Multiple firing of single muscle vasoconstrictor neurons during cardiac dysrhythmias in human heart failure.

Single vasoconstrictor nerve fibers in humans normally fire only once but have the capacity to fire as many as eight times, per cardiac interval. Our laboratory recently demonstrated that the mean firing frequency of individual vasoconstrictor fibers is more than doubled in the sympathoexcitation associated with congestive heart failure (Macefield VG, Rundqvist B, Sverrisdottir YB, Wallin BG, and Elam M. Circulation 100: 1708--1713, 1999). However, the propensity to fire only once per cardiac interval was retained. In the present retrospective study, we tested the hypothesis that vasoconstrictor fibers fire more than once per cardiac interval in response to transient sympathoexcitatory stimuli, providing one mechanism for further increase of an already augmented sympathetic discharge. Six patients with congestive heart failure (New York Heart Association functional class II--IV; left ventricular ejection range 13--37%, average 22%) were studied at rest and during premature ectopic heartbeats. Analyzed for a total of 60 premature beats, the average firing probability of 10 vasoconstrictor fibers increased from 61 to 80% in the prolonged cardiac interval (i.e., reduced diastolic pressure) after premature beats. The incidence of multiple within-burst firing increased markedly, with two spikes being more common than one. Our results illustrate two different mechanisms (increases in firing probability and multiple within-burst firing), and indirectly indicate a third mechanism (recruitment of previously silent fibers), for acute sympathoexcitatory responses.     

Mechanisms of respiratory sinus arrhythmia in patients with mild heart failure

The high-frequency (HF) component of the heart rate variability (HRV) is regarded as an index of cardiac vagal responsiveness. However, when vagal tone is decreased, nonneural mechanisms could account for a significant proportion of the HF component. To test this hypothesis, we examined the HRV spectral power in 20 patients with mild chronic heart failure (CHF) and 11 controls before and during ganglion blockade with trimethaphan camsylate (3-6 mg/min iv). A small HF component was still present during ganglion blockade, and its amplitude did not differ between CHF patients and controls. The average contribution of nonneural oscillations to the HF component was 15% (range 1-77%) in patients with CHF and 3% (range 0. 7-30%) in healthy controls (P < 0.005). During controlled breathing at 0.16 Hz, however, it decreased to 1% (range 0.2-13%) in healthy controls and 5% (range 1-44%) in CHF patients. Our results indicate that the HF component can significantly overestimate cardiac vagal responsiveness in patients with mild CHF. This bias is improved by controlled breathing, since this maneuver increases the vagal contribution to HF without affecting its nonneural component.     

Atrial natriuretic factor as marker of myocardial compromise in Chagas' disease

This study investigated the evolution of plasma atrial natriuretic factor (ANF) in patients in different stages of Chagas' disease and analyzed its usefulness as prognostic factor of the development of myocardial compromise in asymptomatic chagasic patients. Chagas' disease, a determinant of heart failure, is caused by the parasite Trypanosoma cruzi. A total of 21 chagasic patients were studied: 9 in the asymptomatic stage, 6 with conduction defects (CD), and 6 with chronic heart failure (CHF); and 31 controls: 16 healthy, 6 with CD, and 9 with CHF. Plasma ANF radioimmunoassay (RIA) and complementary studies were performed twice for each patient, with an interval period of 12 months. First sample: chagasic patients showed higher ANF levels in the CHF group than in CD and asymptomatic subjects; second sample: the peptide levels were higher in CHF patients than in the asymptomatic group. In non-chagasic CHF patients, ANF levels were higher than in CD patients and controls in both samples. ANF levels were not able to differentiate chagasic asymptomatic and CD patients from healthy subjects and CD controls; meanwhile, chagasic CHF patients showed lower plasma ANF than their controls. Furthermore, ANF is a sensitive marker capable of detecting gradual impairments in cardiac function in all patients studied.     

Detection of low- and high-frequency rhythms in the variability of skin sympathetic nerve activity

Spectral analysis of skin blood flow has demonstrated low-frequency (LF, 0.03-0.15 Hz) and high-frequency (HF, 0.15-0.40 Hz) oscillations, similar to oscillations in R-R interval, systolic pressure, and muscle sympathetic nerve activity (MSNA). It is not known whether the oscillatory profile of skin blood flow is secondary to oscillations in arterial pressure or to oscillations in skin sympathetic nerve activity (SSNA). MSNA and SSNA differ markedly with regard to control mechanisms and morphology. MSNA contains vasoconstrictor fibers directed to muscle vasculature, closely regulated by baroreceptors. SSNA contains both vasomotor and sudomotor fibers, differentially responding to arousals and thermal stimuli. Nevertheless, MSNA and SSNA share certain common characteristics. We tested the hypothesis that LF and HF oscillatory components are evident in SSNA, similar to the oscillatory components present in MSNA. We studied 18 healthy normal subjects and obtained sequential measurements of MSNA and SSNA from the peroneal nerve during supine rest. Measurements were also obtained of the electrocardiogram, beat-by-beat blood pressure (Finapres), and respiration. Spectral analysis showed LF and HF oscillations in MSNA, coherent with similar oscillations in both R-R interval and systolic pressure. The HF oscillation of MSNA was coherent with respiration. Similarly, LF and HF spectral components were evident in SSNA variability, coherent with corresponding variability components of R-R interval and systolic pressure. HF oscillations of SSNA were coherent with respiration. Thus our data suggest that these oscillations may be fundamental characteristics shared by MSNA and SSNA, possibly reflecting common central mechanisms regulating sympathetic outflows subserving different regions and functions.     

Persistent sympathoexcitation long after submaximal exercise in subjects with and without coronary artery disease

There is an increased risk of cardiac events after exercise, which may, in part, be mediated by the sympathoexcitation that accompanies exercise. The duration and extent of this sympathoexcitation following moderate exercise is unknown, particularly in those with coronary artery disease (CAD). Twenty control subjects (mean age, 51 years) and 89 subjects with CAD (mean age, 58 years) underwent two 16-min bicycle exercise sessions followed by 30-45 min of recovery. Session 1 was performed under physiological conditions to peak workloads of 50-100 W. In session 2, parasympathetic blockade with atropine (0.04 mg/kg) was achieved at end exercise at the same workload as session 1. RR interval was continually recorded, and plasma catecholamines were measured at rest and selected times during exercise and recovery. Parasympathetic effect, measured as the difference in RR interval with and without atropine, did not differ between controls and CAD subjects in recovery. At 30 and 45 min of recovery, RR intervals were 12% and 9%, respectively, shorter than at rest. At 30 and 45 min of recovery, plasma norepinephrine levels were 15% and 12%, respectively, higher than at rest. A brief period of moderate exercise is associated with a prolonged period of sympathoexcitation extending >45 min into recovery and is quantitatively similar among control subjects and subjects with CAD, with or without left ventricular dysfunction. Parasympathetic reactivation occurs early after exercise and is also surprisingly quantitatively similar in controls and subjects with CAD. The role of these autonomic changes in precipitating cardiac events requires further evaluation.     

5,7-双羟色胺损毁大鼠中缝背核后底丘脑核的神经活动增强

采用玻璃微电极在体细胞外记录法,观察了5,7-双羟色胺(5,7-dihydroxytryptamine,5,7-DHT)损毁大鼠中缝背核(dorsalraphenucleus,DRN)后,底丘脑核(subthalamicnucleus,STN)神经元电活动的变化。结果发现,对照组和DRN损毁组大鼠STN神经元的放电频率分别是(6.93±6.55)Hz和(11.27±9.31)Hz,DRN损毁组大鼠的放电频率显著高于对照组(P<0.01)。在对照组大鼠,13%的神经元呈现规则放电,46%为不规则放电,41%为爆发式放电;而在DRN损毁组大鼠,具有规则、不规则和爆发式放电的神经元比例分别为9%、14%和77%,爆发式放电的STN神经元比例明显高于对照组(P<0.01)。结果显示,DRN损毁后大鼠STN神经元的放电频率增高,爆发式放电增多,提示在正常大鼠DRN抑制STN神经元的活动。     

血浆B型脑钠肽对心力衰竭和呼吸困难的诊断价值

目的：探讨血浆脑钠肽（BNP）水平在心力衰竭（CHF）T和呼吸困难诊断中的应用。方法：采用免疫荧光快速测试法测定56例已确诊心衰患者、40例心源性呼吸困难患者、29例肺源性呼吸困难患者和30例健康人血浆BNP的含量。结果：心衰组患者血浆BNP水平明显高于对照组,差异显著（P〈0．01）;心源性呼吸困难组患者的BNP值水平（1032．2±879．8pg／ml）与肺源性呼吸困难组患者的BNP值水平（67．1±43．6pg／ml）比较有显著性差异（P〈0．01）。结论：检测BNP水平可为临床诊断CHF及心源性与肺源性呼吸困难的鉴别诊断提供重要依据。     

Leydig neuron activity modulates heartbeat in the medicinal leech

1. Leydig neurons fire spontaneously at low rates (less than 4 Hz), but their activity increases with mechanical stimulation or electrical stimulation of mechanosensory neurons. These conditions also cause acceleration of bursting in heart motor neurons. 2. The firing rate of Leydig cells was found to regulate heart rate in chains of isolated ganglia. When Leydig neurons were made to fire action potentials at relatively high frequencies (ca. 5-10 Hz), however, heart motor neurons ceased bursting and were either silenced or fired erratically. 3. Firing of Leydig neurons at high rates caused bilateral heart interneurons of ganglia 3 or 4 to fire tonically rather than in their normal alternating bursts Tonic firing of these heart interneurons accounts for the prolonged barrages of ipsps recorded in heart motor neurons and the disruption of their normal cyclic activity. 4. Preventing spontaneous activity of Leydig neurons with injected currents in isolated ganglia caused deceleration of the heartbeat rhythm but did not halt oscillation. 5. Electrical stimulation of peripheral nerve roots with Leydig neuron activity suppressed in isolated ganglia caused acceleration of heart rate.     

Combined NO and PG inhibition augments alpha-adrenergic vasoconstriction in contracting human skeletal muscle

Sympathetic alpha-adrenergic vasoconstrictor responses are blunted in the vascular beds of contracting muscle (functional sympatholysis). We tested the hypothesis that combined inhibition of nitric oxide (NO) and prostaglandins (PGs) restores sympathetic vasoconstriction in contracting human muscle. We measured forearm blood flow via Doppler ultrasound and calculated the reduction in forearm vascular conductance in response to alpha-adrenergic receptor stimulation during rhythmic handgrip exercise (6.4 kg) and during a control nonexercise vasodilator condition (using intra-arterial adenosine) before and after combined local inhibition of NO synthase (NOS; via N(G)-nitro-L-arginine methyl ester) and cyclooxygenase (via ketorolac) in healthy men. Before combined inhibition of NO and PGs, the forearm vasoconstrictor responses to intra-arterial tyramine (which evoked endogenous noradrenaline release), phenylephrine (a selective alpha1-agonist), and clonidine (an alpha2-agonist) were significantly blunted during exercise compared with adenosine treatment. After combined inhibition of NO and PGs, the vasoconstrictor responses to all alpha-adrenergic receptor stimuli were augmented by approximately 10% in contracting muscle (P <0.05), whereas the responses to phenylephrine and clonidine were also augmented by approximately 10% during passive vasodilation in resting muscle (P <0.05). In six additional subjects, PG inhibition alone did not alter the vasoconstrictor responses in resting or contracting muscles. Thus in light of our previous findings, it appears that inhibition of either NO or PGs alone does not affect functional sympatholysis in healthy humans. However, the results from the present study indicate that combined inhibition of NO and PGs augments alpha-adrenergic vasoconstriction in contracting muscle but does not completely restore the vasoconstrictor responses compared with those observed during passive vasodilation in resting muscle.     

Ripple-associated high-firing interneurons in the hippocampal CA1 region

By simultaneously recording the activity of individual neurons and field potentials in freely behaving mice, we found two types of interneurons firing at high frequency in the hippocampal CA1 region, which had high correlations with characteristic sharp wave-associated ripple oscillations (100–250 Hz) during slow-wave sleep. The firing of these two types of interneurons highly synchronized with ripple oscillations during slow-wave sleep, with strongly increased firing rates corresponding to individual ripple episodes. Interneuron type I had at most one spike in each sub-ripple cycle of ripple episodes and the peak firing rate was 310±33.17 Hz. Interneuron type II had one or two spikes in each sub-ripple cycle and the peak firing rate was 410±47.61 Hz. During active exploration, their firing was phase locked to theta oscillations with the highest probability at the trough of theta wave. Both two types of interneurons increased transiently their firing rates responding to the startling shake stimuli. The results showed that these two types of high-frequency interneurons in the hippocampal CA1 region were involved in the modulation of the hippocampal neural network during different states.     

ANG II in the paraventricular nucleus potentiates the cardiac sympathetic afferent reflex in rats with heart failure.

Chronic heart failure (CHF) is characterized by sympathoexcitation, and the cardiac sympathetic afferent reflex (CSAR) is a sympathoexcitatory reflex. Our previous studies have shown that the CSAR was enhanced in CHF. In addition, central angiotensin II (ANG II) is an important modulator of this reflex. This study was performed to determine whether the CSAR evoked by stimulation of cardiac sympathetic afferent nerves (CSAN) in rats with coronary ligation-induced CHF is enhanced by ANG II in the paraventricular nucleus (PVN). Under alpha-chloralose and urethane anesthesia, renal sympathetic nerve activity (RSNA) was recorded. The RSNA responses to electrical stimulation (5, 10, 20, and 30 Hz) of the CSAN were evaluated. Bilateral microinjection of the AT1-receptor antagonist losartan (50 nmol) into the PVN had no significant effects in the sham group, but it abolished the enhanced RSNA response to stimulation in the CHF group. Unilateral microinjection of three doses of ANG II (0.03, 0.3, and 3 nmol) into the PVN resulted in dose-related increases in the RSNA responses to stimulation. Although ANG II also potentiated the RSNA response to electrical stimulation in sham rats, the RSNA responses to stimulation after ANG II into the PVN in rats with CHF were much greater than in sham rats. The effects of ANG II were prevented by pretreatment with losartan into the PVN in CHF rats. These results suggest that the central gain of the CSAR is enhanced in rats with coronary ligation-induced CHF and that ANG II in the PVN augments the CSAR evoked by CSAN, which is mediated by the central angiotensin AT1 receptors in rats with CHF.     

Impaired central hemodynamic response and exaggerated vasoconstriction during muscle metaboreflex activation in heart failure patients

The muscle metaboreflex is enhanced in chronic heart failure (CHF) patients, and this fact has been associated with the early fatigue shown by these patients in response to exercise. In animal studies of CHF, it was found that the limited capacity to enhance ventricular performance is responsible for a functional shift from a cardiac output to a systemic vascular resistance (SVR) increase in the mechanism by which the cardiovascular system raises blood pressure in response to the metaboreflex. However, the existence of this functional shift is still unknown in humans. The present study was undertaken to test the hypothesis that a similar hemodynamic response was also present in humans with CHF. The hemodynamic response to metaboreflex activation obtained through postexercise ischemia was assessed in nine patients with CHF and nine healthy controls (CTL) by means of impedance cardiography. The main results were that 1) the blood pressure rise due to the metaboreflex was similar in the two groups; 2) the CTL group achieved the blood pressure response via cardiac output increase, and the CHF group, via SVR increase; and 3) stroke volume was enhanced in the CTL group and decreased in the CHF group. This study demonstrates that in CHF patients, metaboreflex recruitment causes a functional shift from flow increase to peripheral vasoconstriction in the mechanism through which blood pressure is increased. The incapacity to enhance cardiac performance and stroke volume is probably the primary cause of this cardiovascular alteration.     

Calcium signal-dependent plasticity of neuronal excitability developed postnatally

Neuronal plasticity and its development were investigated at pyramidal neurons in the cortical slices of rats. The threshold and probability of firing spikes were measured by using whole-cell recording to assess neuronal excitability. Postsynaptic high frequency activity (HFA) at the pyramidal neurons, evoked by 20 trains (250-ms interval) of five depolarization-pulses (1 ms) at 100 Hz, persistently lowered the threshold and increased the probability of firing spikes. After long-term enhancement of neuronal excitability by HFA was stable, another HFA induced further enhancement. Infusing 1 mM 1,2-bis(2-aminophenoxy)-ethane-N, N,N',N'-tetraacetic acid or 100 microM CaMKII(281-301) into the recording neurons prevented HFA-induced long-term enhancement of neuronal excitability. The infusion of 40 microM calcineurin autoinhibitory peptide enhanced neuronal excitability, which occluded HFA effect. HFA-induced long-term enhancement of intrinsic excitability expressed at most pyramidal neurons after postnatal day (PND) 14, but not at those before PND 9. Our results show a new type of neuronal plasticity induced by physiological activity at cortical neurons, which requires calcium-dependent protein phosphorylation and develops during postnatal period. An upregulation of intrinsic excitability at cortical neurons facilitates their activity and broadens signal codes; consequently, their computational ability is upgraded.     

Determinants of heart rate variability in obstructive sleep apnea syndrome during wakefulness and sleep

Heart rate variability (HRV) is mediated by at least three primary mechanisms: 1) vagal feedback from pulmonary stretch receptors (PSR), 2) central medullary coupling between respiratory and cardiovagal neurons (RCC), and 3) arterial baroreflex (ABR)-induced fluctuations. We employed a noninvasive experimental protocol in conjunction with a minimal model to determine how these sources of HRV are altered in obstructive sleep apnea syndrome (OSAS). Respiration, heart rate, and blood pressure were monitored in eight normal subjects and nine untreated OSAS patients in relaxed wakefulness and stage 2 and rapid eye movement sleep. A computer-controlled ventilator delivered inspiratory pressures that varied randomly from breath to breath. Application of the model to the corresponding subject responses allowed the delineation of the three components of HRV. In all states, RCC gain was lower in OSAS patients than in normal subjects (P < 0.04). ABR gain was also reduced in OSAS patients (P < 0.03). RCC and ABR gains increased from wakefulness to sleep (P < 0.04). However, there was no difference in PSR gain between subject groups or across states. The findings of this study suggest that the adverse autonomic effects of OSAS include impairment of baroreflex gain and central respiratory-cardiovascular coupling, but the component of respiratory sinus arrhythmia that is mediated by lung vagal feedback remains intact.     

Hill muscle model errors during movement are greatest within the physiologically relevant range of motor unit firing rates

This study evaluated the accuracy of Hill-type muscle models during movement. Hill-type models are ubiquitous in biomechanical simulations. They are attractive because of their computational simplicity and close relation to commonly measured experimental variables, but there have been surprisingly few experimental validations of these models during functionally relevant conditions. Our hypothesis was that model errors during movement are largest at the low motor unit firing rates most relevant to normal movement conditions. This hypothesis was evaluated in the cat soleus muscle activated either by electrical stimulation at physiological rates or via the crossed-extension reflex (CXR) thereby obtaining normal patterns of motor unit recruitment and rate modulation. These activation paradigms were applied during continuous movements approximately matched to locomotor length changes. The resulting muscle force was modeled using a common Hill model incorporating independent activation, tetanic length-tension and tetanic force-velocity properties. Errors for this model were greatest for stimulation rates between approximately 10-20Hz. Errors were especially large for muscles activated via the CXR, where most motor units appear to fire within this range. For large muscle excursions, such as those seen during normal locomotion, the errors for naturally activated muscle typically exceeded 50%, supporting our hypothesis and indicating that the Hill model is not appropriate for these conditions. Subsequent analysis suggested that model errors were due to the common Hill model's inability to account for the coupling between muscle activation and force-velocity properties that is most prevalent at the low motor unit firing rates relevant to normal activation.     

The effects of inspiratory intrathoracic pressure production on the cardiovascular response to submaximal exercise in health and chronic heart failure

We sought to determine whether the normal inspiratory intrathoracic pressures (P(ITP)) produced during exercise contribute to the blunted cardiac output and locomotor limb blood flow responses observed in chronic heart failure (CHF). Five chronically instrumented dogs exercised on a treadmill at 2.5 mile/h at 5% grade while healthy or after the induction of tachycardia-induced CHF. We observed several key differences in the cardiovascular responses to changes in the inspiratory P(ITP) excursion between health and CHF; namely, 1) removing approximately 70% of the normally produced inspiratory P(ITP) excursion during exercise (with 15 cmH(2)O inspiratory positive pressure ventilation) significantly reduced stroke volume (SV) in healthy animals by 5 +/- 2% (P < 0.05) but significantly increased SV and cardiac output (Q(TOT)) in animals with CHF by 5 +/- 1% (P < 0.05); 2) doubling the magnitude of the inspiratory P(ITP) excursion had no effect on SV or Q(TOT) in healthy animals but significantly reduced steady-state Q(TOT) and SV in animals with CHF by -4 +/- 3% and -10 +/- 3%, respectively; 3) removing the majority of the normally produced inspiratory P(ITP) excursion had no effect on blood flow distribution in healthy animals but increased hindlimb blood flow (9 +/- 3%, P < 0.05) out of proportion to the increases in Q(TOT); and 4) the only similarity between healthy and CHF animals was that increasing the inspiratory P(ITP) excursion significantly reduced steady-state locomotor limb blood flow by 5 +/- 2% and 6 +/- 3%, respectively (P < 0.05 for both). We conclude that 1) the normally produced inspiratory P(ITP) excursions are required for a maximal SV response to submaximal exercise in healthy animals but detrimental to the SV and Q(TOT) responses to submaximal exercise in CHF, 2) the respiratory muscle ergoreflex tonically restrains locomotor limb blood flow during submaximal exercise in CHF, and 3) excessive inspiratory muscle work further compromises cardiac function and blood flow distribution in both health and CHF.     

Spectral characteristics of skin sympathetic nerve activity in heat-stressed humans

Skin sympathetic nerve activity (SSNA) exhibits low- and high-frequency spectral components in normothermic subjects. However, spectral characteristics of SSNA in heat-stressed subjects are unknown. Because the main components of the integrated SSNA during heat stress (sudomotor/vasodilator activities) are different from those during normothermia and cooling (vasoconstrictor activity), we hypothesize that spectral characteristics of SSNA in heat-stressed subjects will be different from those in subjects subjected to normothermia or cooling. In 17 healthy subjects, SSNA, electrocardiogram, arterial blood pressure (via Finapres), respiratory activity, and skin blood flow were recorded during normothermia and heat stress. In 7 of the 17 subjects, these variables were also recorded during cooling. Spectral characteristics of integrated SSNA, R-R interval, beat-by-beat mean blood pressure, skin blood flow variability, and respiratory excursions were assessed. Heat stress and cooling significantly increased total SSNA. SSNA spectral power in the low-frequency (0.03-0.15 Hz), high-frequency (0.15-0.45 Hz), and very-high-frequency (0.45-2.5 Hz) regions was significantly elevated by heat stress and cooling. Interestingly, heat stress caused a greater relative increase of SSNA spectral power within the 0.45- to 2.5-Hz region than in the other spectral ranges; cooling did not show this effect. Differences in the SSNA spectral distribution between normothermia/cooling and heat stress may reflect different characteristics of central modulation of vasoconstrictor and sudomotor/vasodilator activities.     

Pharmacological characterization of ionic currents that regulate high-frequency spontaneous activity of electromotor neurons in the weakly electric fish, Apteronotus leptorhynchus

The neural circuit that controls the electric organ discharge (EOD) of the brown ghost knifefish (Apteronotus leptorhynchus) contains two spontaneous oscillators. Both pacemaker neurons in the medulla and electromotor neurons (EMNs) in the spinal cord fire spontaneously at frequencies of 500-1,000 Hz to control the EOD. These neurons continue to fire in vitro at frequencies that are highly correlated with in vivo EOD frequency. Previous studies used channel blocking drugs to pharmacologically characterize ionic currents that control high-frequency firing in pacemaker neurons. The goal of the present study was to use similar techniques to investigate ionic currents in EMNs, the other type of spontaneously active neuron in the electromotor circuit. As in pacemaker neurons, high-frequency firing of EMNs was regulated primarily by tetrodotoxin-sensitive sodium currents and by potassium currents that were sensitive to 4-aminopyridine and kappaA-conotoxin SIVA, but resistant to tetraethylammonium. EMNs, however, differed from pacemaker neurons in their sensitivity to some channel blocking drugs. Alpha-dendrotoxin, which blocks a subset of Kv1 potassium channels, increased firing rates in EMNs, but not pacemaker neurons; and the sodium channel blocker muO-conotoxin MrVIA, which reduced firing rates of pacemaker neurons, had no effect on EMNs. These results suggest that similar, but not identical, ionic currents regulate high-frequency firing in EMNs and pacemaker neurons. The differences in the ionic currents expressed in pacemaker neurons and EMNs might be related to differences in the morphology, connectivity, or function of these two cell types.     

Analysis of motor unit firing characteristics in patients with motor neuron diseases

This study was designed to evaluate firing rate variability in patients with upper/lower motor neuron disorders. Twenty healthy subjects and 19 patients with motor neuron disorders participated in the study. Consecutive motor unit action potential pairs from extensor digitorum communis (EDC) muscle were recorded from each subject with trigger-delay line mode. Patients with motor neuron disorders (17.7?±?10.8?ms) showed significantly higher mean time variability of interpotential interval value than healthy volunteers (10.3?±?0.1?ms) (p?相似文献   

Ripple-associated high-firing interneurons in the hippocampal CA1 region

By simultaneously recording the activity of individual neurons and field potentials in freely behaving mice, we found two types of interneurons firing at high frequency in the hippocampal CA1 region, which had high correlations with characteristic sharp wave-associated ripple oscillations (100―250 Hz) during slow-wave sleep. The firing of these two types of interneurons highly synchronized with ripple oscillations during slow-wave sleep, with strongly increased firing rates corresponding to individual ripple episodes. Interneuron type I had at most one spike in each sub-ripple cycle of ripple episodes and the peak firing rate was 310±33.17 Hz. Interneuron type II had one or two spikes in each sub-ripple cycle and the peak firing rate was 410±47.61 Hz. During active exploration, their firing was phase locked to theta oscillations with the highest probability at the trough of theta wave. Both two types of interneurons increased transiently their firing rates responding to the startling shake stimuli. The results showed that these two types of high-frequency interneurons in the hippocampal CA1 region were involved in the modulation of the hippocampal neural network during different states.