Sampling rate, signal bandwidth and related pitfalls in EEG analysis

This submission contains a commentary. (C) 2016 Elsevier B.V. All rights reserved

Analyzing murine electrocardiogram with PhysioToolkit

Quantitative electrocardiogram (ECG) analysis is a very important tool in cardiovascular and neuroedocrine research. It is useful in clinical trials with human beings, as well as in animals such as rabbits, rats, and mice, for example, in studying knockout models. The species of interest differ in their typical baseline heart rate and therefore in the sampling rate in ECG detection. However, for obvious reasons, there are no available analysis programs adjusted to each species. We demonstrate how to use PhysioToolkit, an open source software developed by Massachusetts Institute of Technology for physiologic signal processing and analysis in humans, with murine ECG signals, with full control over analysis options. The procedure can be transferred on any other species in an analogue way. (C) 2010 Elsevier Inc. All rights reserved

The Ca-V 2.3 R-Type Voltage-Gated Ca2+ Channel in Mouse Sleep Architecture

Study Objectives: Voltage-gated Ca2+ channels (VGCCs) are key elements in mediating thalamocortical rhythmicity. Low-voltage activated (LVA) Ca(V)3 T-type Ca2+ channels have been related to thalamic rebound burst firing and to generation of non-rapid eye movement (NREM) sleep. High-voltage activated (HVA) Ca(V)1 L-type Ca2+ channels, on the opposite, favor the tonic mode of action associated with higher levels of vigilance. However, the role of the HVA Non-L-type Ca(V)2.3 Ca2+ channels, which are predominantly expressed in the reticular thalamic nucleus (RTN), still remains unclear. Recently, Ca(V)2.3(-/-) mice were reported to exhibit altered spike-wave discharge (SWD)/absence seizure susceptibility supported by the observation that Ca(V)2.3 mediated Ca2+ influx into RTN neurons can trigger small-conductance Ca2+-activated K+-channel type 2 (SK2) currents capable of maintaining thalamic burst activity. Based on these studies we investigated the role of Ca(V)2.3 R-type Ca2+ channels in rodent sleep. Methods: The role of Ca(V)2.3 Ca2+ channels was analyzed in Ca(V)2.3(-/-) mice and controls in both spontaneous and artificial urethane-induced sleep, using implantable video-EEG radiotelemetry. Data were analyzed for alterations in sleep architecture using sleep staging software and time-frequency analysis. Results: Ca(V)2.3 deficient mice exhibited reduced wake duration and increased slow-wave sleep (SWS). Whereas mean sleep stage durations remained unchanged, the total number of SWS epochs was increased in Ca(V)2.3(-/-) mice. Additional changes were observed for sleep stage transitions and EEG amplitudes. Furthermore, urethane-induced SWS mimicked spontaneous sleep results obtained from Ca(V)2.3 deficient mice. Quantitative Real-time PCR did not reveal changes in thalamic Ca(V)3 T-type Ca2+ channel expression. The detailed mechanisms of SWS increase in Ca(V)2.3(-/-) mice remain to be determined. Conclusions: Low-voltage activated Ca(V)2.3 R-type Ca2+ channels in the thalamocortical loop and extra-thalamocortical circuitries substantially regulate rodent sleep architecture thus representing a novel potential target for pharmacological treatment of sleep disorders in the future

Automatic Detection of Highly Organized Theta Oscillations in the Murine EEG

Theta activity is generated in the septohippocampal system and can be recorded using deep intrahippocampal electrodes and implantable electroencephalography (EEG) radiotelemetry or tether system approaches. Pharmacologically, hippocampal theta is heterogeneous (see dualistic theory) and can be differentiated into type I and type II theta. These individual EEG subtypes are related to specific cognitive and behavioral states, such as arousal, exploration, learning and memory, higher integrative functions, etc. In neurodegenerative diseases such as Alzheimer's, structural and functional alterations of the septohippocampal system can result in impaired theta activity/oscillations. A standard quantitative analysis of the hippocampal EEG includes a Fast-Fourier-Transformation (FFT)-based frequency analysis. However, this procedure does not provide details about theta activity in general and highly-organized theta oscillations in particular. In order to obtain detailed information on highly-organized theta oscillations in the hippocampus, we have developed a new analytical approach. This approach allows for time-and cost-effective quantification of the duration of highly-organized theta oscillations and their frequency characteristics

Spontaneous long-term and urethane induced hippocampal EEG power, activity and temperature data from mice lacking the Ca(v)3.2 voltage-gated Ca2+ channel

This article provides raw relative electroencephalographic (EEG) power, temperature and activity data from controls and Ca-v 3.2 deficient mice. Radiotransmitter implantation was carried out in male experimental mice under ketamine/xylazine narcosis. Following a recovery period, radiotelemetric EEG recordings from the hippocampal CA1 region were obtained under spontaneous 24 h long-term conditions and post urethane injection. Relative EEG power values (%) for 2 s epochs were analysed for the following frequency ranges: delta 1 (81 , 0.5-4 Hz), delta 2 (82 , 1-4 Hz), theta 1 (01 , 4-8 Hz), theta 2 (02 , 4-12 Hz), alpha (alpha, 8-12 Hz), sigma (sigma, 12- 16 Hz), beta 1 (beta 1 , 12-30 Hz), beta 2 (beta 2 , 16-24 Hz), beta 3 (beta 3 , 16-30 Hz), gamma low (gamma(low) , 30-50 Hz), gamma mid (gamma(mid) , 50-70 Hz), gamma high (gamma(high) , 70-100 Hz), gamma rip-ples (yripples, 80-200 Hz), and gamma fast ripples (y(fast) ripples, 20 0-50 0 Hz). In addition, subcutaneous temperature and rel-ative activity data were analysed for both the light and dark cycle of two long-term recordings. The same type of data was obtained post urethane injection. Detailed information is provided for the age and body weight of the experimen-tal animals, the technical specifications of the radiofrequency transmitter, the stereotaxic coordinates for the intracerebral, deep and epidural, surface EEG electrodes, the electrode fea-tures, the filtering and sampling characteristics, the analysed EEG frequency bands and the data acquisition parameters. EEG power data, temperature and activity data are avail-able at MENDELEY DATA (doi: 10.17632/x53km5sby6.1 , URL: http://dx.doi.org/10.17632/x53km5sby6.1 ). Raw EEG data are available at zenodo (https://zenodo.org/ ). (C) 2021 The Authors. Published by Elsevier Inc

Altered Theta Oscillations and Aberrant Cortical Excitatory Activity in the 5XFAD Model of Alzheimer's Disease

Alzheimer's disease (AD) is an age-related neurodegenerative disorder characterized by impairment of memory function. The 5XFAD mouse model was analyzed and compared with wild-type (WT) controls for aberrant cortical excitability and hippocampal theta oscillations by using simultaneous video-electroencephalogram (EEG) monitoring. Seizure staging revealed that 5XFAD mice exhibited cortical hyperexcitability whereas controls did not. In addition, 5XFAD mice displayed a significant increase in hippocampal theta activity from the light to dark phase during nonmotor activity. We also observed a reduction in mean theta frequency in 5XFAD mice compared to controls that was again most prominent during nonmotor activity. Transcriptome analysis of hippocampal probes and subsequent qPCR validation revealed an upregulation of Plcd4 that might be indicative of enhanced muscarinic signalling. Our results suggest that 5XFAD mice exhibit altered cortical excitability, hippocampal dysrhythmicity, and potential changes in muscarinic signaling

Enhanced hippocampal type II theta activity AND altered theta architecture in mice lacking the Ca(v)3.2 T-type voltage-gated calcium channel

T-type Ca2+ channels are assumed to contribute to hippocampal theta oscillations. We used implantable video-EEG radiotelemetry and qPCR to unravel the role of Ca(v)3.2 Ca2+ channels in hippocampal theta genesis. Frequency analysis of spontaneous long-term recordings in controls and Ca(v)3.2(-/-) mice revealed robust increase in relative power in the theta (4-8 Hz) and theta-alpha (4-12 Hz) ranges, which was most prominent during the inactive stages of the dark cycles. Urethane injection experiments also showed enhanced type II theta activity and altered theta architecture following Ca(v)3.2 ablation. Next, gene candidates from hippocampal transcriptome analysis of control and Ca(v)3.2(-/-) mice were evaluated using qPCR. Dynein light chain Tctex-Type 1 (Dynlt1b) was significantly reduced in Ca(v)3.2(-/-) mice. Furthermore, a significant reduction of GABA A receptor delta subunits and GABA B1 receptor subunits was observed in the septohippocampal GABAergic system. Our results demonstrate that ablation of Ca(v)3.2 significantly alters type II theta activity and theta architecture. Transcriptional changes in synaptic transporter proteins and GABA receptors might be functionally linked to the electrophysiological phenotype

Data Acquisition and Analysis In Brainstem Evoked Response Audiometry In Mice

Brainstem evoked response audiometry (BERA) is of central relevance in the clinical neurophysiology. As other evoked potential (EP) techniques, such as visually evoked potentials (VEPs) or somatosensory evoked potentials (SEPs), the auditory evoked potentials (AEPs) are triggered by the repetitive presentation of identical stimuli, the electroencephalographic (EEG) response of which is subsequently averaged resulting in distinct positive (p) and negative (n) deflections. In humans, both the amplitude and the latency of individual peaks can be used to characterize alterations in synchronization and conduction velocity in the underlying neuronal circuitries. Importantly, AEPs are also applied in basic and preclinical science to identify and characterize the auditory function in pharmacological and genetic animal models. Even more, animal models in combination with pharmacological testing are utilized to investigate for potential benefits in the treatment of sensorineural hearing loss (e.g., age-or noise-induced hearing deficits). Here we provide a detailed and integrative description of how to record auditory brainstem-evoked responses (ABRs) in mice using click and tone-burst application. A specific focus of this protocol is on pre-experimental animal housing, anesthesia, ABR recording, ABR filtering processes, automated wavelet-based amplitude growth function analysis, and latency detection

Gender specific click and tone burst evoked ABR datasets from mice lacking the Ca(v)2.3 R-type voltage-gated calcium channel

This data article provides raw auditory evoked brainstem responses (ABRs) from controls and Ca(v)2.3 transgenics, i.e. heterozygous Ca(v)2.3 (broken vertical bar) (/-) and Ca(v)2.3(-/-) null mutants. Gender specific ABR recordings were performed in age-matched animals under ketamine/xylazine narcosis. Data presented here include ABRs upon both click and tone burst presentation in the increasing SPL mode using a commercially available ABR setup from Tucker Davis Technologies Inc. (TDT, USA). Detailed information is provided for the sound attenuating cubicle, electrical shielding, electrode parameters, stimulus characteristics and architecture, sampling rate, filtering processes and ABR protocol application during the course of data acquisition and recording. The later are important for subsequent analysis of click and tone burst related hearing thresholds, amplitude growth function and peak latencies. (C) 2018 The Authors. Published by Elsevier lnc

Ca(v)3.2 T-Type Calcium Channels Are Physiologically Mandatory for the Auditory System

Voltage-gated Ca2+ channels (VGCCs) play key roles in auditory perception and information processing within the inner ear and brainstem. Pharmacological inhibition of low voltage-activated (LVA) T-type Ca2+ channels is related to both age- and noise induced hearing loss in experimental animals and may represent a promising approach to the treatment of auditory impairment of various etiologies. Within the LVA Ca2+ channel subgroup, Ca(v)3.2 is the most prominently expressed T-type channel entity in the cochlea and auditory brainstem. Thus, we performed a complete gender specific click and tone burst based auditory brainstem response (ABR) analysis of Ca(v)3.2(+/-) and Ca(v)3.2(-/-) mice, including i.a. temporal progression in hearing loss, amplitude growth function and wave latency analysis as well as a cochlear qPCR based evaluation of other VGCCs transcripts. Our results, based on a self-programmed automated wavelet approach, demonstrate that both heterozygous and Ca(v)3.2 null mutant mice exhibit age-dependent increases in hearing thresholds at 5 months of age. In addition, complex alterations in WI-IV amplitudes and latencies were detected that were not attributable to alterations in the expression of other VGCCs in the auditory tract. Our results clearly demonstrate the important physiological role of Ca(v)3.2 VGCCs in the spatiotemporal organization of auditory processing in young adult mice and suggest potential pharmacological targets for interventions in the future. (C) 2019 The Author(s). Published by Elsevier Ltd on behalf of IBRO