Time Course Of Increase Research Articles

Delayed increase of acetylcholine quantal size induced by the activity-dependent release of endogenous CGRP but not ATP in neuromuscular junctions.

In mouse motor synapses tetanic neuromuscular activity (30Hz, 2min) led to a delayed posttetanic potentiation of amplitude and duration of spontaneous miniature endplate potentials (MEPPs). Microelectrode recordings of MEPPs before and after nerve stimulation showed an increase in MEPP amplitude and time course by 30% and 15%, respectively, without changes in their frequency. Peak effect was detected 20min after tetanic activity and progressively faded throughout the next 40min of recording. The revealed potentiation of MEPPs was fully preserved in preparations from pannexin 1 knockout mice. It means, that myogenic ATP released via pannexin 1 channels from contracting muscle fibers is not likely to participate in the described phenomenon. But posttetanic potentiation of MEPPs was fully prevented by competitive antagonist of calcitonin gene-related peptide (CGRP) receptors CGRP8-37 , ryanodine receptors inhibitor ryanodine and by vesicular acetylcholine transporter inhibitor vesamicol. It is suggested that the combination of intensive synaptic and contractile activity in neuromuscular junctions is required to induce Ca2+ -dependent exocytosis of endogenous CGRP. The accumulation of CGRP in the synaptic cleft and its presynaptic activity may induce posttetanic potentiation of MEPP amplitude due to CGRP-stimulated acetylcholine loading into vesicles and subsequent increase of quantal size.

Bukhuldaria vietnamensis mediated induced wilt resistance in chickpea

The efficacy of root dipping with Bukhuldaria vietnamensis isolate KM2 (Bv-KM2) an antagonist of Fusarium oxysporum was evaluated to improve the tolerance mechanism of chickpea against wilt. The increase in activity of key ROS enzymes of root tissues viz., peroxidase, catalase and superoxide dismutase was reported with the increase in time course of infection in resistance and susceptible varieties at 1 and 5 DAI. The pre-treatment with Bv-KM2 helps to maintain the higher level of ROS enzymes in susceptible variety JG-62, hence imparts resistance against Foc stress. In resistant variety WR-315 it further improves resistance towards Foc stress through enhanced production of ROS enzymes. The role of phenolic compounds and polyamines was studied from root tissues using HPTLC at 5 DAI. Among the polyphenols, ferulic acid was found to be constitutively expressing in both varieties over the treatment condition, the salicylic acid was found in resistant variety WR-315 over the treatment whereas it was found to be induced in susceptible variety JG-62. Four polyamines were detected through HPTLC of which two were unidentified where as two were identified as cadvarine and spermine. One of unidentified polyamiens (P2) was reported only in resistant variety WR-315 under different treatment conditions. Overall the Bv-KM2 treatment leads to alteration in ROS enzymes, polyphenols and polyamines which result in improved tolerance to Foc in both resistant and susceptible varieties.

Heart Rate Responses in the Diving Reflex among Aerobically Trained and Untrained Men

The mechanisms of the diving reflex involve the simultaneous activation of the sympathetic and parasympathetic nervous systems (PNS). The enhanced PNS capabilities as achieved through aerobic training has been investigated in the diving reflex, specifically vagally-mediated bradycardia, and the research remains controversial. PURPOSE: The current study was conducted to evaluate heart rate responses associated with the diving reflex in aerobically trained and untrained men. METHODS: Using 2 x 3 mixed factorial ANOVA, lowest heart rate achieved, percent heart rate reduction, and time course of heart rate reduction were compared between aerobically untrained (n = 7) and trained (n = 9) men while breath holding in air, water at 15 °C, and water at 0 °C. RESULTS: Results showed that trained men did not differ in percent heart rate reduction or lowest heart rate achieved, although there was a tendency for lowest heart rate achieved in the trained group (p = .06). A significant interaction was found for time course (p = .01), where trained men took significantly longer to reach a plateau in heart rate in the air compared to untrained men. No differences in training status were found for time course in the two water conditions. However, a linear increase in time course for untrained men in the water conditions indicated a potentially delayed response by the PNS with the diving reflex. CONCLUSION: No additional clarification on the impact of training status on the diving reflex has been made except that an effect may lie in the timing of the response of the PNS.

Dye sorption and swelling of poly(vinyl alcohol) hydrogels in Congo red aqueous solution

The swelling behavior of cylindrical poly(vinyl alcohol) (PVA) hydrogels, prepared by means of γ-ray irradiation technique with different irradiation doses have been investigated. The cylindrical gels with ca. 0.2 mm diameter were immersed in various concentrations of Congo red (CR) solutions, and the time course of the swelling degree of the gels were microscopically measured. The swelling degree was increased with the increase in polymer content and time course, but decreased with increasing the irradiation dose. The sorption experiment of CR onto PVA hydrogels was also carried out. CR concentrations of the solutions before and after the sorption were determined spectrophotometrically. Higher irradiation dose of hydrogels had higher dye uptakes. This result reveals that the gels were strongly crosslinked, and the CR anions were bound to PVA as bridges between the hydroxyl groups of PVA. The effect of incorporation of dye on the chemical structure of PVA hydrogels was studied by using differential scanning calorimetry (DSC), and Fourier transform infrared (FTIR) spectroscopy. The results of DSC analysis showed that the melting temperatures of CR-PVA hydrogels are significantly lower than that of PVA hydrogels alone. It is possible to conclude that PVA structure has a significant loss of crystallinity when PVA interacts with CR. FTIR spectra of PVA hydrogels and CR-PVA hydrogels showed the absorption regions of the specific functional groups associated with hydroxyl groups of PVA confirming the formation of cross-links between them. The results showed that the interaction between PVA hydrogels and CR affect the swelling and sorption properties of the hydrogels. Open image in new window

The sea anemone Bunodosoma caissarum toxin BcIII modulates the sodium current kinetics of rat dorsal root ganglia neurons and is displaced in a voltage-dependent manner

Sea anemone toxins bind to site 3 of the sodium channels, which is partially formed by the extracellular linker connecting S3 and S4 segments of domain IV, slowing down the inactivation process. In this work we have characterized the actions of BcIII, a sea anemone polypeptide toxin isolated from Bunodosoma caissarum, on neuronal sodium currents using the patch clamp technique. Neurons of the dorsal root ganglia of Wistar rats (P5–9) in primary culture were used for this study ( n = 65). The main effects of BcIII were a concentration-dependent increase in the sodium current inactivation time course (IC 50 = 2.8 μM) as well as an increase in the current peak amplitude. BcIII did not modify the voltage at which 50% of the channels are activated or inactivated, nor the reversal potential of sodium current. BcIII shows a voltage-dependent action. A progressive acceleration of sodium current fast inactivation with longer conditioning pulses was observed, which was steeper as more depolarizing were the prepulses. The same was observed for other two anemone toxins (CgNa, from Condylactis gigantea and ATX-II, from Anemonia viridis). These results suggest that the binding affinity of sea anemone toxins may be reduced in a voltage-dependent manner, as has been described for α-scorpion toxins.

Influence of State-2 transition on the proton motive force across the thylakoid membrane in spinach chloroplasts

The proton motive force (pmf) across the thylakoid membrane is composed of the proton gradient and the membrane potential, which promotes millisecond-delayed light emission (ms-DLE). In this study, the time courses of LHC II phosphorylation and ms-DLE were investigated in spinach chloroplast during State-2 transition. Red light illumination resulted in an exponential rise in LHC II phosphorylation and a biphasic time course of ms-DLE. The phospho-LHC II appeared upon approximately 1 min illumination. The phosphorylation level increased exponentially when illumination was elongated to 20 min. The t((1/2) )of saturated LHC II phosphorylation was estimated 4-5 min under present illumination. During this process, the amplitudes of ms-DLE increased transiently to a maximal amplitude within 0.5 min illumination, and the reached maximum of the fast phase of ms-DLE was approximately 140% of the dark control. Then, ms-DLE decreased from the maximum. After > or =3 min illumination, ms-DLE decreased to a lower level than the dark control. In the presence of uncouplers and inhibitors, the transient increase in the biphasic time course of ms-DLE was removed by nigericin and DCMU, and the sequential decrease was delayed by DCCD. The time course was not affected significantly by valinomycin and DBMIB. Moreover, the level of LHC II phosphorylation was enhanced by nigericin, valinomycin and DCCD, and was inhibited completely by DCMU and partially by DBMIB. Taken together, we proposed that the PS II photochemical activity remained unaffected even with a higher level of LHC II phosphorylation, which was reflected by the effect of DCCD on the time course of ms-DLE. Probably, the evidence of LHC II phosphorylation is the rearrangement of LHC II-PS II complex and the thylakoid, a feedback to light-exposure, rather than the redistribution of excitation energy from PS II to PS I.

Parallel processing in cerebral cortex of the marmoset monkey: effect of reversible SI inactivation on tactile responses in SII.

1. Responsiveness within the hand region of the second somatosensory area of cortex (SII) was investigated in the marmoset monkey (Callithrix jacchus) in association with cooling-induced, reversible inactivation of the primary somatosensory area, SI. The aims were to determine whether thalamocortical systems in this primate species are organized according to a serial scheme in which tactile information is conveyed from the thalamus to SI and thence to SII as the next hierarchical level of processing and to establish whether primates are fundamentally different, in this respect, from mammals in which tactile information is conveyed in parallel from the thalamus to both SI and SII. 2. Inactivation of the SI had area was achieved when the temperature at the face of the silver cooling block over this SI region was lowered to < or = 13 degrees C. Inactivation was confirmed by abolition of the SI surface potential evoked by a brief tap stimulus to the hand and by the abolition of responsiveness in single SI neurons located beneath and around the edge of the block. 3. The effect of SI inactivation on SII-evoked potentials was investigated in 20 experiments by simultaneous recording of the SI- and SII-evoked potentials. The SII response was never abolished and was unchanged in the majority (12/20) of experiments. In the remainder, the SII-evoked potentials underwent a reduction in amplitude that was usually < 30% but never > 50%. 4. Tactile responsiveness was examined quantitatively in 47 individual SII neurons of different functional classes before, during, and after the inactivation of SI. Controlled tactile stimuli consisted of trains of sinusoidal vibration or rectangular pulses delivered to the glabrous or hairy skin of the hand. 5. Thirteen of the 47 SII neurons (28%) were unaffected in their response levels in association with SI inactivation. The remaining 34 SII neurons underwent some reduction in responsiveness, but in only 6% (3/47) was responsiveness abolished by SI inactivation. As the same range of functional classes of tactile neurons were represented among the affected and unaffected SII neurons, there was no evidence for a differential susceptibility among SII tactile neurons to the effect of SI inactivation. 6. Where reductions in amplitude of the SII-evoked potential or in response levels of SII neurons were observed, the effects were not attributable to direct spread of cooling from SI to the SII hand area as there was no cooling-induced prolongation of either the evoked potential or spike waveform in SII, an effect that is known to precede cooling-induced reductions in responsiveness. 7. These lines of evidence indicate that reductions in SII responsiveness in association with SI inactivation may be attributable to a loss of a background facilitatory influence rather than to a blockage of a component of peripheral input that comes over a putative serial path to SII via SI. First, as SI was cooled, there was a progressive increase in latency and time course of the SI responses before their disappearance, but no comparable delay in the SII responses as might be expected if SI were placed earlier than SII in a strict hierarchical scheme of thalamocortical processing. Second, SI inactivation failed to bring about a tightening in the phase-locking of SII responses to vibrotactile stimuli as might have been expected if the inputs to the SII neurons come via both a direct path from the thalamus and an indirect intracortical path via SI. Blockage of the indirect intracortical pathway through SI might be expected to reduce temporal dispersion in the input to SII neurons and result in an improvement in phase-locking in the SII responses to skin vibration. Third, the background activity of some SII neurons was reduced during SI inactivation along with the reduction in their responses to tactile stimulation.

Potentiation by ACE inhibitors of the dilator response to bradykinin in the coronary microcirculation: interaction at the receptor level.

1. To examine the possibility that angiotensin-converting enzyme (ACE) inhibitors modulate the action of bradykinin at the receptor level, their effect on the dilator response to bradykinin was studied in the isolated saline-perfused heart of the rabbit. 2. Continuous infusion of bradykinin (10 nM) elicited a transient decrease in coronary perfusion pressure (CPP) and increased prostacyclin (PGI2) release which returned to baseline values within 30 min. 3. Subsequent co-infusion of ramiprilat (> or = 10 nM) or moexiprilat, but not of the less potent ACE inhibitor n-octyl-ramipril (RA-octyl), caused another fall in CPP and an increase in PGI2 release, the magnitude and time course of which were almost identical to the first response to bradykinin. No change in CPP or PGI2 release was observed when the ACE inhibitors were administered in the absence of exogenous bradykinin. 4. Infusion of D-Arg[Hyp3]-bradykinin (10 nM), a specific B2-receptor agonist which was significantly more resistant to degradation by ACE than bradykinin, produced virtually identical changes in CPP and PGI2 release when compared to bradykinin. Subsequent co-infusion of ramiprilat was similarly effective in restoring the fall in CPP and increase in PGI2 release elicited by D-Arg[Hyp3]-bradykinin as in the presence of bradykinin. 5. In concentrations which should block the degradation of bradykinin by ACE in the coronary vascular bed, two ACE substrates, hippuryl-L-histidyl-L-leucine (0.2 mM) and angiotensin I (0.3 microM), were unable to elicit a significant change in CPP or PGI2 release while ramiprilat and another ACE inhibitor, quinaprilat, were still active in the presence of these substrates. 6. To reveal the potential B2-receptor action of ramiprilat, its effect on the constrictor response to bradykinin was studied in the rabbit isolated jugular vein. Ramiprilat (0.1 MicroM), but not RA-octyl (1 MicroM),potentiated the endothelium-independent, B2-receptor-mediated constrictor response to bradykinin, but not that to the thromboxane-mimetic U46619 (9,11-dideoxy-ll alpha,9 alpha-epoxymethano-prostaglandin F2.).Moreover, ramiprilat but not RA-octyl caused a concentration-dependent, B2-receptor antagonist sensitive increase in tone when administered alone.7. These findings suggest that an interaction of ACE inhibitors with the B2-receptor or its signal transduction pathway rather than an accumulation of bradykinin within the vascular wall is responsible for the restoration of the endothelial response to bradykinin (dilatation, PGI2 release) in the coronary vascular bed of the rabbit.

Effects of tetraethylammonium on the depolarizing after‐potential and passive properties of lizard myelinated axons.

1. Intra-axonal recordings were obtained from myelinated axons innervating a lizard skeletal muscle. 2. Bath application of tetraethylammonium (TEA, 1-10 mM) depolarized the resting potential, prolonged the action potential and increased the amplitude and duration of the ensuing passive depolarizing after-potential (DAP) in a dose-dependent and reversible manner. TEA increased the axonal input resistance and the slow time constant of the passive voltage response, not only in depolarized axons, but also in resting and hyperpolarized axons. The resting input resistance was tripled in 10 mM-TEA. 3. TEA's effects on the resting potential and action potential usually approached a steady state within 5 min, whereas TEA's effects on input resistance and on the amplitude and time course of the DAP increased progressively for 10-15 min or more, and persisted for 10-15 min after removal of TEA from the bath. 4. 4-Aminopyridine (4-AP, 1 mM), which prolonged the action potential by about the same extent as 10 mM-TEA, did not depolarize the resting potential or increase the resting input resistance, and produced a much smaller increase in DAP time course than 10 mM-TEA. Gallamine (1 mM) had effects more similar to those of TEA. 5. These results suggest that the resting input conductance and DAP time course in lizard motor axons are controlled in part by K+ channels that are blocked by TEA and gallamine, but not by 4-AP. The slow development of the TEA-induced increase in input resistance and DAP time course suggests that some of these channels are located in paranodal or internodal axolemma. 6. In TEA and gallamine additional depolarizing potentials were superimposed on the falling phase of the action potential and on the passive DAP. These superimposed potentials were abolished by 1 mM-Mn2+, and were probably caused by Ca2+ influx into motor terminals.

Increased ponto-geniculo-occipital (PGO) wave frequency following central administration of neostigmine.

In all mammals so far investigated the occurrence of ponto-geniculo-occipital (PGO) waves precedes the onset and maintenance of desynchronized (D) sleep. As unitary electrographic events, PGO waves provide an index for quantitative evaluation of physiological D sleep or the D sleep-like state evoked by centrally administered acetylcholinesterase inhibitors. The present study characterized PGO wave frequency and time course following central administration of neostigmine bromide (Neo). The results show that Neo produced a dose-dependent increase in PGO wave frequency and time course when injected into brainstem regions other than areas containing putative PGO wave generating neurons. These results support the concept that PGO waves and D sleep are generated by an anatomically distributed network of cholinoceptive neurons.

Mechanisms of action of CO 2 on the visual response of Galleria mellonella

Carbon dioxide modifies the visual response recorded from the compound eye of the moth Galleria mellonella. Changes brought about include an increase in latency and time course, as well as the loss of a phasic negativegoing transient. Treating the preparation with either organic or inorganic acid vapours affects the time course of the tonic negative receptor potential, initially by increasing it and then decreasing it. Acids have no effect on the latency of the response, but there is a marked increase in amplitude of the phasic negative component. The resting potential in the eye is also sensitive to acids and CO 2. Changes in resting level, however, do not appear to effect the response significantly. Acids and bases have reciprocal effects on the time course of the response. Acids and CO 2 have different effects on the phasic negative transient and CO 2 can reverse amplitude increases caused by acid. We consider the changes in the visual response brought about by the addition of CO 2 of two kinds. Changes in time course are probably due to a shifting of pH in the eye, while the abolition of the phasic negative component is probably due to a CO 2-specific reaction.

The mechanism of the facilitatory action of edrophonium in cat skeletal muscle.

1. The effects of edrophonium have been observed in the transversely cut tenuissimus muscle of the cat.2. Concentrations of edrophonium 10(-7)M to 10(-5)M increased the amplitude of the end-plate potential (e.p.p.) but produced no greater increase in time course than previously observed in curarized muscle.3. When the e.p.p. and gross nerve action potential were recorded simultaneously, antidromic discharges were observed in the motor nerve concomitantly with repetitive e.p.ps in the presence of edrophonium.4. Edrophonium produced no effect on the input resistance or equilibrium potential of the end-plate.5. The fractional release of transmitter was significantly increased by edrophonium but there was no increase in the quantal release of transmitter in the transversely cut muscle preparation.6. In curarized muscle edrophonium also increased the quantal release, the size of the available store of transmitter and the rate of refilling of the available store.7. It is concluded that edrophonium facilitates transmission to skeletal muscle by inducing a repetitive antidromic discharge in the nerve, following orthodromic stimulation. The antidromic discharge propagates by axon reflex to other nerve terminals of the same motor unit producing repetitive e.p.ps. It is also suggested that edrophonium antagonizes tubocurarine by acting as a partial agonist at the motor nerve terminal.