Transient Increase In Amplitude Research Articles

Passivity Breakdown and Crack Propagation Mechanisms of Lean Duplex (UNS S32001) Stainless Steel Reinforcement in High Alkaline Solution Under Stress Corrosion Cracking

The passivity breakdown and subsequent stress corrosion cracking (SCC) of Type 2001 lean duplex stainless steel (UNS S32001) reinforcement were investigated in a highly alkaline environment containing chlorides at a low temperature. Electrochemical analysis and mechanical testing were utilized to characterize the passive film development. Fractographic analysis was performed, correlating microstructure and corrosion performance, to reveal preferential crack paths. A chloride threshold below 4 wt% Cl− for a high alkaline environment was elucidated, with pitting susceptibility factor values close to unity, having a threshold critical areal cation vacancy concentration for passivity breakdown close to the 1013 cm−2. Pit initiation leading to passivity breakdown and crack nucleation in 4 wt% Cl− was triggered for stresses above σy, developing a low-frequency peak (0.1 Hz to 0.01 Hz) of the cracking process. Current peak deconvolution demonstrated passivity breakdown was triggered by the intensification in the rate of Type II transient and exposure time, while an increase in transient amplitude was related to the crack propagation. The α phase served as a nucleation site for pits, whose propagation was arrested at the γ phase. Predominant intergranular-SCC morphology through the α/γ interface was developed following anodic dissolution given the more active nature of the α phase (most active path); minor transgranular-SCC propagated through γ phase when high-stress concentration was reached, corresponding to slip-step dissolution.

Temperature dependence of single-event transients in SiGe heterojunction bipolar transistors for cryogenic applications

We experimentally demonstrate that the dominant mechanism of single-event transients in silicon-germanium heterojunction bipolar transistors (SiGe HBTs) can change with decreasing temperature from +20 °C to −180 °C. This is accomplished by using a new well-designed cryogenic experimental system suitable for a pulsed-laser platform. Firstly, when the temperature drops from +20 °C to −140 °C, the increased carrier mobility drives a slight increase in transient amplitude. However, as the temperature decreases further below −140 °C, the carrier freeze-out brings about an inflection point, which means the transient amplitude will decrease at cryogenic temperatures. To better understand this result, we analytically calculate the ionization rates of various dopants at different temperatures based on Altermatt’s new incomplete ionization model. The parasitic resistivities with temperature on the charge-collection pathway are extracted by a two-dimensional (2D) TCAD process simulation. In addition, we investigate the impact of temperature on the novel electron-injection process from emitter to base under different bias conditions. The increase of the emitter–base junction’s barrier height at low temperatures could suppress this electron-injection phenomenon. We have also optimized the built-in voltage equations of a high current compact model (HICUM) by introducing the impact of incomplete ionization. The present results and methods could provide a new reference for effective evaluation of single-event effects in bipolar transistors and circuits at cryogenic temperatures, and could provide a new evidence of the potential of SiGe technology in applications in extreme cryogenic environments.

Distractor-induced deafness: The effect of multiple auditory distractors on conscious target processing

Conscious access to a target stimulus embedded in a rapid serial visual presentation can be impaired by the preceding presentation of multiple task-irrelevant distractors. While this phenomenon – labeled distractor-induced blindness (DIB) – is established in vision, it is unknown whether a similar effect can be observed in the auditory modality. Considering the differences in the processing of visual and auditory stimuli, modality-specific effects in the inhibitory mechanisms triggered by distractors can be expected. First, we aimed to find evidence for a distractor-induced deafness (DID) for auditory targets in a behavioral experiment. The target was defined by a transient increase in amplitude in a continuous sinusoidal tone, which was to be detected if accompanied or preceded by a deviant tone (cue). Both events were embedded in separate streams in a binaural rapid serial auditory presentation. Distractors preceded the cue and shared the target's features. As previously observed for DIB, a failure to detect the auditory target critically relied on the presentation of multiple distractor episodes. This DID effect was followed up in a subsequent event-related brain potentials (ERP) study to identify the signature of target detection. In contrast to missed targets, hits were characterized by a larger frontal negativity and by a more pronounced centro-parietal P3b wave. Whereas the latter process was also observed in the visual domain, indicating a post-perceptual updating process, the frontal negativity was exclusively observed for auditory DID. This modality-specific process might signal that early attentional control processes support conscious access to relevant auditory events.

P1-20. Respiratory changes after lesions of the medullary raphe nuclei

It is known that respiratory movements change after chemical or electrical stimulation of the midline regions of the brain stem, including raphe obscurus, raphe pallidus and raphe magnus. We previously reported that neurons located in these regions had respiratory-related activity and a part of the neurons projected to the phrenic nuclei, suggesting the midline regions are involved in the control of respiration. However, it is unclear whether or not these neurons play a crucial role in respiration. To elucidate the role, we tested effects of chemical lesions of the medullary raphe nuclei on respiration using spontaneously breathing Sprague–Dawley rats which were anesthetized with pentobarbital sodium. Local injection of kainic acid into the medullary midline induced a transient increase in amplitude and frequency of diaphragm activities, and the frequency subsequently decreased. Then, apnea was elicited 20 min after the injection. Injection sites were located 1.5–3.0 mm rostral to the obex. The results suggest that the caudal medullary raphe nuclei may participate in the control of respiratory movements in rats.

Antecedent occipital alpha band activity predicts the impact of oculomotor events in perceptual switching.

Oculomotor events such as blinks and saccades transiently interrupt the visual input and, even though this mostly goes undetected, these brief interruptions could still influence the percept. In particular, both blinking and saccades facilitate switching in ambiguous figures such as the Necker cube. To investigate the neural state antecedent to these oculomotor events during the perception of an ambiguous figure, we measured the human scalp electroencephalogram (EEG). When blinking led to perceptual switching, antecedent occipital alpha band activity exhibited a transient increase in amplitude. When a saccade led to switching, a series of transient increases and decreases in amplitude was observed in the antecedent occipital alpha band activity. Our results suggest that the state of occipital alpha band activity predicts the impact of oculomotor events on the percept.

The neuromagnetic response to spoken sentences: Co-modulation of theta band amplitude and phase

Speech elicits a phase-locked response in the auditory cortex that is dominated by theta (3–7Hz) frequencies when observed via magnetoencephalography (MEG). This phase-locked response is potentially explained as new phase-locked activity superimposed on the ongoing theta oscillation or, alternatively, as phase-resetting of the ongoing oscillation. The conventional method used to distinguish between the two hypotheses is the comparison of post- to prestimulus amplitude for the phase-locked frequency across a set of trials. In theory, increased amplitude indicates the presence of additive activity, while unchanged amplitude points to phase-resetting. However, this interpretation may not be valid if the amplitude of ongoing background activity also changes following the stimulus. In this study, we employ a new approach that circumvents this problem. Specifically, we utilize a fine-grained time–frequency analysis of MEG channel data to examine the co-modulation of amplitude change and phase coherence in the post-stimulus theta-band response. If the phase-locked response is attributable solely to phase-resetting of the ongoing theta oscillation, then amplitude and phase coherence should be uncorrelated. In contrast, additive activity should produce a positive correlation. We find significant positive correlation not only during the onset response but also throughout the response period. In fact, transient increases in phase coherence are accompanied by transient increases in amplitude in accordance with a “signal plus background” model of the evoked response. The results support the hypothesis that the theta-band phase-locked response to attended speech observed using MEG is dominated by additive phase-locked activity.

Imperatoxin Induces a Biphasic Response in Ca2+ Sparks

Imperatoxin induces a biphasic response in Ca2+ sparksImperatoxin A (IpTxa), isolated from the venom of the African scorpion Pandinus imperator, has been shown to specifically activate ryanodine receptors (RyR) and to be capable of translocating across cell membranes. IpTxa enhances [3H]ryanodine binding to sarcoplasmic reticulum (SR) and stabilizes subconducting states in single channels. We previously demonstrated that IpTxa alters the amplitude of calcium transients in intact field-stimulated cells, causing a rapid increase in transient amplitude. This is followed by a gradual decrement in amplitude to a new steady state at lower amplitude than in control. The current study seeks to clarify how IpTxa acts on RyRs to perturb Ca2+ handling in cardiomyocytes. We employed visualization of IpTxa-modified Ca2+ sparks in saponin-permeabilized cells to facilitate direct titration of RyRs with known concentrations of IpTxa, ranging from 500pM to 50nM. In addition, we modified our sparks protocol to enable a comparison of the caffeine-releasable SR Ca2+ load before and after treatment with the toxin. Our results demonstrate that IpTxa induces a biphasic RyR response, typified by a transient increase in spark frequency, amplitude, FWHM, and FDHM, which is rapidly followed by a sharp decrease in the same parameters. Comparison of pre- and post-toxin caffeine-releasable SR Ca2+ consistently reveals that SR content has been reduced as a result of IpTxa perfusion to approximately 75% of control. These results are consistent with the biphasic response observed in Ca2+ transient experiments. We believe that IpTxa sensitizes RyR to luminal Ca2+, leading to increased Ca2+ release and subsequent depletion of Ca2+ from the SR. Our findings have exciting implications for translational research into cardiac diseases such as catecholaminergic polymorphic ventricular tachycardia, in which acute RyR hyperactivity is hypothesized to trigger arrhythmias leading to sudden cardiac death.

Experience‐dependent increase in spine calcium evoked by backpropagating action potentials in layer 2/3 pyramidal neurons in rat somatosensory cortex

In spines on basal dendrites of layer 2/3 pyramidal neurons in somatosensory barrel cortex, calcium transients evoked by back-propagating action potentials (bAPs) were investigated (i) along the length of the basal dendrite, (ii) with postnatal development and (iii) with sensory deprivation during postnatal development. Layer 2/3 pyramidal neurons were investigated at three different ages. At all ages [postnatal day (P)8, P14, P21] the bAP-evoked calcium transient amplitude increased with distance from the soma with a peak at around 50 microm, followed by a gradual decline in amplitude. The effect of sensory deprivation on the bAP-evoked calcium was investigated using two different protocols. When all whiskers on one side of the rat snout were trimmed daily from P8 to P20-24 there was no difference in the bAP-evoked calcium transient between cells in the contralateral hemisphere, lacking sensory input from the whisker, and cells in the ipsilateral barrel cortex, with intact whisker activation. When, however, only the D-row whiskers on one side were trimmed the distribution of bAP-evoked calcium transients in spines was shifted towards larger amplitudes in cells located in the deprived D-column. In conclusion, (i) the bAP-evoked calcium transient gradient along the dendrite length is established at P8, (ii) the calcium transient increases in amplitude with age and (iii) this increase is enhanced in layer 2/3 pyramidal neurons located in a sensory-deprived barrel column that is bordered by non-deprived barrel columns.

Cholinergic short-term conditioning and activation of ATP-sensitive K+ current in cat atrial myocytes.

In atrial myocytes, an initial exposure to acetylcholine (ACh1) exerts a short-term conditioning effect such that a second ACh exposure (ACh2) activates ATP-sensitive K+ current (IK,ATP). The purpose of the present study was to determine the mechanism underlying the short-term conditioning induced by ACh that results in subsequent ACh-induced activation of IK.ATP. Cat atrial myocytes were studied using a nystatin-perforated patch whole cell recording method. Changes in L-type Ca2+ current (ICa,L) amplitude were used as an index of relative changes in cyclic AMP (cAMP). The results show that when atrial myocytes are treated with two consecutive exposures to 10 microM ACh separated by a recovery interval, ACh2 activates a larger increase in potassium conductance (gK+) than ACh1. The additional ACh2-induced increase in gK+ is selectively blocked by 10 microM glibenclamide, identifying the current as IK,ATP. Moreover, ICa,L activated immediately after the withdrawal of ACh1 exhibited a transient increase in amplitude above control (+ 76%), consistent with rebound stimulation of cAMP. Rp-cAMPs (50 microM), a selective antagonist of cAMP-dependent protein kinase A, blocked the rebound stimulation of ICa,L and abolished ACh2-induced activation of IK,ATP. Thapsigargin (5 microM), an inhibitor of Ca2+ ATPase in the sarcoplasmic reticulum (SR), abolished ACh2-induced activation of IK,ATP without decreasing rebound stimulation of ICa,L. Rebound stimulation of ICa,L and ACh2-induced activation of IK,ATP both varied as a function of ACh1 duration. We conclude that withdrawal of an initial ACh exposure elicits a rebound cAMP-mediated stimulation of SR Ca2+ uptake. This mechanism induces a short-term conditioning in atrial myocytes such that a subsequent ACh exposure activates IK,ATP. The present results demonstrate novel cholinergic signaling mechanisms in the regulation of IK,ATP.

Roles of cerebral perfusion pressure and neurotransmitters in changes of evoked potentials induced by hypoxia

AIM: We studied the effects of hypoxia on excitability of the brain with evoked potentials and membrane transmitter release. METHODS: Dogs were anesthetized with pentobarbital sodium and artificially ventilated. (1) In a hypoxia group, somatosensory evoked potential (SEP) and auditory brain-stem response (ABR) were measured to study the brain behavior in response to sensory input during hypoxia. Electric stimulation for SEP and acoustic stimulation for ABR were generated in a fixed sequence, i.e., once for SEP and 4 times for ABR, and one ensemble of SEP data and 4 ensembles of ABR data were stored for 500 msec. We averaged 20 ensembles of SEP data and 80 ensembles of ABR data every 10 seconds. After room air ventilation (control period), dogs were exposed to a 5%O2-95%N 2 gaseous mixture for 5 min (hypoxic period) and returned to room air (recovery period). ABR and SEP (EPs) were monitored throughout the periods. (2) In a barostat group, systemic arterial pressure was clamped at 120 mmHg to artificially stabilize cerebral peffusion pressure (CPP), because the hydrodynamics influence edema spreading and tissue impedance. Other procedures were the same as used in the hypoxia group. (3) In an/n vivo voltammetry (IW) group, neurotransmitter metabolitcs were measured throughout the control, hypoxic and recovery periods. RESULTS: In the hypoxia group, amplitude of EPs showed transient increase in response to hypoxia, accompanied by an increase in CPP. This phenomenon preceded a decrease in amplitude. In the barostat group, the amplitude also increased during the hypoxic period, though CPP was maintained at the same level as the control period. This finding suggests that the volume conductor properties are not involved in the transient increase in amplitude of EPs in response to hypoxia. In the IVV group, 5-HIAA transiently increased in response to hypoxia, in the same fashion with the change of EPs. DISCUSSION: The transient increase of neurotransmitter metabolite might be a reflection of enhanced transmitter release associated with a transient increase in membrane excitability. In conclusion, hypoxia transiently enhances membrane excitability, and results in transient increases of amplitude of EPs and neurotransmitter metabolite.

High-rate sequential sampling of auditory brain-stem and somatosensory evoked responses in hypoxia

We developed a high-rate sequential recording technique that allowed simultaneous measurements of both auditory brain-stem response (ABR) and somatosensory evoked potential (SEP) every 10 sec. Using this method, a transient increase in amplitude of all the ABR and SEP components in response to hypoxia in dogs could be detected. The increase in amplitude preceded the prolongation of latency. Our study showed that there were succesive changes of evoked potentials in response to hypoxia. A transient increase in amplitude is the first to occur, followed by a latency prolongation and an amplitude decrease for both ABRs and SEPs.

5-Hydroxytryptamine increases excitability of CA1 hippocampal pyramidal cells.

In the presence of spiperone to block the 5-HT1A-mediated inhibition of pyramidal cell activity, 5-hydroxytryptamine (serotonin, 5-HT) produces a rapid transient increase in amplitude of the extracellularly recorded population spike from area CA1 of the hippocampus. Intracellular recording techniques in area CA1 of rat hippocampal slices were used to identify the ionic mechanism and to characterize the 5-HT receptor mediating this excitatory response to 5-HT. Most of the experiments were conducted in the presence of spiperone to block the 5HT1A hyperpolarization. Since spiperone also has high affinity for 5-HT2 receptors, any response mediated by 5-HT2 receptors would also be blocked. Bath perfusion of the slice with 5-HT increased the rectification of pyramidal cells in the subthreshold region, increased the resistance, and increased the amplitude of subthreshold excitatory postsynaptic potentials (EPSPs) to initiate spike firing. The 5-HT2,1C-selective agonist DOI mimicked this effect of 5-HT, and the 5-HT2,1C antagonist ketanserin (1 microM) blocked the effect of DOI. There was no change in the amplitude of the slow afterhyperpolarization (sAHP) or the amplitude of evoked inhibitory postsynaptic potentials (IPSPs). The increase in rectification and EPSP amplitude by 5-HT occurred even in the presence of the 5-HT4-selective antagonist BRL 24924 to prevent the decrease in amplitude of the sAHP by 5-HT. We conclude that 5-HT produces a fast excitatory response by increasing subthreshold conductance in CA1 hippocampal pyramidal cells. The identity of the receptor mediating this response was not conclusively identified, but resembled the 5-HT1C receptor.

Electrophysiology of neuroeffector transmission in the isolated, innervated trachea of the guinea‐pig

Intracellular recordings were made from cells of the guinea-pig trachealis muscle. Some cells were electrically quiescent while others exhibited spontaneous slow waves. In quiescent cells, stimulation of the cervical vagus nerve evoked transient depolarization. Occasionally there was a single depolarization, but more often there were several fluctuations in potential. In spontaneously active cells, vagal stimulation induced a transient increase in amplitude of the slow waves without affecting their frequency. Depolarizing responses could be obtained with a single pulse applied to the vagus nerve, and responses increased in amplitude with number of pulses (up to 16 pulses), and with frequency of stimulation (up to 20 Hz). Depolarization did not give rise to spike discharge. Responses to vagal stimulation were blocked by atropine. In the presence of neostigmine, vagally-mediated depolarization was augmented and abortive spikes were observed in a number of cells. In quiescent cells, repetitive stimulation of the sympathetic stellate ganglion evoked slight hyperpolarization. In spontaneously active cells, sympathetic stimulation evoked attenuation, or temporary cessation of slow wave discharge, with or without hyperpolarization. Sympathetic-induced hyperpolarization and suppression of slow waves were both blocked by propranolol, but unaffected by phentolamine. Electrical changes associated with sympathetic stimulation may be of minor importance in the initiation of relaxation.

Field potentials, inhibition and the effect of pentobarbitone in the rat olfactory cortex slice.

1. Field potentials were evoked in slices of rat olfactory cortex by stimulating the lateral olfactory tract. In addition to previously described components of the wave-form, a further distinct surface-negative potential of low amplitude and long duration (I-wave) has been described. 2. Pentobarbitone, at concentrations of 10(-5) M and above, markedly enhanced enhanced the amplitude and duration of the I-wave with only minimal effect on other components of the field potential. 3. The I-wave was reversibly reduced by the GABA antagonists bicuculline and picrotoxin and was also attenuated at rapid rates of stimulation. Low chloride medium usually caused a transient increase in amplitude of the I-wave followed by a gradual reduction, suggesting that a chloride-mediated depolarization was involved. 4. Evoked inhibition, which was most probably post-synaptic, occurred in parallel with the I-wave. This was monitored as a suppression of, or increase in latency of the population spike evoked by a second stimulus at appropriate intervals after the first. Pentobarbitone substantially increased the duration of the post-synpatic inhibition, without obvious changes in the presynaptic inhibitory phenomenon associated with antidromic firing in the lateral olfactory tract. 5. It is proposed that the I-wave is the field potential representation of a population depolarizing i.p.s.p. and that the main action of pentobarbitone is to enhance this inhibition.

The effects of VIP on intestinal motility study onex vivo perfused isolated canine jejunal loops

The effects of VIP on intestinal motility were studied on isolated canine jejunal loops ex vivo perfused at normothermia, under pulsatile flow with heparinized, oxygenated and nonrecirculated canine whole blood, by means of an intraluminal balloon. VIP was administered intraarterially either by 1 min injections or by long-time infusions. The results showed that for arterial concentrations of the polypeptide ranging between 25 pg/ml and 300-500 pg/ml a fast but short-lasting relaxant effect was observed. For higher concentrations VIP usually produced a biphasic response: The relaxant effect is followed by an increase of the basal muscular tone often accompanied, for concentrations higher than about 25 ng/ml, by a marked and transient increase in amplitude of the intestinal rhythmic contractions. During long-time infusions a biphasic response was also observed but both effects were of short duration. A cholingeric origin of the secondary contracting phase was expected but could not be demonstrated because, at blood concentrations at which atropine affected the biphasic response, not only was the contractile effect abolished but also the initial relaxing phase. It is suggested that the secondary contraction may be a "rebound excitation" of myogenic nature or a result of noncholingeric excitatory fiber stimulations. The short-lasting relaxant effect observed under the present experimental conditions, even during long-time infusion of the polypeptide, fails to argue for an important physiological role of VIP as an hormonal inhibitor of intestinal motility. The biphasic response, however, might have a physiological significance in so far as the aboral propulsion of the intestinal content requires a muscular inhibition which rapidly changes to contraction.

Cochlear Pathology with Experimental Acoustic Trauma

Cochlear pathology due to noise exposure were investigated by chiefly experimental approaches. Among a variety of the experimental procedures were predominantly employed optical microscopy and scanning and transmission electron microscopy for morphological examination and evoked response audiometry.Experimental animals used were guinea-pigs and mice. They were exposed to pure tone of 500, 2, 000 and 4, 000Hz with 110-120 dB SPL for various durations from 10 minutes to 15 days consecutively, or to a shock sound. Immediately and in different periods of time within 2 months after the completion of the exposure, the cochlea was examined and the extent of the lesions ranging initial sign to advanced degeneration was minutely clarified.Besides, it was demonstrated that the immature cochlea is less affected by sound injury while vulnerability of the mature cochlea is much intensified by concomitant medication with aminoglycoside drugs.Changes in auditory function were studied by evoked response auditometry at the stage in which no morphological change was found, and, as a result, a transient increase in amplitude of the course of recovery from the sound injury.

On the mechanism of action of intra-amniotic hypertonic saline treatment in rabbits.

Summary. A study was made into the effects of hypertonic saline upon the intra-uterine pressure in non-pregnant and pregnant rabbits. In non-pregnant rabbits intra-luminal administration of hypertonic saline caused an almost immediate transient increase in amplitude and frequency of uterine pressure cycles, a response which was abolished by prior treatment with progesterone. In pregnant rabbits, provided all placentae were damaged by the treatment, intra-amniotic administration of 20% NaCl resulted in abortion of all foetuses in 56 ± 7·3 hr SE. If one conceptus escaped damage pregnancy was not interrupted. Furthermore, treatment with 25 μg/day oestradiol propionate prevented abortion. Of the procedures carried out, only dislocation of the placentae also caused abortion, whereas pregnancy was not terminated by extra-amniotic administration of hypertonic saline, by cutting the umbilical cords (i.e. causing foetal death), nor by the intra-amniotic administration of normal (0·9%) saline. The abortion produced by both intra-amniotic hypertonic saline and dislocation of the placentae could be prevented by oestrogen administration, but not if ovariectomy were combined with placental dislocation. From these results, it is concluded that intra-amniotic hypertonic saline induced abortion in rabbits by interrupting the luteotrophic function of the placenta which resulted in loss of the luteal function essential for the defence of pregnancy.