliar faces. We investigated whether modulations in specific frequency bands can be dissociated in time, space and by experimental manipulation. Both, MEG and iEEG data, show that decreases in alpha/beta power specifically predicted the encoding of words, but not faces, whereas increases in gamma power and decreases in theta power predicted memory formation irrespective of material. Critically, these different oscillatory signatures of memory encoding were evident in different brain regions. Moreover, high frequency gamma power increases occurred significantly earlier compared to low frequency theta power decreases. These results speak against a “spectral tilt” and demonstrate that brain oscillations in different frequency bands serve different functions for memory encoding.

scholarly journals Decreased Phase–Amplitude Coupling Between the mPFC and BLA During Exploratory Behaviour in Chronic Unpredictable Mild Stress-Induced Depression Model of Rats

2021 ◽  
Vol 15 ◽  
Author(s):  
Zihe Wang ◽  
Qingying Cao ◽  
Wenwen Bai ◽  
Xuyuan Zheng ◽  
Tiaotiao Liu
Keyword(s):  
Basolateral Amygdala ◽  
Low Frequency ◽  
Exploratory Behaviour ◽  
Control Group ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Field Potentials ◽  
High Gamma ◽  
Phase Amplitude

Depression is a common neuropsychiatric illness observed worldwide, and reduced interest in exploration is one of its symptoms. The control of dysregulated medial prefrontal cortex (mPFC) over the basolateral amygdala (BLA) is related to depression. However, the oscillation interaction in the mPFC-BLA circuit has remained elusive. Therefore, this study used phase–amplitude coupling (PAC), which provides complicated forms of information transmission by the phase of low-frequency rhythm, modulating the amplitude of high-frequency rhythm, and has a potential application for the treatment of neurological disease. The chronic unpredictable mild stress (CUMS) was used to prepare the rat models of depression. Moreover, multichannel in vivo recording was applied to obtain the local field potentials (LFPs) of the mPFC, the BLA in rats in control, and CUMS groups, while they explored the open field. The results showed prominent coupling between the phase of theta oscillation (4–12 Hz) in the mPFC and the amplitude of high-gamma oscillation (70–120 Hz) in the BLA. Compared to the control group, this theta–gamma PAC was significantly decreased in the CUMS group, which was accompanied by the diminished exploratory behaviour. The results indicate that the coupling between the phase of theta in the mPFC and the amplitude of gamma in the BLA is involved in exploratory behaviour, and this decreased coupling may inhibit exploratory behaviour of rats exposed to CUMS.

Electroencephalographic Recordings of Focal Seizures in Patients Affected by Periventricular Nodular Heterotopia: Role of the Heterotopic Nodules in the Genesis of Epileptic Discharges

2004 ◽  
Vol 19 (3) ◽  
pp. 369-377
Author(s):  
Giorgio Battaglia ◽  
Silvana Franceschetti ◽  
Luisa Chiapparini ◽  
Elena Freri ◽  
Stefania Bassanini ◽  
...  
Keyword(s):  
Brain Regions ◽  
Periventricular Nodular Heterotopia ◽  
Focal Seizures ◽  
Ictal Eeg ◽  
Epileptic Discharges ◽  
Nodular Heterotopia ◽  
Eeg Recordings ◽  
Drug Resistant Epilepsy ◽  
Video Eeg

Patients affected by periventricular nodular heterotopia are frequently characterized by focal drug-resistant epilepsy. To investigate the role of periventricular nodules in the genesis of seizures, we analyzed the electroencephalographic (EEG) features of focal seizures recorded by means of video-EEG in 10 patients affected by different types of periventricular nodular heterotopia and followed for prolonged periods of time at the epilepsy center of our institute. The ictal EEG recordings with surface electrodes revealed common features in all patients: all seizures originated from the brain regions where the periventricular nodular heterotopia were located; EEG patterns recorded on the leads exploring the periventricular nodular heterotopia were very similar both at the onset and immediately after the seizure's end in all patients. Our data suggest that seizures are generated by abnormal anatomic circuitries, including the heterotopic nodules and adjacent cortical areas. The major role of heterotopic neurons in the genesis and propagation of epileptic discharges must be taken into account when planning surgery for epilepsy in patients with periventricular nodular heterotopia. ( J Child Neurol 2005;20:369—377).

scholarly journals SAT-606 Distribution of Beta Klotho Gene Expression in the Mouse Brain

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Bianca S Bono ◽  
Persephone A Miller ◽  
Nikita K Koziel Ly ◽  
Melissa J Chee
Keyword(s):  
Basolateral Amygdala ◽  
Piriform Cortex ◽  
Brain Regions ◽  
Brain Atlas ◽  
Hypothalamic Nucleus ◽  
Fibroblast Growth Factor 21 ◽  
Lateral Olfactory Tract ◽  
Hypothalamic Area ◽  
Low Levels ◽  
The Brain

Abstract Fibroblast growth factor 21 (FGF21) has emerged as a critical endocrine factor for understanding the neurobiology of obesity, such as by the regulation thermogenesis, food preference, and metabolism, as well as for neuroprotection in Alzheimer’s disease and traumatic brain injury. FGF21 is synthesized primarily by the liver and pancreas then crosses the blood brain barrier to exert its effects in the brain. However, the sites of FGF21 action in the brain is not well-defined. FGF21 action requires the activation of FGF receptor 1c as well as its obligate co-receptor beta klotho (KLB). In order to determine the sites of FGF21 action, we mapped the distribution of Klb mRNA by in situ hybridization using RNAscope technology. We labeled Klb distribution throughout the rostrocaudal axis of male wildtype mice by amplifying Klb hybridization using tyramine signal amplification and visualizing Klb hybridization using Cyanine 3 fluorescence. The resulting Klb signal appears as punctate red “dots,” and each Klb neuron may express low (1–4 dots), medium (5–9 dots), or high levels (10+ dots) of Klb hybridization. We then mapped individual Klb expressing neuron to the atlas plates provided by the Allen Brain Atlas in order to determine Klb distribution within the substructures of each brain region, which are defined by Nissl-based parcellations of cytoarchitectural boundaries. The distribution of Klb mRNA is widespread throughout the brain, and the brain regions analyzed thus far point to notable expression in the hypothalamus, amygdala, hippocampus, and the cerebral cortex. The highest expression of Klb was localized to the suprachiasmatic nucleus in the hypothalamus, which contained low and medium Klb-expressing neurons in the lateral hypothalamic area and ventromedial hypothalamic nucleus while low expressing Klb neurons were seen in the paraventricular and dorsmedial hypothalamic nucleus. Hippocampal Klb expression was limited to the dorsal region and largely restricted to the pyramidal cell layer of the dentate gyrus, CA3, CA2, and CA1 but at low levels only. In the amygdala, low and medium Klb expressing cells were seen in lateral amygdala nucleus while low levels were observed in the basolateral amygdala nucleus. Cortical Klb expression analyzed thus far included low Klb-expressing neurons in the olfactory areas, including layers 2 and 3 of piriform cortex and nucleus of the lateral olfactory tract. These findings are consistent with the known roles of FGF21 in the central regulation of energy balance, but also implicates potentially wide-ranging effects of FGF21 such as in executive functions.

scholarly journals Orientation of Temporal Interference for Non-Invasive Deep Brain Stimulation in Epilepsy

2020 ◽  
Author(s):  
Florian Missey ◽  
Evgeniia Rusina ◽  
Emma Acerbo ◽  
Boris Botzanowski ◽  
Romain Carron ◽  
...  
Keyword(s):  
Electric Fields ◽  
Brain Regions ◽  
Intracranial Stimulation ◽  
Epileptogenic Zone ◽  
Implanted Electrodes ◽  
Non Invasive ◽  
Gamma Range ◽  
Wide Range ◽  
Drug Resistant Epilepsy ◽  
Intracranial Electrodes

AbstractIn patients with focal drug-resistant epilepsy, electrical stimulation from intracranial electrodes is frequently used for the localization of seizure onset zones and related pathological networks. The ability of electrically stimulated tissue to generate beta and gamma range oscillations, called rapid-discharges, is a frequent indication of an epileptogenic zone. However, a limit of intracranial stimulation is the fixed physical location and number of implanted electrodes, leaving numerous clinically and functionally relevant brain regions unexplored. Here, we demonstrate an alternative technique relying exclusively on nonpenetrating surface electrodes, namely an orientation-tunable form of temporally-interfering (TI) electric fields to target the CA3 of the mouse hippocampus which focally evokes seizure-like events (SLEs) having the characteristic frequencies of rapid-discharges, but without the necessity of the implanted electrodes. The orientation of the topical electrodes with respect to the orientation of the hippocampus is demonstrated to strongly control the threshold for evoking SLEs. Additionally, we demonstrate the use of square waves as an alternative to sine waves for TI stimulation. An orientation-dependent analysis of classic implanted electrodes to evoke SLEs in the hippocampus is subsequently utilized to support the results of the minimally-invasive temporally-interfering fields. The principles of orientation-tunable TI stimulation seen here can be generally applicable in a wide range of other excitable tissues and brain regions, overcoming several limitations of fixed electrodes which penetrate tissue.

scholarly journals Dissociable oscillatory networks support gain and loss processing in human orbitofrontal cortex

2021 ◽  
Author(s):  
Ignacio Saez ◽  
Jack Lin ◽  
Edward Chang ◽  
Josef Parvizi ◽  
Robert T. Knight ◽  
...  
Keyword(s):  
Neural Activity ◽  
Orbitofrontal Cortex ◽  
Low Frequency ◽  
Brain Regions ◽  
Reward Processing ◽  
Neural Oscillations ◽  
Beta Band ◽  
Neuronal Ensembles ◽  
Gain And Loss

AbstractHuman neuroimaging and animal studies have linked neural activity in orbitofrontal cortex (OFC) to valuation of positive and negative outcomes. Additional evidence shows that neural oscillations, representing the coordinated activity of neuronal ensembles, support information processing in both animal and human prefrontal regions. However, the role of OFC neural oscillations in reward-processing in humans remains unknown, partly due to the difficulty of recording oscillatory neural activity from deep brain regions. Here, we examined the role of OFC neural oscillations (<30Hz) in reward processing by combining intracranial OFC recordings with a gambling task in which patients made economic decisions under uncertainty. Our results show that power in different oscillatory bands are associated with distinct components of reward evaluation. Specifically, we observed a double dissociation, with a selective theta band oscillation increase in response to monetary gains and a beta band increase in response to losses. These effects were interleaved across OFC in overlapping networks and were accompanied by increases in oscillatory coherence between OFC electrode sites in theta and beta band during gain and loss processing, respectively. These results provide evidence that gain and loss processing in human OFC are supported by distinct low-frequency oscillations in networks, and provide evidence that participating neuronal ensembles are organized functionally through oscillatory coherence, rather than local anatomical segregation.

scholarly journals Acute stress enhances adult rat hippocampal neurogenesis and activation of newborn neurons via secreted astrocytic FGF2

eLife ◽  
2013 ◽  
Vol 2 ◽  
Author(s):  
Elizabeth D Kirby ◽  
Sandra E Muroy ◽  
Wayne G Sun ◽  
David Covarrubias ◽  
Megan J Leong ◽  
...  
Keyword(s):  
Basolateral Amygdala ◽  
Acute Stress ◽  
Memory Function ◽  
Brain Regions ◽  
Hippocampal Neurogenesis ◽  
Mammalian Brain ◽  
Stress Hormone ◽  
Adult Rat ◽  
Neural Stem Progenitor Cells ◽  
Newborn Neurons

Stress is a potent modulator of the mammalian brain. The highly conserved stress hormone response influences many brain regions, particularly the hippocampus, a region important for memory function. The effect of acute stress on the unique population of adult neural stem/progenitor cells (NPCs) that resides in the adult hippocampus is unclear. We found that acute stress increased hippocampal cell proliferation and astrocytic fibroblast growth factor 2 (FGF2) expression. The effect of acute stress occurred independent of basolateral amygdala neural input and was mimicked by treating isolated NPCs with conditioned media from corticosterone-treated primary astrocytes. Neutralization of FGF2 revealed that astrocyte-secreted FGF2 mediated stress-hormone-induced NPC proliferation. 2 weeks, but not 2 days, after acute stress, rats also showed enhanced fear extinction memory coincident with enhanced activation of newborn neurons. Our findings suggest a beneficial role for brief stress on the hippocampus and improve understanding of the adaptive capacity of the brain.

scholarly journals Causal connectivity abnormalities of regional homogeneity in children with attention deficit hyperactivity disorder: a rest-state fMRI study

ADMET & DMPK ◽  
2017 ◽  
Vol 5 (4) ◽  
pp. 242-252 ◽  
Author(s):  
Dechun Zhao ◽  
Shuxing Zheng ◽  
Li Yang ◽  
Yin Tian
Keyword(s):  
Attention Deficit Hyperactivity Disorder ◽  
Attention Deficit ◽  
Low Frequency ◽  
Brain Regions ◽  
Regional Homogeneity ◽  
Support Vector ◽  
Attention And Memory ◽  
Causality Analysis ◽  
Hyperactivity Disorder ◽  
Significant Difference

The present study aimed to investigate individual differences of causal connectivity between brain regions in attention deficit hyperactivity disorder (ADHD) which was a psychiatric disorder. Resting-state functional magnetic resonance imaging (R-fMRI) data of typically-developing controls (TDC) children group and combined ADHD (ADHD-C) children group were distinguished by the support vector machine (SVM) with linear kernel function, based on regional homogeneity (ReHo), amplitude of low frequency fluctuation (ALFF) and fractional ALFF (FALFF). The highest classification accuracy yielded by ReHo was 90.91 %. Furthermore, the granger causality analysis (GCA) method based on the classified weight map of regions of interesting (ROIs) showed that five causal flows existed significant difference between TDC and ADHD-C. That is, the averaged GCA values of three causal connections (i.e. left VLPFC à left CC1, right PoCG à left CC1, and right PoCG à right CC2) for ADHD-C were separately stronger than those for TDC. And the other two connections (i.e. right FEF à right SOG and right CC1 à right SOG) were weaker for ADHD-C than those for TDC. In addition, only two causality flows (i.e. left VLPFC à left CC1 and right PoCG à right CC2) presented that their GCA values were positively correlation with ADHD index scores, respectively. Our findings revealed that ADHD children represented widespread abnormalities in the causality connectivity, especially involved in the attention and memory related regions. And further provided evidence that the potential neural causality flows could play a key role in characterizing individual’s ADHD.

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