脑室注射哌仑西平减弱应激所致颈动脉窦压力感受器反射的重调定

目的探讨中枢胆碱能M_1受体在应激条件下对颈动脉窦压力感受器反射（CSR）的影响。方法健康雄性SD大鼠随机分成非应激组（n=12）和应激组（n=12）,后者接受不可逃避的足底电击,每日2次,每次持续2h。应激1周的SD大鼠,经筛选、麻醉后孤离双侧颈动脉窦区,将不同窦内压（ISP）与其对应的平均动脉压（MAP）值进行Logistic曲线拟合,求得ISP-MAP、ISP-增益（Gain）关系曲线及其特征参数,观察侧脑室微量注射选择性胆碱能M_1受体拮抗剂哌仑西平（PRZ）对CSR的影响。结果侧脑室注射PRZ（1.0 mmol/L,5μl）导致应激大鼠ISP-MAP关系曲线后半程明显下移（P〈0.05）,ISP-Gain关系曲线中部明显上移（P〈0.05）,反射参数中饱和压和最大增益时的窦内压值减少（P〈0.05）,而反射最大Gain加大（P〈0.05）;侧脑室注射相同剂量、容积的PRZ对非应激大鼠CSR的各项指标均无明显影响（P〉0.05）;侧脑室注射PRZ不能使应激的CSR水平恢复到非应激水平（P〈0.05）。结论中枢胆碱能M_1受体参与应激对CSR功能抑制性重调定;除此之外,应激调节中尚有其他神经机制因素的参与。     

Effects of age and cortical infarction on EEG dynamic changes associated with spike wave discharges in F344 rats

Rodent models of absence seizures are used to investigate the network properties and regulatory mechanisms of the seizure's generalized spike and wave discharge (SWD). As rats age, SWDs occur more frequently, suggesting aging-related changes in the regulation of the corticothalamic mechanisms generating the SWD. We hypothesized that brain resetting mechanisms – how the brain “resets” itself to a more normal functional state following a transient period of abnormal function, e.g., a SWD – are impaired in aged animals and that brain infarction would further affect these resetting mechanisms. The main objective of this study was to determine the effects of aging, infarction, and their potential interaction on the resetting of EEG dynamics assessed by quantitative EEG (qEEG) measures of linear (signal energy measured by amplitude variation; signal frequency measured by mean zero-crossings) and nonlinear (signal complexity measured by the pattern match regularity statistic and the short-term maximum Lyapunov exponent) brain EEG dynamics in 4- and 20-month-old F344 rats with and without brain infarction. The main findings of the study were: 1) dynamic resetting of both linear and nonlinear EEG characteristics occurred following SWDs; 2) animal age significantly affected the degree of dynamic resetting in all four qEEG measures: SWDs in older rats exhibited a lower degree of dynamic resetting; 3) infarction significantly affected the degree of dynamic resetting only in terms of EEG signal complexity: SWDs in infarcted rats exhibited a lower degree of dynamic resetting; and 4) in all four qEEG measures, there was no significant interaction effect between age and infarction on dynamic resetting. We conclude that recovery of the brain to its interictal state following SWDs was better in young adult animals compared with aged animals, and to a lesser degree, in age-matched controls compared with infarction-injured animal groups, suggesting possible effects of brain resetting mechanisms and/or the disruption of the epileptogenic network that triggers SWDs.     

Entrainment and coupling of the hamster suprachiasmatic clock by daily dark pulses

The circadian rhythm of locomotor activity of hamsters kept in constant light (LL) can split into two distinct components that, in steady state, lie 180 degrees apart. The splitting phenomenon is the result of antiphase circadian oscillations between left and right sides of the suprachiasmatic nuclei (SCN), the master circadian clock in mammals. In unsplit hamsters housed in LL, a single dark pulse produces a phase-shift of the wheel-running activity rhythm, accompanied by a transient down-regulation of clock gene expression in the SCN. In the present study, we evaluated the effects of daily 1-hr dark pulses on wheel-running activity rhythm and on the expression of clock and nonclock proteins in the SCN of Syrian hamsters exposed to LL conditions. The results show that a daily 1-hr dark pulse entrained the rhythm of wheel-running activity of unsplit hamsters. In addition, in split animals, unimodal coupling of the two locomotor activity components was produced by daily 1-hr dark pulses. In the SCN, the effects of entrainment and unimodal coupling of the two separate components by dark observed in behavior were also evident in the bilateral expression of the proteins c-FOS, p-ERK, PERIOD 1, and calbindin. These results show that the bilaterally asymmetric SCN clock, underlying split circadian behavior, can be recoupled in phase and entrained by short daily dark exposure, indicating the synchronizing potency of darkness on the main circadian clock.     

Effects of inspiratory impedance on the carotid–cardiac baroreflex response in humans

Abstract. We were interested in a therapeutic device designed to increase carotid–cardiac baroreflex sensitivity (BRS) since high BRS is associated with a lower risk for development of hypotension in humans with experimentally–induced central hypovolemia. We hypothesized that spontaneous breathing through an impedance threshold device (ITD) designed to increase negative intrathoracic pressure during inspiration and elevate arterial blood pressure would acutely increase BRS in humans.We tested this hypothesis by measuring heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressures, and carotid-cardiac BRS in 10 female and 10 male subjects breathing through a face mask at three separate ITD conditions: (a) 6 cm H₂O; (b) 12 cm H₂O; and (c) a control (0 cm H₂O). HR was increased (P = 0. 013) from 64 ± 3 bpm during control to 68 ± 3 bpm at 6 cm H₂O ITD and 71 ± 4 bpm at 12 cm H₂O ITD breathing conditions. During ITD breathing, BRS was not altered but responses were shifted to higher arterial pressures. However, SBP and DBP were elevated for both the 6 and 12 cm H₂O conditions compared to the 0 cm H₂O condition, but returned to control (sham) levels by 30 minutes after cessation of ITD breathing. There were no gender effects for BRS or any hemodynamic responses to breathing through the ITD. We conclude that breathing with inspiratory impedance at relatively low pressures can increase baseline arterial blood pressure, i. e., reset the operational point for SBP on the baroreflex stimulus–response relationship, in healthy subjects. This resetting of the cardiac baroreflex may represent a mechanism that allows blood pressure to increase without a reflex–mediated reduction in HR.     

Dynamics of intergestural timing: a perturbation study of lip-larynx coordination

In this study, downward-directed mechanical perturbations were applied to the lower lip during both repetitive (/…pæpæpæ…/) and discrete (/p ’sæpæpl/) utterances in order to examine the perturbation-induced changes of intergestural timing between syllables (i.e., between the bilabial and laryngeal gestures for successive /p/’s) and within phonemes (i.e., between the bilabial and laryngeal gestures within single /p/’s ). Our findings led us to several conclusions. First, steady-state (phase-resetting) analyses of the repetitive utterances indicated both that ”permanent” phase shifts existed for both the lips and the larynx after the system returned to its pre-perturbation rhythm and that smaller steady-state shifts occurred in the relative phasing of these gestures. These results support the hypothesis that central intergestural dynamics can be reset by peripheral articulatory events. Such resetting was strongest when the perturbation was delivered within a ”sensitive phase” of the cycle, during which the downwardly directed lower-lip perturbation opposed the just-initiated, actively controlled bilabial closing gesture for /p/. Although changes in syllable duration were found for other perturbed phases, these changes were simply transient effects and did not indicate a resetting of the central ”clock.” Second, analyses of the transient portions of the perturbed cycles of the repetitive utterances indicated that the perturbation-induced steady-state phase shifts are almost totally attributable to changes occurring during the first two perturbed cycles. Finally, the transient changes in speech timing induced by perturbations in the discrete sequences appeared to share a common dynamical basis with the changes to the repetitive sequences. We conclude by speculating on the type of dynamical system that could generate these temporal patterns.     

Evoked activity and EEG phase resetting in the genesis of auditory Go/NoGo ERPs

Current views of the genesis of the event-related potential (ERP) contrast the phase-reset and evoked activity models. In the former, a portion of the ongoing electroencephalographic (EEG) activity becomes phase-locked at stimulus onset; in the latter, processing in the brain contributes additional time-locked activity at each trial. This study aimed to explore these perspectives in an auditory Go/NoGo task. The interactions between these processes were examined using the amplitudes and topographies of pre- and post-stimulus EEGs in traditional bands, and the averaged ERPs, together with time-frequency analysis. Results indicate that both evoked activity and phase locking of ongoing EEG activity contribute substantially to the different Go and NoGo ERP components. Phase locking contributes most strongly to the early exogenous ERP components, with evoked brain activity related to cognitive processing contributing strongly to the endogenous ERP components. Evidence also suggests that extensive phase realignments may generate the power increases associated with early exogenous components. It is concluded that exogenous ERP components arise substantially from phase-resetting mechanisms involving ongoing EEG activity. In contrast, the endogenous components are substantially produced by evoked activity in various frequency bands, and their differences reflect differential cortical processing required for appropriate responding to the Go vs. NoGo stimuli.     

压力感受反射快速重调定感受器成分与中枢成分的比较

家兔18只,乌拉坦麻醉,切断主动脉神经、迷走神经与一侧窦神经.以健侧颈动脉窦内方波形式保持压刺激(HP)和电刺激同侧窦神经模拟保持压(SN),分别诱导同一窦压力感受反射快速重调定。结果显示,HP 组重调发展的程度与速率皆高于 SN 组。重调发展的时程关系 HP 组近似对数形式;SN 组近似直线形式。HP 组重调的发展对中枢压力感受反射效应无明显影响,SN 组的重调导致压力感受反射机能显著下降.提示压力感受反射中枢成分的重调是整体血压调定点浮动的主导因素。     

Resetting of aortic baroreceptors with non-myelinated afferent fibers in spontaneously hypertensive rats

The phenomenon of resetting and the possible mechanisms responsible for it were investigated in aortic baroreceptors having unmyelinated axons. Recordings were obtained from 31 aortic baroreceptor C-fibers in 20 normotensive Wistar Kyoto rats (WKY) and 37 baroreceptor C-fibers in 11 spontaneously hypertensive rats (SHR). The recordings were obtained from the left aortic nerve of an in vitro aortic nerve-aortic arch preparation. The thresholds for activation of baroreceptor C-fibers were not different between SHR's and WKY's at 16 weeks of age (139±7 and 133±5 mmHg, respectively). However, the thresholds for activation in SHR at 36 weeks of age were considerably higher (163±4 mmHg) indicating resetting of the receptors in the older rats. The pressure-discharge curves were not different between SHR's and WKY's at 16 weeks of age and WKY's at 35 weeks of age, but were shifted to the right for SHR's at 36 weeks of age. The receptors showed greater responses to pulsatile pressures than to steady state pressures at the same mean level of pressure. We found that aortic C-fibers were not reset during the early established phase of hypertension in SHR's because of enhanced receptor strain sensitivity. This is likely to be of importance for tonic vasomotor control at this time. In later stages of hypertension and despite enhanced strain sensitivity the endings were reset to higher pressures probably due to an increased collagen content in the aortic wall.     

Resetting of DDD Pacemakers Due to EMI

Multiprogrammable pacemakers have long been subject to inappropriate reprogramming and electromagnetic interference (EMI). A limited clinical experience with DDD pacing systems precludes the significance of such phenomena in these units. Since August 1981, in a series of 140 DDD systems, certain units demonstrated consistent and reproducible resetting to the back-up modes caused by electrocautery. One unit was permanently reset to the VOO mode. These observations suggest the need for renewed caution at the time of surgery; they also underscore the importance of a thorough understanding of any DDD system and careful follow-up so that such phenomena will not be misinterpreted as pacemaker failure, resulting in erroneous pacemaker removal.