Slow Wave Frequency Research Articles

Brain electrical activity in female Major Depressive Disorder patients

Background: Quantitative EEG provides insight to the brain activity associated with depressive illness. Frontal asymmetry and changes of slow wave frequencies brain activity have been found as the characteristic features of Major Depressive Disorder (MDD). Objective: To assess the brain activity by power spectral analysis of EEG in female patients with MDD. Methods: This observational study was carried on 20 female MDD patients (age 20-40 years) enrolled from the Department of Psychiatry, Bangabandhu Sheikh Mujib Medical University, Shahbag, Dhaka. Twenty (20) healthy volunteers of the same age were considered the control group. For the study, EEG was recorded for 3 minutes in eye closed position by EEG data acquisition device, EEG Traveler BrainTech 32+ CMEEG-01, India. Power spectral analysis of EEG data was done by BT40 analysis software. For statistical analysis, the Mann-Whitney U test was done. Results: Significantly higher Absolute power of delta and theta brain wave, and lower alpha and beta brain wave activity was observed in female MDD patients compared to control in all most all electrodes in all cortical regions. Conclusion: MDD patients showed low excitable brain state and characteristic feature of high slow frequency wave and low fast frequency wave in MDD which can be diagnosed by quantitative EEG analysis. J Bangladesh Soc Physiol 2023;18(2): 53-62

A planar mounted SQUID full-tensor module for magnetoenterogram denoising detection

Magntoenterogram (MENG) is a functional imaging method with great clinical potential for non-invasive diagnosis of intestinal diseases. In measurements of MENG, the cardiac artifacts are a strong biological source of interference. Based on wire-wound SQUID gradiometers, we constructed a planar mounted full-tensor compensation module for MENG system, which can obtain cardiac artifacts while suppressing ambient noise, so as to denoise MENG signals without increasing external ECG recording channels. The cardiac artifacts are regressed out from the full-tensor compensation module outputs, which can denoise the MENG measurements. Using this module, the SNR is about 70 dB better than the raw data. At last, 36-point array MENG signals were detected successfully and the contour map of jejunal slow-wave frequency (SWF) was consistent with the jejunal area (one part of the small intestine). This method will save costs and avoid the new electromagnetic interferences introduced by ECG equipment. It will lay a good foundation for the rapid clinical application of the MENG system.

Cerebral Gray Matter May Not Explain Sleep Slow-Wave Characteristics after Severe Brain Injury.

Sleep slow waves are the hallmark of deeper non-rapid eye movement sleep. It is generally assumed that gray matter properties predict slow-wave density, morphology, and spectral power in healthy adults. Here, we tested the association between gray matter volume (GMV) and slow-wave characteristics in 27 patients with moderate-to-severe traumatic brain injury (TBI, 32.0 ± 12.2 years old, eight women) and compared that with 32 healthy controls (29.2 ± 11.5 years old, nine women). Participants underwent overnight polysomnography and cerebral MRI with a 3 Tesla scanner. A whole-brain voxel-wise analysis was performed to compare GMV between groups. Slow-wave density, morphology, and spectral power (0.4-6 Hz) were computed, and GMV was extracted from the thalamus, cingulate, insula, precuneus, and orbitofrontal cortex to test the relationship between slow waves and gray matter in regions implicated in the generation and/or propagation of slow waves. Compared with controls, TBI patients had significantly lower frontal and temporal GMV and exhibited a subtle decrease in slow-wave frequency. Moreover, higher GMV in the orbitofrontal cortex, insula, cingulate cortex, and precuneus was associated with higher slow-wave frequency and slope, but only in healthy controls. Higher orbitofrontal GMV was also associated with higher slow-wave density in healthy participants. While we observed the expected associations between GMV and slow-wave characteristics in healthy controls, no such associations were observed in the TBI group despite lower GMV. This finding challenges the presumed role of GMV in slow-wave generation and morphology.

High-energy pacing inhibits slow-wave dysrhythmias in the small intestine.

The motility of the gastrointestinal tract is coordinated in part by rhythmic slow waves, and disrupted slow-wave patterns are linked to functional motility disorders. At present, there are no treatment strategies that primarily target slow-wave activity. This study assessed the use of pacing to suppress glucagon-induced slow-wave dysrhythmias in the small intestine. Slow waves in the jejunum were mapped in vivo using a high-resolution surface-contact electrode array in pigs (n = 7). Glucagon was intravenously administered to induce hyperglycemia. Slow-wave propagation patterns were categorized into antegrade, retrograde, collision, pacemaker, and uncoupled activity. Slow-wave characteristics such as period, amplitude, and speed were also quantified. Postglucagon infusion, pacing was applied at 4 mA and 8 mA and the resulting slow waves were quantified spatiotemporally. Antegrade propagation was dominant throughout all stages with a prevalence of 55 ± 38% at baseline. However, glucagon infusion resulted in a substantial and significant increase in uncoupled slow waves from 10 ± 8% to 30 ± 12% (P = 0.004) without significantly altering the prevalence of other slow-wave patterns. Slow-wave frequency, amplitude, and speed remained unchanged. Pacing, particularly at 8 mA, significantly suppressed dysrhythmic slow-wave patterns and achieved more effective spatial entrainment (85%) compared with 4 mA (46%, P = 0.039). This study defined the effect of glucagon on jejunal slow waves and identified uncoupling as a key dysrhythmia signature. Pacing effectively entrained rhythmic activity and suppressed dysrhythmias, highlighting the potential of pacing for gastrointestinal disorders associated with slow-wave abnormalities.NEW & NOTEWORTHY Glucagon was infused in pigs to induce hyperglycemia and the resulting slow-wave response in the intact jejunum was defined in high resolution for the first time. Subsequently, with pacing, the glucagon-induced dysrhythmias were suppressed and spatially entrained for the first time with a success rate of 85%. The ability to suppress slow-wave dysrhythmias through pacing is promising in treating motility disorders that are associated with intestinal dysrhythmias.

Multichannel mapping of in vivo rat uterine myometrium exhibits both high and low frequency electrical activity in non-pregnancy

The uterus exhibits intermittent electrophysiological activity in vivo. Although most active during labor, the non-pregnant uterus can exhibit activity of comparable magnitude to the early stages of labor. In this study, two types of flexible electrodes were utilized to measure the electrical activity of uterine smooth muscle in vivo in anesthetized, non-pregnant rats. Flexible printed circuit electrodes were placed on the serosal surface of the uterine horn of six anesthetized rats. Electrical activity was recorded for a duration of 20–30 min. Activity contained two components: high frequency activity (bursts) and an underlying low frequency ‘slow wave’ which occurred concurrently. These components had dominant frequencies of 6.82 ± 0.63 Hz for the burst frequency and 0.032 ± 0.0055 Hz for the slow wave frequency. There was a mean burst occurrence rate of 0.76 ± 0.23 bursts per minute and mean burst duration of 20.1 ± 6.5 s. The use of multiple high-resolution electrodes enabled 2D mapping of the initiation and propagation of activity along the uterine horn. This in vivo approach has the potential to provide the organ level detail to help interpret non-invasive body surface recordings.

Pulsed Vibro-Acoustic Analysis Technique for Monitoring Bone Health in Preterm Infants: A Pilot Study.

Despite advances in neonatal care, metabolic bone disease of prematurity (MBDP) remains a common problem in preterm infants. The development of non-invasive and affordable diagnostic approaches can be highly beneficial in the diagnosis and management of preterm infants at risk of MBDP. In this study, we present an ultrasound method called pulsed vibro-acoustic analysis to investigate the progression of bone mineralization in infants over time versus weight and postmenstrual age. The proposed pulsed vibro-acoustic analysis method is used to evaluate the vibrational characteristics of the bone. This method uses the acoustic radiation force of ultrasound to vibrate the bone. The generated acoustic waves are detected using a hydrophone placed on the skin over the tibia. The frequency of vibration and the speeds of received acoustic waves have information regarding the material property of the bone. We examined the feasibility of this method through an in vivo study consisting of 25 preterm and 10 full term infants. The pulsed vibro-acoustic data were acquired longitudinally in preterm infants with multiple visits and at a single visit in full term infants. Speed of sound and mean peak frequency of slow and fast sound waves recorded by hydrophone were used to analyze bone mineralization progress. Linear mixed model was used for statistical analysis in characterizing the mineralization progress in preterm infants compared to data from full term subjects. Significance changes in wave parameters (speed of sound and mean peak frequency) with respect to the postmenstrual age and weight in preterm infants were observed with p-values less than 0.05. Statistical significances in speed of sound measurement for both fast and slow waves were observed between preterm and full term infants, with p-values of <0.01 and 0.02, respectively. The results of this pilot study indicate the potential use of vibro-acoustic analysis for monitoring the progression of bone mineralization in preterm infants.

Transmission of slow waves in Masimo O3 near infrared spectroscopy measures

IntroductionCerebral autoregulation (CA) dysfunction is a key complication following brain injury. CA assessment using near-infrared spectroscopy (NIRS) offers a promising alternative to the current non-invasive standard, cerebral blood flow velocity (CBFV) measured with transcranial Doppler. Research questionCan autoregulatory slow waves (frequency range 0.005–0.05 Hz) associated with spontaneous and induced changes in ABP in healthy volunteers be detected by parameters measured with the Masimo O3 NIRS device? MethodsABP, CBFV and Masimo O3 parameters were measured in 10 healthy volunteers at baseline and during ABP oscillations induced by squat/stand manoeuvres. Transmission of slow waves was assessed with power spectral density and coherence analysis in NIRS signals and compared to that of CBFV. ResultsAt baseline, slow waves were detected with sufficient power that substantially exceeded the signals’ measurement resolution in all parameters except cerebral oxygen saturation. During ABP oscillations in the 0.033 Hz range (induced by squat/stand), the power of slow waves increased in all parameters in a similar pattern, with total (cHb) and oxygenated (O2Hb) haemoglobin concentrations most closely mirroring CBFV (median standardised power [first-third quartile], baseline vs squat/stand: CBFV 0.35 [0.28–0.42] vs 0.50 [0.45–0.62], O2Hb 0.47 [0.33–0.68] vs 0.61 [0.59–0.69]). Coherence with ABP increased for both CBFV and NIRS measures from low at baseline (<0.4) to high during induced changes (>0.8). ConclusionSpontaneous fluctuations in ABP can be observed in analysed Masimo O3 metrics to a varying degree. The clinical utility of Masimo O3 signals in CA assessment requires further investigation in brain injury patients.

Effects of weaning on intestinal longitudinal muscle-myenteric plexus function in piglets.

Weaning piglets usually suffer from severe diarrhea (commonly known as postweaning diarrhea, PWD) along with intestinal motility disorder. Intestinal peristalsis is mainly regulated by the longitudinal muscle-myenteric plexus (LM-MP). To understand the relationship between intestinal LM-MP function and the development of PWD, we compared the intestinal electrical activity, and the transcriptional profile of the LM-MP between 21-day-old piglets (just weaned, n=7) and 24-day-old piglets (suffered the most severe weaning stress, n=7). The results showed that 24-day-old piglets exhibited different degrees of diarrhea. A significant increase in the slow-wave frequency in the ileum and colon was observed in 24-day-old piglets, while c-kit expression in the intestinal LM-MPs was significantly decreased, indicating that PWD caused by elevated slow-wave frequency may be associated with loss of c-kit. The real-time quantitative PCR (RT-qPCR) and enzyme-linked immunosorbent assay (ELISA) showed that intestinal LM-MPs in 24-day-old piglets may undergo inflammation and oxidative stress. Significant increases in 8-hydroxy-2'-deoxyguanosine and decreases in thioredoxin suggest that weaning may lead to DNA damage in the LM-MP of 24-day-old piglets. In addition, activating transcription factor 3 was significantly upregulated, indicating nerve damage in the LM-MP of 24-day-old piglets. The transcriptomic results showed that most of the differentially expressed genes in the ileal LM-MP after weaning were downregulated and closely related to the cell cycle process. Subsequent RT-qPCR analysis showed that the relative expression of p21 was upregulated, while the expression of cyclin A2, cyclin B1, and proliferating cell nuclear antigen was downregulated in the ileal and colonic LM-MP of 24-day-old piglets, suggesting that weaning may inhibit cell proliferation and cause G1/S cell cycle arrest in ileal and colonic LM-MP. In conclusion, weaning may lead to cell cycle arrest by causing DNA damage in the LM-MP, impairing intestinal motility regulation, and ultimately leading to diarrhea in piglets.

Effect of Propofol on Heart Rate and Its Coupling to Cortical Slow Waves in Humans.

Propofol causes significant cardiovascular depression and a slowing of neurophysiological activity. However, literature on its effect on the heart rate remains mixed, and it is not known whether cortical slow waves are related to cardiac activity in propofol anesthesia. The authors performed a secondary analysis of electrocardiographic and electroencephalographic data collected as part of a previously published study where n = 16 healthy volunteers underwent a slow infusion of propofol up to an estimated effect-site concentration of 4 µg/ml. Heart rate, heart rate variability, and individual slow electroencephalographic waves were extracted for each subject. Timing between slow-wave start and the preceding R-wave was tested against a uniform random surrogate. Heart rate data were further examined as a post hoc analysis in n = 96 members of an American Society of Anesthesiologists Physical Status II/III older clinical population collected as part of the AlphaMax trial. The slow propofol infusion increased the heart rate in a dose-dependent manner (mean ± SD, increase of +4.2 ± 1.5 beats/min/[μg ml-1]; P < 0.001). The effect was smaller but still significant in the older clinical population. In healthy volunteers, propofol decreased the electrocardiogram R-wave amplitude (median [25th to 75th percentile], decrease of -83 [-245 to -28] μV; P < 0.001). Heart rate variability showed a loss of high-frequency parasympathetic activity. Individual cortical slow waves were coupled to the heartbeat. Heartbeat incidence peaked about 450 ms before slow-wave onset, and mean slow-wave frequency correlated with mean heart rate. The authors observed a robust increase in heart rate with increasing propofol concentrations in healthy volunteers and patients. This was likely due to decreased parasympathetic cardioinhibition. Similar to non-rapid eye movement sleep, cortical slow waves are coupled to the cardiac rhythm, perhaps due to a common brainstem generator.

The hierarchy of coupled sleep oscillations reverses with aging in humans.

A well-orchestrated coupling hierarchy of slow waves and spindles during slow wave sleep supports memory consolidation. In old age, duration of slow wave sleep and number of coupling events decreases. The coupling hierarchy deteriorates, predicting memory loss and brain atrophy. Here, we investigate the dynamics of this physiological change in slow wave-spindle coupling in a frontocentral electroencephalography position in a large sample (N=340, 237 female, 103 male) spanning most of the human lifespan (ages 15-83). We find that, instead of changing abruptly, spindles gradually shift from being driven by-, to driving slow waves with age, reversing the coupling hierarchy typically seen in younger brains. Reversal was stronger the lower the slow wave frequency, and starts around midlife (∼age 40-48), with an established reversed hierarchy at age 56-83. Notably, coupling strength remains unaffected by age. In older adults, deteriorating slow wave-spindle coupling, measured using phase slope index (PSI) and number of coupling events, is associated with blood plasma glial fibrillary acidic protein (GFAP) levels, a marker for astrocyte activation. Data-driven models suggest decreased sleep time and higher age lead to fewer coupling events, paralleled by increased astrocyte activation. Counterintuitively, astrocyte activation is associated with a back-shift of the coupling hierarchy (PSI) towards a "younger" status along with increased coupling occurrence and strength, potentially suggesting compensatory processes. As the changes in coupling hierarchy occur gradually starting at midlife, we suggest there exists a sizable window of opportunity for early interventions to counteract undesirable trajectories associated with neurodegeneration.Significance StatementEvidence accumulates that sleep disturbances and cognitive decline are bi-directionally and causally linked forming a vicious cycle. Improving sleep quality could break this cycle. One marker for sleep quality is a clear hierarchical structure of sleep oscillations. Previous studies showed that sleep oscillations decouple in old age. Here, we show that, rather, the hierarchical structure gradually shifts across the human lifespan and reverses in old age, while coupling strength remains unchanged. This shift is associated with markers for astrocyte activation in old age. The shifting hierarchy resembles brain maturation, plateau, and wear processes. This study furthers our comprehension of this important neurophysiological process and its dynamic evolution across the human lifespan.

Optogenetic targeting of astrocytes restores slow brain rhythm function and slows Alzheimer’s disease pathology

Patients with Alzheimer’s disease (AD) exhibit non-rapid eye movement (NREM) sleep disturbances in addition to memory deficits. Disruption of NREM slow waves occurs early in the disease progression and is recapitulated in transgenic mouse models of beta-amyloidosis. However, the mechanisms underlying slow-wave disruptions remain unknown. Because astrocytes contribute to slow-wave activity, we used multiphoton microscopy and optogenetics to investigate whether they contribute to slow-wave disruptions in APP/PS1 mice. The power but not the frequency of astrocytic calcium transients was reduced in APP/PS1 mice compared to nontransgenic controls. Optogenetic activation of astrocytes at the endogenous frequency of slow waves restored slow-wave power, reduced amyloid deposition, prevented neuronal calcium elevations, and improved memory performance. Our findings revealed malfunction of the astrocytic network driving slow-wave disruptions. Thus, targeting astrocytes to restore circuit activity underlying sleep and memory disruptions in AD could ameliorate disease progression.

Modulatory dynamics mark the transition between anesthetic states of unconsciousness

Unconsciousness maintained by GABAergic anesthetics, such as propofol and sevoflurane, is characterized by slow-delta oscillations (0.3 to 4 Hz) and alpha oscillations (8 to 14 Hz) that are readily visible in the electroencephalogram. At higher doses, these slow-delta-alpha (SDA) oscillations transition into burst suppression. This is a marker of a state of profound brain inactivation during which isoelectric (flatline) periods alternate with periods of the SDA patterns present at lower doses. While the SDA and burst suppression patterns have been analyzed separately, the transition from one to the other has not. Using state-space methods, we characterize the dynamic evolution of brain activity from SDA to burst suppression and back during unconsciousness maintained with propofol or sevoflurane in volunteer subjects and surgical patients. We uncover two dynamical processes that continuously modulate the SDA oscillations: alpha-wave amplitude and slow-wave frequency modulation. We present an alpha modulation index and a slow modulation index which characterize how these processes track the transition from SDA oscillations to burst suppression and back to SDA oscillations as a function of increasing and decreasing anesthetic doses, respectively. Our biophysical model reveals that these dynamics track the combined evolution of the neurophysiological and metabolic effects of a GABAergic anesthetic on brain circuits. Our characterization of the modulatory dynamics mediated by GABAergic anesthetics offers insights into the mechanisms of these agents and strategies for monitoring and precisely controlling the level of unconsciousness in patients under general anesthesia.

Involvement of sympathetic nerve activation in acupoint application induced improvement of gastric ulcer and motility in rats with gastric ulcer

To observe the effect of mustard oil application at "Liangmen" (ST21) on gastric ulcer (GU) and gastric motility and its association with the sympathetic nerve activity in rats with GU, so as to provide experimental basis for improvement of GU by acupoint application. Thirty-nine male SD rats were randomly divided into control (n=7), model, acupoint application (AA), medication (guanethidine, an adrenergic sympathetic antagonist) and AA+medication groups (n=8 in each of the latter 4 groups). The GU model was made by applying acetic acid-immersed filter paper onto the gastric antrum. For rats of the AA and AA+medication groups, 50% mustard oil was applied to left ST21 for 10 min, once a day, for 9 consecutive days. Rats of the medication and AA+medication groups received intraperitoneal injection of guanethidine solution (40 mg/kg) beginning from the modeling day on, once a day for 10 consecutive days. The rat's body weight of each group was recorded on the 0th, 1st, 3rd, 7th and 9th day. The intragastric peristaltic wave frequency and the myoelectrical activity (frequency of slow waves, and integration of fast waves) of the gastric smooth muscle were recorded by using PowerLab data acquisition system. The gastric ulcer area was measured after the rats were executed, and histopathological changes of gastric antrum tissues (histopathological score including epithelial cell injury, submucosal edema, hemorrhagic injury, inflammatory cell infiltration score) were observed after H.E. staining. Compared with the control group, the body weight ratio, frequency of gastric peristaltic waves and slow wave frequency of gastric smooth muscle were significantly decreased (P<0.001, P<0.05), while the ulcer area, total histopathological score, epithelial cell injury score, submucosal edema score, hemorrhagic injury score and inflammatory cell infiltration score were significantly increased in the model group (P<0.05, P<0.001). Relevant to the model group, the AA group had a significant increase in the body weight ratio, frequency of gastric peristaltic waves, slow wave frequency, integration of fast waves (P<0.05, P<0.001), and a considerable decrease in the ulcer area, total histopathological score, epithelial cell injury score, submucosal edema score, hemorrhagic injury score and inflammatory cell infiltration score (P<0.05, P<0.001), and the medication group has a significantly decrease in the frequency of gastric peristaltic waves (P<0.05). In comparison with the AA group, the body weight ratio, frequency of gastric peristaltic waves and slow wave frequency of gastric smooth muscle in both medication and AA+medication groups, and the integration of fast waves in the medication group were obviously lower (P<0.05, P<0.001, P<0.01), whereas the levels of ulcer area, total pathological score, submucosal edema score, hemorrhagic injury score and inflammatory cell infiltration score in both medication and AA+medication groups, and the epithelial cell injury score in medication group were significantly higher (P<0.05, P<0.001). Application of mustard oil at acupoint ST21 can effectively remit GU caused by acetic acid and regulate gastric rhythmic contraction, which was mediated by sympathetic nerve.

Sleep waves in a large-scale corticothalamic model constrained by activities intrinsic to neocortical networks and single thalamic neurons.

Many biophysical and non-biophysical models have been able to reproduce the corticothalamic activities underlying different EEG sleep rhythms but none of them included the known ability of neocortical networks and single thalamic neurons to generate some of these waves intrinsically. We built a large-scale corticothalamic model with a high fidelity in anatomical connectivity consisting of a single cortical column and first- and higher-order thalamic nuclei. The model is constrained by different neocortical excitatory and inhibitory neuronal populations eliciting slow (<1 Hz) oscillations and by thalamic neurons generating sleep waves when isolated from the neocortex. Our model faithfully reproduces all EEG sleep waves and the transition from a desynchronized EEG to spindles, slow (<1 Hz) oscillations, and delta waves by progressively increasing neuronal membrane hyperpolarization as it occurs in the intact brain. Moreover, our model shows that slow (<1 Hz) waves most often start in a small assembly of thalamocortical neurons though they can also originate in cortical layer 5. Moreover, the input of thalamocortical neurons increases the frequency of EEG slow (<1 Hz) waves compared to those generated by isolated cortical networks. Our simulations challenge current mechanistic understanding of the temporal dynamics of sleep wave generation and suggest testable predictions.

Effect of electroacupuncture at "Zusanli" (ST36) and "Tianshu" (ST25) on intestinal function and autonomic nerve balance in rats with irritable bowel syndrome

To study whether electroacupuncture (EA) of "Zusanli" (ST36) combined with "Tianshu" (ST25) has a synergistic effect in regulating the colonic function and autonomic nerve balance in rats with irritable bowel syndrome (IBS). Male Wistar rats were randomly divided into control, model, EA-ST36, and EA-ST36+ST25 groups, with 14 rats in each group. The IBS model was established by using water avoidance stress method. The visceral hypersensitivity was measured using the abdominal wall retraction reflex (AWR). The rectus abdominis electromyogram (EMG), intestinal electrical activity, and electrocardiogram (ECG) were recorded using a PowerLab data acquisition and analysis system. The contents of serum cAMP and cGMP were determined by ELISA, the expression levels of colonic tyrosine hydroxylase (TH) and choline acetyl-transferase (ChAT) proteins were determined by immunofluorescence staining and Western blot, respectively. Compared with the control group, the model group had an evident increase in the levels of AWR, LF, LF/HF, ChAT protein expression, cAMP and cGMP contents and cAMP/cGMP ratio (P<0.001, P<0.05), and a marked decrease in the levels of HF, frequency of slow waves of intestinal EMG, visceral pain threshold (PT), immunoactivity and expression of TH protein (P<0.05, P<0.001). In contrast to the model group, the levels of AWR, LF, LF/HF, ChAT protein expression and immunoactivity, cAMP and cGMP contents and ratio of cAMP/cGMP were significantly reduced (P<0.001, P<0.05, P<0.01), whereas the levels of frequency of slow waves of intestinal EMG, PT, and the immunoactivity and expression of TH were considerably increased (P<0.001, P<0.05) in both EA-ST36 and EA-ST36+ST25 groups. EA of both ST36 and ST36+ST25 can relieve visceral pain, and reduce sympathetic activity to improve autonomic nerve balance, but without apparent synergistic effect between EA-ST36 and EA-ST25 in rats with IBS.

Effects of PAR2 Gene Knockout on Visceral Sensitivity, Stress Behaviors, and Colonic Electrical Activities in Irritable Bowel Syndrome.

Irritable bowel syndrome (IBS) could seriously affect the patient's health quality by its recurrence. There is a great medical and social need to explore the mechanisms and new treatment strategies of IBS. To explore the influence of protease-activated receptor 2 (PAR2) gene knockout on IBS visceral sensitivity, stress behaviors, and colonic electrical activities. The PAR2 gene knockout and IBS model rats were generated and divided into PAR2+/+ wild control (WC) group, PAR2+/+ wild IBS model (WM) group, PAR2-/- knockout control (KC) group and PAR2-/- knockout IBS model (KM) group. The stress behaviors scores, minimum rectal fluid injection capacity threshold value of abdominal withdrawal reflex (AWR) = 3, and the colonic electrical activities indexes were recorded and the experimental results were analyzed statistically. (1) PAR2 gene deletion and IBS models were successfully generated. (2) The scores of aggressive and exploratory behaviors in WM and KM groups were higher than WC and KC groups (p < 0.05). The grooming behavior scores in WC and KC groups were higher than the WM and KM groups (p < 0.05). WM group had the highest aggressive and exploratory behavior scores; WC group had the highest grooming behavior scores. (3) The minimum rectal fluid injection capacity threshold value of AWR = 3 in WM and KM groups were lower than WC and KC groups (p < 0.05); WM group had the lowest value. (4) The maximum amplitude and wave frequency of colonic fast and slow waves in WM and WC groups were greater than in the KM and KC groups, respectively (p < 0.05). The amplitude index and number of colonic contraction waves in WM and KM groups were greater than the WC and KC groups (p < 0.05). Colonic electrical activity indexes were highest in the WM group. The PAR2 gene deletion could have a beneficial effect on visceral sensitivity, stress behaviors and colonic electrical activities in rats with IBS.

Modulation of colonic function in irritable bowel syndrome rats by electroacupuncture at ST25 and the neurobiological links between ST25 and the colon.

Irritable bowel syndrome (IBS) is a chronic functional gastrointestinal disease characterized by abdominal pain and defecation disorders. Acupuncture therapy positively affects IBS, with ST25 being the main point. However, ST25 has mostly been used in conjunction with other acupoints. This study aimed to observe the therapeutic effect of electroacupuncture at ST25 alone in IBS and the neurobiological mechanism of ST25 associated with the colon. First, we observed the effect of electroacupuncture at ST25 on the visceral pain threshold and slow-wave discharge of the colon in IBS model rats. Second, we explored the neurobiological mechanism of ST25 associated with the colon using a neural tracer technique. The results showed that (1) electroacupuncture at ST25 alone can alleviate visceral hypersensitivity and restore normal slow-wave frequency and rhythm of the colon in IBS rats; (2) there is a close neuroanatomical connection between ST25 and the colon, i.e., in the dorsal root ganglion (DRG), ST25 is similar in innervation to the colon, mainly in the T8-L1 segment, while the presence of double-labeled positive neurons is present in a part of the DRG; retrogradely labeled motor neurons associated with ST25 were observed in the anterior horn of the spinal cord, and retrogradely labeled sympathetic postganglionic neurons associated with ST25 were observed in the sympathetic nerve chain. These findings suggested that the DRGs and the dorsal horn of the spinal cord are important targets for electroacupuncture at ST25 to reduce visceral hypersensitivity in IBS rats. The sympathetic ganglia may be an important site for ST25 to regulate intestinal motility. The neurobiological mechanism of ST25 action in IBS rats should be further investigated in the future by combining related techniques, such as pseudorabies virus, optogenetics, calcium imaging, and electrophysiology.

Effect of ketamine, an NMDA-receptor antagonist, on gastric myoelectric activity in experimental pigs

Summary: Introduction: Preclinical studies in experimental pigs are carried out mostly under general anaesthesia. Ketamine is commonly used for induction of anaesthesia. However, there are concerns that ketamine, an NMDA-receptor antagonist, may influence gastric motor function. The aim of this study was to investigate porcine gastric myoelectric activity by means of electrogastrography (EGG). Methods: Seventeen female animals (mean weight 36.2±3.8 kg) were enrolled. Drugs used for induction of anaesthesia were: Group A (n=5): medetomidine 0.1 mg/kg i. m.; butorphanol 0.3 mg/kg i. m.; midazolam 0.3 mg/kg i. m.; Group B (n=6): azaperon 2.2 mg/kg i. m.; Group C (n=6): ketamine 20 mg/kg i. m.; azaperon 2.2 mg/kg i. m., followed in all groups by i.v. 1% propofol (repeated one-mL boluses, 10–12 mL in total). EGG recording started 15 min. after the induction administration and lasted 30 min. Results were evaluated as the dominant frequency of gastric slow waves (DF) and EGG power (areas of amplitudes). Results: In total, 510 one-minute EGG intervals were assessed. DFs were (mean ± standard deviation): 1.4±0.4 (Group A), 1.3±0.3 (Group B) and 0.2±0.1 cycles per min. (Group C). The differences between group C and groups A and B were statistically significant (p&lt;0.001). Median power (IQR) was 0.13 (0.02–0.44; Group A), 0.13 (0.03–0.54; Group B) and 0.30 V2 (0.07–1.44; Group C). The difference between groups A and C was of borderline significance (p=0.066; type 2 error beta 0.295). Conclusions: Ketamine, administered even in a single intramuscular dose, affected myoelectric function of the porcine stomach. Therefore, it should be avoided in gastrointestinal motility studies in experimental pigs. Key words: ketamine – NMDA (N-methyl-D-aspartate) -receptor antagonist – electrogastrography – myoelectrical activity – experimental pigs

The bioelectrical conduction system around the ileocecal junction defined through in vivo high-resolution mapping in rabbits.

Coordinated contractions across the small and large intestines via the ileocecal junction (ICJ) are critical to healthy gastrointestinal function and are in part governed by myoelectrical activity. In this study, the spatiotemporal characteristics of the bioelectrical conduction across the ICJ and its adjacent regions were quantified in anesthetized rabbits. High-resolution mapping was applied from the terminal ileum (TI) to the sacculus rotundus (SR), across the ICJ and into the beginning of the large intestine at the cecum ampulla coli (AC). Orally propagating slow wave patterns in the SR did not entrain the TI. However, aborally propagating patterns from the TI were able to entrain the SR. Bioelectrical activity was recorded within the ICJ and AC, revealing complex interactions of slow waves, spike bursts, and bioelectrical quiescence. This suggests the involvement of myogenic coordination when regulating motility between the small and large intestines. Mean slow wave frequency between regions did not vary significantly (13.74-17.16 cycles/min). Slow waves in the SR propagated with significantly faster speeds (18.51 ± 1.57 mm/s) compared with the TI (14.05 ± 2.53 mm/s, P = 0.0113) and AC (9.56 ± 1.56 mm/s, P = 0.0001). Significantly higher amplitudes were observed in both the TI (0.28 ± 0.13 mV, P = 0.0167) and SR (0.24 ± 0.08 mV, P = 0.0159) within the small intestine compared with the large intestine AC (0.03 ± 0.01 mV). We hypothesize that orally propagating slow waves facilitate a motor-brake pattern in the SR to limit outflow into the ICJ, similar to those previously observed in other gastrointestinal regions.NEW & NOTEWORTHY Competing slow wave pacemakers were observed in the terminal ileum and sacculus rotundus. Prevalent oral propagation in the sacculus rotundus toward the terminal ileum potentially acts as a brake mechanism limiting outflow. Slow waves and periods of quiescence at the ileocecal junction suggest that activation may depend on the coregulatory flow and distention pathways. Slow waves and spike bursts in the cecum impart a role in the coordination of motility.

Frontal grey matter microstructure is associated with sleep slow waves characteristics in late midlife.

The ability to generate slow waves (SW) during non-rapid eye movement (NREM) sleep decreases as early as the 5th decade of life, predominantly over frontal regions. This decrease may concern prominently SW characterized by a fast switch from hyperpolarized to depolarized, or down-to-up, state. Yet, the relationship between these fast and slow switcher SW and cerebral microstructure in ageing is not established. We recorded habitual sleep under EEG in 99 healthy late midlife individuals (mean age = 59.3 ± 5.3 years; 68 women) and extracted SW parameters (density, amplitude, frequency) for all SW as well as according to their switcher type (slow vs. fast). We further used neurite orientation dispersion and density imaging (NODDI) to assess microstructural integrity over a frontal grey matter region of interest (ROI). In statistical models adjusted for age, sex, and sleep duration, we found that a lower SW density, particularly for fast switcher SW, was associated with a reduced orientation dispersion of neurites in the frontal ROI (p = 0.018, R2β* = 0.06). In addition, overall SW frequency was positively associated with neurite density (p = 0.03, R2β* = 0.05). By contrast, we found no significant relationships between SW amplitude and NODDI metrics. Our findings suggest that the complexity of neurite organization contributes specifically to the rate of fast switcher SW occurrence in healthy middle-aged individuals, corroborating slow and fast switcher SW as distinct types of SW. They further suggest that the density of frontal neurites plays a key role for neural synchronization during sleep. EudraCT 2016-001436-35.