Electrophysiological Mechanisms Research Articles

High-definition transcranial direct current stimulation modulates theta response during a Go-NoGo task in traumatic brain injury

ObjectiveHigh Definition transcranial Direct Current Stimulation (HD-tDCS) has been shown to improve cognitive performance in individuals with chronic traumatic brain injury (TBI), although electrophysiological mechanisms remain unclear. MethodsVeterans with TBI underwent active anodal (N = 15) vs sham (N = 10) HD-tDCS targeting the pre-supplementary motor area (pre-SMA). A Go-NoGo task was conducted simultaneously with electroencephalography (EEG) at baseline and after intervention completion. ResultsWe found increased theta event-related spectral perturbation (ERSP) and inter-trial phase coherence (ITPC) during Go in the frontal midline electrodes overlying the pre-SMA after active HD-tDCS intervention, but not after sham. We also found increased theta phase coherence during Go between the frontal midline and left posterior regions after active HD-tDCS. A late increase in alpha-theta ERSP was found in the left central region after active HD-tDCS. Notably, lower baseline theta ERSP/ITPC in the frontal midline region predicted more post-intervention improvement in Go performance only in the active group. ConclusionsThere are local and interregional oscillatory changes in response to HD-tDCS modulation in chronic TBI. SignificanceThese findings may guide future research in utilizing EEG time–frequency metrics not only to measure interventional effects, but also in selecting candidates who may optimally respond to treatment.

Functional Connectivity Increases in Response to High-Definition Transcranial Direct Current Stimulation in Patients with Chronic Disorder of Consciousness.

Highlights Functional connectivity induced by HD-tDCS in DLPFC has different trends in CRS-R score improvers and non-improvers.An increase in theta PLV in the left frontal–parietooccipital region was significantly associated with CRS-R changes.DOC patients with increased PLV of the alpha band in the intra-bifrontal region have a better prognosis than those without. High-definition transcranial direct current stimulation (HD-tDCS) has been shown to play an important role in improving consciousness in patients with disorders of consciousness (DOCs), but its neuroelectrophysiological evidence is still lacking. To better explain the electrophysiological mechanisms of the effects of HD-tDCS on patients with DOCs, 22 DOC patients underwent 10 anodal HD-tDCS sessions of the left dorsolateral prefrontal cortex (DLPFC). This study used the Coma Recovery Scale-Revised (CRS-R) to assess the level of consciousness in DOC patients. According to whether the CRS-R score increased before and after stimulation, DOC patients were divided into a responsive group and a non-responsive group. By comparing the differences in resting-state EEG functional connectivity between different frequency bands and brain regions, as well as the relationship between functional connectivity values and clinical scores, the electrophysiological mechanism of the clinical effects of HD-tDCS was further explored. The change of the phase locking value (PLV) on the theta frequency band in the left frontal–parietooccipital region was positively correlated with the change in the CRS-R scores. As the number of interventions increased, we observed that in the responsive group, the change in PLV showed an upward trend, and the increase in the PLV appeared in the left frontal–parietooccipital region at 4–8 Hz and in the intra-bifrontal region at 8–13 Hz. In the non-responsive group, although the CRS-R scores did not change after stimulation, the PLV showed a downward trend, and the decrease in the PLV appeared in the intra-bifrontal region at 8–13 Hz. In addition, at the three-month follow-up, patients with increased PLV in the intra-bifrontal region at 8–13 Hz after repeated HD-tDCS stimulation had better outcomes than those without. Repeated anodal stimulation of the left DLPFC with HD-tDCS resulted in improved consciousness in some patients with DOCs. The increase in functional connectivity in the brain regions may be associated with the improvement of related awareness after HD-tDCS and may be a predictor of better long-term outcomes.

Multisensory integration of anticipated cardiac signals with visual targets affects their detection among multiple visual stimuli

Many studies have elucidated the multisensory processing of different exteroceptive signals (e.g., auditory-visual stimuli), but less is known about the multisensory integration of interoceptive signals with exteroceptive information. Here, we investigated the perceptual outcomes and electrophysiological brain mechanisms of cardio-visual integration by using participants’ electrocardiogram signals to control the color change of a visual target in dynamically changing displays. Reaction times increased when the target change coincided with strong cardiac signals concerning the state of cardiovascular arousal (i.e., presented at the end of ventricular systole), compared to when the target change occurred at a time when cardiac arousal was relatively low (i.e., presented at the end of ventricular diastole). Moreover, the concurrence of the target change and cardiac arousal signals modulated the event-related potentials and the beta power in an early period (~100 ms after stimulus onset), and decreased the N2pc and the beta lateralization in a later period (~200 ms after stimulus onset). Our results suggest that the multisensory integration of anticipated cardiac signals with a visual target negatively affects its detection among multiple visual stimuli, potentially by suppressing sensory processing and reducing attention toward the visual target. This finding highlights the role of cardiac information in visual processing and furthers our understanding of the brain dynamics underlying multisensory perception involving both interoception and exteroception.

Abstract P1098: Atrial Deletion Of AMPK Promotes Atrial Oxidative Stress And The Formation Of Delayed Afterdepolarizations Within The Inter-atrial Pulmonary Vein Junction

Atrial specific AMPK deletion leads to spontaneous onset of AF. Electrophysiological mechanisms underlying this heightened propensity remain unknown. We hypothesized that AMPK inactivation forms atrial triggered activity leading to atrial ectopy and AF initiation, in large part, by promoting atrial oxidative stress. Methods: We performed detailed ex vivo atrial optical action potential (AP) mapping on the posterior surface of hearts from mice with atrial deletion of AMPK a1/a2 (AMPK-dKO) (via Cre recombinase driven by sarcolipin) vs littermate controls (Ctrl), both during steady state pacing and following challenge with right atrial stimulus trains designed to promote calcium overload. Mitochondrial (mito) ultrastructure and markers of atrial oxidative stress were measured. To assess the functional impact of atrial oxidative stress, AMPK-dKO mice underwent chronic in vivo treatment with EUK-134 (EUK, 25mg/Kg SQ, 3X/wk) for 16 wks. Results: AMPK-dKO (7/11) but not Ctrl (0/5) hearts exhibited subthreshold delayed afterdepolarizations (DAD) that were consistently localized within a discrete inter-atrial region corresponding with the pulmonary veins (PV) junction. These triggers coincided with atrial oxidative stress indexed by a significant (p<0.05) decrease in GSH/GSSG, PRDX3, SOD2, and increase in nitrotyrosine expression along with atrial mito swelling, decreased count and loss of cristae density. Chronic EUK treatment of AMPK-dKO suppressed the incidence (83% to 40%) and frequency (1.81±0.98/s to 0.083±0.08/s) of PV triggers abrogating the genesis of post-pacing atrial AP ectopy originating from the PV (4/5 vs 0/5). Serial in vivo ECG recordings in a subset of AMPK-dKO mice showed reorganization of the RR vs RR+1 relationship following 16 wks of EUK treatment consistent with decreased incidence of premature atrial complexes. Expression of total and S368 phosphorylated Cx43 were both reduced in the atria of AMPK-dKO mice vs Ctrl and restored by EUK reflecting reversal of pathological molecular remodeling by in vivo ROS scavenging. Conclusions: AMPK deletion promotes formation of left atrial ectopy from DAD sources within the PV region. AMPK plays a central role in the prevention of atrial oxidative stress and associated arrhythmias.

Arrhythmias and Their Electrophysiological Mechanisms in Takotsubo Syndrome: A Narrative Review.

Takotsubo syndrome (TTS), an acute and usually reversible condition, is associated with both tachy- and bradyarrhythmias. Such arrhythmias can be life-threatening, e.g. ventricular tachycardia and fibrillation, and associated with cardiac arrest. Others, such as atrioventricular block, persist and require long-term device therapy. In this narrative review, we aim to provide a summary of the current literature on arrhythmias in TTS and their clinical sequelae. PubMed and Medline databases were searched with various permutations of TTS, arrhythmias and beta-adrenoceptors. After application of exclusion criteria and review, 84 articles were included. Although there are no specific electrocardiograph (ECG) findings in TTS to differentiate it from ST-elevation myocardial infarction, suggestive patterns include small QRS amplitude, ST segment elevation without reciprocal ST depression and prolonged QT interval. Atrial tachyarrhythmias (incidence of 5-15%) are associated with a more unwell patient cohort. Ventricular arrhythmias (incidence 4-14%) are often associated with prolonged QT interval and are a cause of sudden death in TTS. Bradyarrhythmias are less common (incidence 1.3-2.5%), but have been reported with TTS, and usually persist beyond the acute phase. Takotsubo syndrome, though considered primarily a disease of the myocardium, carries multiple arrhythmic manifestations that affect short- and long-term prognosis. The management of such arrhythmias represents a constantly evolving area of research.

Consensus guidelines on the construct validity of rodent models of restless legs syndrome.

ABSTRACTOur understanding of the causes and natural course of restless legs syndrome (RLS) is incomplete. The lack of objective diagnostic biomarkers remains a challenge for clinical research and for the development of valid animal models. As a task force of preclinical and clinical scientists, we have previously defined face validity parameters for rodent models of RLS. In this article, we establish new guidelines for the construct validity of RLS rodent models. To do so, we first determined and agreed on the risk, and triggering factors and pathophysiological mechanisms that influence RLS expressivity. We then selected 20 items considered to have sufficient support in the literature, which we grouped by sex and genetic factors, iron-related mechanisms, electrophysiological mechanisms, dopaminergic mechanisms, exposure to medications active in the central nervous system, and others. These factors and biological mechanisms were then translated into rodent bioequivalents deemed to be most appropriate for a rodent model of RLS. We also identified parameters by which to assess and quantify these bioequivalents. Investigating these factors, both individually and in combination, will help to identify their specific roles in the expression of rodent RLS-like phenotypes, which should provide significant translational implications for the diagnosis and treatment of RLS.

Electrophysiological Mechanism Underlying Vagal Nerve Activity in Mice

The autonomic nervous system, which consists of sympathetic and parasympathetic nerves, plays an important role in the regulation of various functions of body organs. Recent studies have reported that vagal afferents that transmit information from the periphery to the brain function as an important signal pathway for dissemination of details regarding nutritional status, as well as the cardiovascular system and inflammation. In this review, we describe the measurement analysis of vagal nerve activity in mice using an in vivo electrophysiological method and account for the role and mechanism of action of vagal nerves in homeostasis.

Electrophysiologic Mechanism of Conversion of Atrial Fibrillation to Sinus Rhythm

Electrophysiologic Mechanism of Conversion of Atrial Fibrillation to Sinus Rhythm

Arrhythmogenesis of surgical atrial incisions and lesions in Maze procedure: insights from high-resolution mapping of atrial tachycardias.

Atrial tachycardias (ATs) frequently develop after a surgical Maze procedure. We aimed to elucidate the electrophysiologic mechanisms and their arrhythmogenic substrates of these ATs. We retrospectively reviewed 20 patients (14 females, mean age of 55.5 ± 8.6 years) with post-Maze ATs who underwent high-resolution mapping at three institutions. The slow conduction areas, reentry circuits, voltage signals, complex electrograms, and their correlation with the surgical incisions and lesions placed in the surgical Maze procedures were analyzed. Thirty-six ATs with a mean cycle length of 260.0 ± 67.6 ms were mapped in these patients. Among them, 22 (61.1%) were anatomical macro-reentrant ATs (AMAT), 12 (33.3%) non-AMATs (localized ATs), and 2 (5.6%) focal ATs, respectively. Epicardial conduction bridges were observed in 6/20 (30.0%) patients and 7/36 (19.4%) ATs. Different arrhythmogenic substrates were identified in these ATs, including slow conduction regions within the previous lesion areas or between the incisions and anatomical structures, the prolonged activation pathways caused by the short lesions connecting the tricuspid annulus, and the circuits around the long incisions and/or lesions. Reentry is the main mechanism of the post-Maze ATs. The pro-arrhythmic substrates are most likely caused by surgical incisions and lesions. The slow conduction regions and the protected channels yielded from these areas are the major arrhythmogenic factors.

Supraventricular tachycardias: the underlying mechanisms and the choice of treatment options

The lecture is devoted to one of the most pressing problems of cardiology – the paroxysmal heart rhythm disorders in clinical practice. Supraventricular tachycardias (SVTs) is a common group of cardiac arrhythmias that requires a diagnostic search to establish the mechanisms of formation and selection of optimal treatment tactics. The basic principles of determination of SVTs and their electrophysiological mechanisms are reviewed. The clinical picture and ECG diagnostics of certain forms of tachycardia are outlined. The causes of wide QRS complex tachycardias, and electrocardiographic criteria for the differential diagnosis between ventricular and supraventricular tachycardias with conduction aberration are presented. The key aspects of the diagnosis of wide QRS complex tachycardias are discussed. The emergency care and long-term therapy for SVTs with narrow and wide QRS complexes are presented. According to updated 2019 ESC Guidelines for the management of patients with SVTs, the treatment options and the algorithms for the management of patients with SVT are shown. What should and should not be done? What’s new in 2019 Guidelines? The antiarrhythmic drugs and their use are given, and the principles of catheter treatment of tachycardia are stated.

The Spatial Reach of Neuronal Coherence and Spike-Field Coupling across the Human Neocortex.

Neuronal coherence is thought to be a fundamental mechanism of communication in the brain, where synchronized field potentials coordinate synaptic and spiking events to support plasticity and learning. Although the spread of field potentials has garnered great interest, little is known about the spatial reach of phase synchronization, or neuronal coherence. Functional connectivity between different brain regions is known to occur across long distances, but the locality of synchronization across the neocortex is understudied. Here we used simultaneous recordings from electrocorticography (ECoG) grids and high-density microelectrode arrays to estimate the spatial reach of neuronal coherence and spike-field coherence (SFC) across frontal, temporal, and occipital cortices during cognitive tasks in humans. We observed the strongest coherence within a 2-3 cm distance from the microelectrode arrays, potentially defining an effective range for local communication. This range was relatively consistent across brain regions, spectral frequencies, and cognitive tasks. The magnitude of coherence showed power law decay with increasing distance from the microelectrode arrays, where the highest coherence occurred between ECoG contacts, followed by coherence between ECoG and deep cortical local field potential (LFP), and then SFC (i.e., ECoG > LFP > SFC). The spectral frequency of coherence also affected its magnitude. Alpha coherence (8-14 Hz) was generally higher than other frequencies for signals nearest the microelectrode arrays, whereas delta coherence (1-3 Hz) was higher for signals that were farther away. Action potentials in all brain regions were most coherent with the phase of alpha oscillations, which suggests that alpha waves could play a larger, more spatially local role in spike timing than other frequencies. These findings provide a deeper understanding of the spatial and spectral dynamics of neuronal synchronization, further advancing knowledge about how activity propagates across the human brain.SIGNIFICANCE STATEMENT Coherence is theorized to facilitate information transfer across cerebral space by providing a convenient electrophysiological mechanism to modulate membrane potentials in spatiotemporally complex patterns. Our work uses a multiscale approach to evaluate the spatial reach of phase coherence and spike-field coherence during cognitive tasks in humans. Locally, coherence can reach up to 3 cm around a given area of neocortex. The spectral properties of coherence revealed that alpha phase-field and spike-field coherence were higher within ranges <2 cm, whereas lower-frequency delta coherence was higher for contacts farther away. Spatiotemporally shared information (i.e., coherence) across neocortex seems to reach farther than field potentials alone.

Electrophysiological characteristics and possible mechanism of bipolar pacing in left bundle branch pacing

Left bundle branch pacing is a physiological pacing modality with a low and stable threshold. The electrophysiological characteristics and mechanisms of bipolar pacing remain unclear. This study aimed to assess the electrophysiological characteristics of bipolar pacing of left bundle branch pacing and to infer the mechanisms underlying each electrocardiogram and electrogram waveform morphology. A total of 65 patients who strictly met the criteria for left bundle branch capture were enrolled. The changes in the morphology of the electrocardiogram and electrogram during the threshold testing with different outputs on unipolar and bipolar pacing were recorded. The electrophysiological characteristics were then analyzed. Four distinct morphologies and 3 different types of transitions during bipolar pacing threshold testing were identified; we labeled the 4 types of morphologies as nonselective (NS)-bipolar-left bundle (LB), NS-cathodal-LB, selective (S)-cathodal-LB, and left ventricular septal-cathodal. Except left ventricular septal-cathodal, the other 3 types (NS-bipolar-LB, NS-cathodal-LB, and S-cathodal-L) had a short and constant V6 R-wave peak time (RWPT) (64.8 ± 7.7 ms vs 65.7 ± 7.8 ms vs 65.7 ± 7.3 ms). The paced QRS (P-QRS) complex was the narrowest in NS-bipolar-LB rather than in NS-cathodal-LB (118.2 ± 14.2 ms vs 133.8 ± 15.8 ms; P < .001). NS-bipolar-LB had a higher threshold than did NS-cathodal-LB (2.5 ± 1.2 V vs 0.8 ± 0.4 V; P < .001). With a higher output on bipolar pacing, NS-bipolar-LB capture had the shortest V6 RWPT, V1 RWPT, and P-QRS. S-cathodal-LB capture had the longest V1 RWPT and P-QRS complex.

The influence of temporal unpredictability on the electrophysiological mechanisms of neural entrainment.

Neural entrainment, or the synchronization of endogenous oscillations to exogenous rhythmic events, has been postulated as a powerful mechanism underlying stimulus prediction. Nevertheless, studies that have explored the benefits of neural entrainment on attention, perception, and other cognitive functions have received criticism, which could compromise their theoretical and clinical value. Therefore, the aim of the present study was [1] to confirm the presence of entrainment using a set of pre-established criteria and [2] to establish whether the reported behavioral benefits of entrainment remain when temporal predictability related to target appearance is reduced. To address these points, we adapted a previous neural entrainment paradigm to include: a variable entrainer length and increased target-absent trials, and instructing participants to respond only if they had detected a target, to avoid guessing. Thirty-six right-handed women took part in this study. Our results indicated a significant alignment of neural activity to the external periodicity as well as a persistence of phase alignment beyond the offset of the driving signal. This would appear to indicate that neural entrainment triggers preexisting endogenous oscillations, which cannot simply be explained as a succession of event-related potentials associated with the stimuli, expectation and/or motor response. However, we found no behavioral benefit for targets in-phase with entrainers, which would suggest that the effect of neural entrainment on overt behavior may be more limited than expected. These results help to clarify the mechanistic processes underlying neural entrainment and provide new insights on its applications.

Carbamazepine Increases the Risk of Sudden Cardiac Arrest by a Reduction of the Cardiac Sodium Current.

Aim: To assess the risk of sudden cardiac arrest (SCA) associated with the use of carbamazepine (CBZ) and establish the possible underlying cellular electrophysiological mechanisms. Methods: The SCA risk association with CBZ was studied in general population cohorts using a case–control design (n = 5,473 SCA cases, 21,866 non-SCA controls). Effects of 1–100 µM CBZ on action potentials (APs) and individual membrane currents were determined in isolated rabbit and human cardiomyocytes using the patch clamp technique. Results: CBZ use was associated with increased risk of SCA compared with no use (adjusted odds ratio 1.90 [95% confidence interval: 1.12–3.24]). CBZ reduced the AP upstroke velocity of rabbit and human cardiomyocytes, without prominent changes in other AP parameters. The reduction occurred at ≥30 µM and was frequency-dependent with a more pronounced reduction at high stimulus frequencies. The cardiac sodium current (INa) was reduced at ≥30 μM; this was accompanied by a hyperpolarizing shift in the voltage-dependency of inactivation. The recovery from inactivation was slower, which is consistent with the more pronounced AP upstroke velocity reduction at high stimulus frequencies. The main cardiac K+ and Ca2+ currents were unaffected, except reduction of L-type Ca2+ current by 100 µM CBZ. Conclusion: CBZ use is associated with an increased risk of SCA in the general population. At concentrations of 30 µM and above, CBZ reduces AP upstroke velocity and INa in cardiomyocytes. Since the concentration of 30 µM is well within the therapeutic range (20–40 µM), we conclude that CBZ increases the risk of SCA by a reduction of the cardiac INa.

Analysis of Electrophysiological Mechanisms of N-Deacetyllapaconitine Monochlorhydrate, the Main Metabolite of Lappaconitine Hydrobromide.

In in vitro experiments on isolated rat hippocampal neurons, we studied the electrophysiological mechanisms of the antiarrhythmic effects of N-deacetyllappaconitine monochlorhydrate (DALCh), active metabolite of lappaconitine hydrobromide (allapinin). Electrical activity of neurons was recorded by the patch-clamp method in the whole cell configuration. It was shown that DALCh increased the duration of both slow and fast depolarization phases and decreased the amplitude of the action potential. DALCh effectively inhibited transmembrane currents of Na+ ions and partially K+ ions through the corresponding transmembrane voltage-gated ion channels. Thus, DALCh, in contrast to lappaconitine hydrobromide, belongs not to 1C, but to the 1A class of antiarrhythmics according to the Vaughan-Williams classification.

High-Definition Transcranial Direct Current Stimulation of the Dorsolateral Prefrontal Cortex Modulates the Electroencephalography Rhythmic Activity of Parietal Occipital Lobe in Patients With Chronic Disorders of Consciousness.

BackgroundDisorders of consciousness (DOC) are a spectrum of pathologies affecting one’s ability to interact with the external world. At present, High-Definition Transcranial Direct Current Stimulation (HD-tDCS) is used in many patients with DOC as a non-invasive treatment, but electrophysiological research on the effect of HD-tDCS on patients with DOC is limited.ObjectivesTo explore how HD-tDCS affects the cerebral cortex and examine the possible electrophysiological mechanisms underlying the effects of HD-tDCS on the cerebral cortex.MethodsA total of 19 DOC patients were assigned to HD-tDCS stimulation. Each of them underwent 10 anodal HD-tDCS sessions of the left dorsolateral prefrontal cortex (DLPFC) over 5 consecutive days. Coma Recovery Scale-Revision (CRS-R) scores were recorded to evaluate the consciousness level before and after HD-tDCS, while resting-state electroencephalography (EEG) recordings were obtained immediately before and after single and multiple HD-tDCS stimuli. Depending on whether the CRS-R score increased after stimulation, we classified the subjects into responsive (RE) and non-responsive (N-RE) groups and compared the differences in power spectral density (PSD) between the groups in different frequency bands and brain regions, and also examined the relationship between PSD values and CRS-R scores.ResultsFor the RE group, the PSD value of the parieto-occipital region increased significantly in the 6–8 Hz frequency band after multiple stimulations by HD-tDCS. After a single stimulation, an increase in PSD was observed at 10–13 and 13–30 Hz. In addition, for all subjects, a positive correlation was observed between the change in PSD value in the parieto-occipital region at 10–13 and 6–8 Hz frequency band and the change in CRS-R score after a single stimulation.ConclusionRepeated anodal HD-tDCS of the left DLPFC can improve clinical outcomes in patients with DOC, and HD-tDCS-related increased levels of consciousness were associated with increased parieto-occipital PSD.

Consortin: a potential modulator of ventricular conduction

Abstract Funding Acknowledgements Type of funding sources: None. Background Consortin, encoded by the CNST gene, is a ubiquitously expressed protein putatively involved in trafficking of connexins to the plasma membrane. In the heart, connexins form gap junctions, which are essential for cardiac conduction. Reduced levels and abnormal cellular distribution of connexins have been found in patients with heart failure, atrial fibrillation, arrhythmogenic cardiomyopathy and Brugada syndrome. Purpose To decipher the role of Consortin in cardiac electrophysiology. Methods Homozygous Cnst knockout mice (Cnst-/-) were generated using CRISPR-Cas9 technology. Consortin expression was assessed by Western blot analysis. Cardiac conduction parameters were recorded by electrocardiography in anesthetized wild-type (WT) and Cnst-/- male and female littermates aged 3-6 months. Conduction velocity (CV) was determined in Langendorff-perfused hearts by optical mapping of the right ventricle (RV) at a pacing cycle length of 120 ms. Data were analyzed by Student’s t­-test and P values &amp;lt; 0.05 were considered significant. Results Western blot analysis confirmed the presence of Consortin in WT mouse hearts, and its absence in Cnst-/- hearts. Heart rate, P-wave duration and PR-interval did not differ between groups, whereas QRS interval was significantly prolonged in Cnst-/- (mean±SEM 8.7±1.3 ms, n=13) compared to WT mice (7.9±1.1ms, n=13; (p=0.0009)). Hearts were structurally normal, and heart weight:body weight ratio was similar between groups. Preliminary optical mapping at the RV of Langendorff-perfused hearts demonstrated a lower, although not significantly different, transversal CV in Cnst-/- (56±4.3 cm/s, n=6) compared to WT (65±7.1 cm/s; n=3; p=0.31), whereas longitudinal CV was similar between groups (Cnst-/- 80±4.2 cm/s versus WT 83±9.1 cm/s; p=0.74). No differences were observed in RV effective refractory period (p=0.59). Conclusion These preliminary findings support a modulatory role of Consortin in ventricular conduction. Current efforts are aimed at elucidating the underlying electrophysiological and molecular mechanisms, including the impact of Consortin on cardiac connexins.

PtNPs/PEDOT:PSS-Modified Microelectrode Arrays Reveal Electrophysiological Activities of Different Neurons in Medial Amygdala of Mice Under Innate Fear.

The medial amygdala (MA) plays an important role in the innate fear circuit. However, the electrophysiological mechanism of MA for processing innate fear needs to be further explored. In this study, we fabricated microelectrode arrays (MEAs) with detecting sites arranged to match the location and shape of MA in mice and detected the electrophysiology in freely behaving mice under 2-methyl-2-thiazoline (2MT)-induced fear. The detection performance of MEA is improved by modifying metal nanoparticles and conductive polymers (PtNPs/PEDOT:PSS). After modification, the impedance magnitude and phase of electrodes were decreased to 27.0 ± 2.3 kΩ and −12.30 ± 0.52°, respectively, leading to a signal-to-noise ratio of 10. Its electrochemical stability and mechanical stability were also verified by cyclic voltammetry (CV) sweeping and ultrasonic vibration. MEAs were then implanted into the MA of mice, and the electrophysiology and behavioral characteristics were synchronously recorded and analyzed. The results showed that 2MT induced strong defensive behaviors in mice, accompanied by increases in the average spike firing rate and local field potential (LFP) power of MA neurons. According to principles commonly applied to cortical extracellular recordings, the recorded neurons are divided into two classes based on waveforms. Statistics showed that about 37% of type 1 neurons (putative GABAergic neurons) and 87% of type 2 neurons (putative glutamatergic neurons) were significantly activated under innate fear. At the same time, the firing rate of some activated neurons had a good linear correlation with the freezing rate.

BS-526-01 THE EFFECT OF CHRONIC NICOTINE EXPOSURE ON CARDIAC ELECTROPHYSIOLOGY IN THE RABBIT HEART

Tobacco smoke exposure is associated with increased risk for atrial and ventricular arrhythmias. However, the individual components of tobacco smoke that may promote arrhythmias and the underlying electrophysiological mechanisms are unknown. Nicotine (NIC) is a major component of tobacco smoke and emerging tobacco products, including e-cigarettes.

BS-400-49 THE EFFECT OF CHRONIC NICOTINE EXPOSURE ON CARDIAC ELECTROPHYSIOLOGY IN THE RABBIT HEART

Tobacco smoke exposure is associated with increased risk for atrial and ventricular arrhythmias. However, the individual components of tobacco smoke that may promote arrhythmias and the underlying electrophysiological mechanisms are unknown. Nicotine (NIC) is a major component of tobacco smoke and emerging tobacco products, including e-cigarettes.