Reliability of spike propagation in arborizations of dorsal root fibers studied by analysis of postsynaptic potentials mediated by electrotonic coupling in the frog spinal cord

1996 ◽  
Vol 76 (5) ◽  
pp. 3451-3459 ◽  
Author(s):  
A. E. Dityatev ◽  
H. P. Clamann
Keyword(s):  
Synaptic Transmission ◽  
Dorsal Root ◽  
Slow Component ◽  
Electrical Coupling ◽  
Fast Component ◽  
Branch Points ◽  
Positive Component ◽  
Postsynaptic Potentials ◽  
Baseline Noise ◽  
Different Temperatures

1. Postsynaptic potentials were recorded in lumbar motoneurons of the frog in response to electrical activation of dorsal roots. After chemical synaptic transmission was blocked by replacing Ca2+ with Mg2+ in the superfusion medium, it was confirmed that the remaining electrical excitatory postsynaptic potentials (EEPSPs) recorded in motoneurons consisted of potential changes-produced by electrical coupling between the motoneurons and the stimulated axons. The EEPSPs could then be used as an assay to study the reliability of spike propagation into presynaptic terminals. 2. EEPSPs typically consisted of three components. The first was a small positive deflection (prespike or presynaptic volley) that could also be recorded extracellularly. The second component was a spikelike fast positive component and the third was a slow positive component that followed the second but had a distinct maximum and a slow decay. The amplitude of the fast component did not correlate with that of either the prespike or the slow component. 3. 4-Aminopyridine (0.1 mM), which widens action potentials by blocking K+ channels, increased the amplitude and width of EEPSPs. Heptanol (1-4 mM), which is known to be a blocker of electrical coupling, could block EEPSPs. 4. The amplitudes of EEPSPs evoked by dorsal root stimulation were compared at different temperatures (7.5-19.5 degrees C). A slight decrease of the amplitude of the fast component with increasing temperature (Q10 = 0.8) was within limits predicted by resistance-capacitance filtering of the presynaptic spike at the different temperatures, suggesting that the temperature does not affect propagation of the spike in this synapse. 5. The amplitude of the fast component of EEPSPs evoked by single-pulse and paired-pulse stimulation did not fluctuate more than the baseline noise in 37 experiments in which the SD of baseline noise was < 100 microV. We conclude that electrical synaptic transmission does not fluctuate intermittently in this system, and that branch points conduct or fail to conduct for periods of time longer than the longest period in the analyzed experiments.

P2X Receptor–Mediated Ionic Currents in Dorsal Root Ganglion Neurons

1999 ◽  
Vol 82 (3) ◽  
pp. 1590-1598 ◽  
Author(s):  
Edward C. Burgard ◽  
Wende Niforatos ◽  
Tim van Biesen ◽  
Kevin J. Lynch ◽  
Edward Touma ◽  
...  
Keyword(s):  
Dorsal Root ◽  
Slow Component ◽  
Ionic Currents ◽  
P2x Receptors ◽  
Fast Component ◽  
Dorsal Root Ganglion Neurons ◽  
P2x Receptor ◽  
Receptor Subtype ◽  
Nociceptive Neurons ◽  
Ganglion Neurons

Nociceptive neurons in the dorsal root ganglia (DRG) are activated by extracellular ATP, implicating P2X receptors as potential mediators of painful stimuli. However, the P2X receptor subtype(s) underlying this activity remain in question. Using electrophysiological techniques, the effects of P2X receptor agonists and antagonists were examined on acutely dissociated adult rat lumbar DRG neurons. Putative P2X-expressing nociceptors were identified by labeling neurons with the lectin IB4. These neurons could be grouped into three categories based on response kinetics to extracellularly applied ATP. Some DRG responses (slow DRG) were relatively slowly activating, nondesensitizing, and activated by the ATP analogue α,β-meATP. These responses resembled those recorded from 1321N1 cells expressing recombinant heteromultimeric rat P2X2/3 receptors. Other responses (fast DRG) were rapidly activating and desensitized almost completely during agonist application. These responses had properties similar to those recorded from 1321N1 cells expressing recombinant rat P2X3 receptors. A third group (mixed DRG) activated and desensitized rapidly (P2X3-like), but also had a slow, nondesensitizing component that functionally prolonged the current. Like the fast component, the slow component was activated by both ATP and α,β-meATP and was blocked by the P2X antagonist TNP-ATP. But unlike the fast component, the slow component could follow high-frequency activation by agonist, and its amplitude was potentiated under acidic conditions. These characteristics most closely resemble those of rat P2X2/3 receptors. These data suggest that there are at least two populations of P2X receptors present on adult DRG nociceptive neurons, P2X3 and P2X2/3. These receptors are expressed either separately or together on individual neurons and may play a role in the processing of nociceptive information from the periphery to the spinal cord.

V˙o 2 and heart rate kinetics in cycling: transitions from an elevated baseline

2001 ◽  
Vol 90 (6) ◽  
pp. 2081-2087 ◽  
Author(s):  
S. E. Bearden ◽  
R. J. Moffatt
Keyword(s):  
Heart Rate ◽  
Base Excess ◽  
Slow Component ◽  
Lactate Concentration ◽  
Fast Component ◽  
Square Wave ◽  
Mean Response Time ◽  
Rate Kinetics ◽  
Component Amplitude ◽  
Heart Rate Kinetics

The purpose of this study was to examine oxygen consumption (V˙o 2) and heart rate kinetics during moderate and repeated bouts of heavy square-wave cycling from an exercising baseline. Eight healthy, male volunteers performed square-wave bouts of leg ergometry above and below the gas exchange threshold separated by recovery cycling at 35%V˙o 2 peak.V˙o 2 and heart rate kinetics were modeled, after removal of phase I data by use of a biphasic on-kinetics and monoexponential off-kinetics model. Fingertip capillary blood was sampled 45 s before each transition for base excess, HCO[Formula: see text] and lactate concentration, and pH. Base excess and HCO[Formula: see text] concentration were significantly lower, whereas lactate concentration and pH were not different before the second bout. The results confirm earlier reports of a smaller mean response time in the second heavy bout. This was the result of a significantly greater fast-component amplitude and smaller slow-component amplitude with invariant fast-component time constant. A role for local oxygen delivery limitation in heavy exercise transitions with unloaded but not moderate baselines is presented.

scholarly journals Mechanism of retraction of the trailing edge during fibroblast movement.

1981 ◽  
Vol 90 (1) ◽  
pp. 187-200 ◽  
Author(s):  
W T Chen
Keyword(s):  
Slow Component ◽  
Fast Component ◽  
Slow Phase ◽  
Main Body ◽  
Elastic Recoil ◽  
Forward Movement ◽  
Trailing Edge ◽  
Fast Phase ◽  
Focal Contacts

Retraction of the taut, trailing portion of a moving chick heart fibroblast in vitro is an abrupt dynamic process. Upon retraction, the fibroblast tail always ruptures, leaving a small amount of itself attached to the substratum by focal contacts. Time-lapse cinemicrography shows that retraction produces a sudden, massive movement of both surface and cytoplasmic material toward a cluster of focal contacts near the main body of the cell. The appearance of folds on the upper cell surface at this time and the absence of endocytotic vesicles are consistent with this forward movement. Retraction of the trailing edge, either occurring naturally or produced artificially with a microneedle, consists of an initial fast component followed and overlapped by a slow component. Upon artificial detachment in the presence of iodoacetate, dinitrophenol, and sodium fluoride, and at 4 degrees C, the slow component is strongly inhibited and the fast one only slightly inhibited. Moreover of the bundles of microfilaments oriented parallel to the long axis of the tail seen in TEM. Most of the birefringence is lost during the fast phase and the rest during the slow phase of retraction. Concurrently, the bundles of microfilaments disappear during the fast phase of retraction and are replaced by a microfilament meshwork. All of these results are consistent with the hypothesis that the initial fast component of retraction is a passive elastic recoil, associated with the oriented bundles of microfilaments, and that the slow component of retraction is an active contraction, associated with a meshwork of microfilaments.

Enhanced NMDAR-dependent epileptiform activity is controlled by oxidizing agents in a chronic model of temporal lobe epilepsy

1996 ◽  
Vol 76 (6) ◽  
pp. 4185-4189 ◽  
Author(s):  
J. C. Hirsch ◽  
O. Quesada ◽  
M. Esclapez ◽  
H. Gozlan ◽  
Y. Ben-Ari ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Ex Vivo ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Nmda Antagonist ◽  
Pyramidal Cells ◽  
Resting Membrane Potential ◽  
Postsynaptic Potentials ◽  
Epileptiform Discharges ◽  
Late Part

1. Graded N-methyl-D-aspartate receptor (NMDAR)-dependent epileptiform discharges were recorded from ex vivo hippocampal slices obtained from rats injected a week earlier with an intracerebroventricular dose of kainic acid. Intracellular recordings from pyramidal cells of the CA1 area showed that glutamate NMDAR actively participated in synaptic transmission, even at resting membrane potential. When NMDAR were pharmacologically isolated, graded burst discharges could still be evoked. 2. The oxidizing reagent 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB, 200 microM, 15 min) suppressed the late part of the epileptiform burst that did not recover after wash but could be reinstated by the reducing agent tris (2-carboxyethyl) phosphine (TCEP, 200 microM, 15 min) and again abolished with the NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 3. Pharmacologically isolated NMDAR-mediated responses were decreased by DTNB (56 +/- 10%, mean +/- SD, n = 6), an effect reversed by TCEP. 4. When only the fast glutamateric synaptic component was blocked, NMDA-dependent excitatory postsynaptic potentials (EPSPs) could be evoked despite the presence of underlying fast and slow inhibitory postsynaptic potentials (IPSPs). DTNB decreased EPSPs to 48 +/- 12% (n = 5) of control. 5. Since a decrease of the NMDAR-mediated response by +/- 50% is sufficient to suppress the late part of the burst, we suggest that epileptiform activity can be controlled by manipulation of the redox sites of NMDAR. Our observations raise the possibility of developing new anticonvulsant drugs that would spare alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-R (AMPAR)-mediated synaptic responses and decrease NMDAR-mediated synaptic transmission without blocking it completely.

Simulations of fast component and slow component of SMBI on HL-2A tokamak

2017 ◽  
Vol 26 (5) ◽  
pp. 055201 ◽  
Author(s):  
Yong-Fu Shi ◽  
Zhan-Hui Wang ◽  
Qi-Long Ren ◽  
Ai-Ping Sun ◽  
De-Liang Yu ◽  
...  
Keyword(s):  
Slow Component ◽  
Fast Component

Anoxia produces smaller changes in synaptic transmission, membrane potential, and input resistance in immature rat hippocampus

1989 ◽  
Vol 62 (4) ◽  
pp. 882-895 ◽  
Author(s):  
E. Cherubini ◽  
Y. Ben-Ari ◽  
K. Krnjevic
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Mossy Fibers ◽  
Input Resistance ◽  
Resting Potential ◽  
Inward Rectification ◽  
Adult Rats ◽  
Ca1 Neurons ◽  
Postsynaptic Potentials ◽  
Ca3 Neurons

1. The reversible blocking effect of brief anoxia (2-4 min) on synaptic transmission was studied in submerged hippocampal slices (kept mostly at 34 degrees), obtained from adult (greater than 120 g) and very young (6-50 g) Wistar rats. Excitatory postsynaptic potentials (EPSPs) were recorded with extra- and intracellular electrodes, sometimes simultaneously: in CA1, they were evoked by stratum radiation stimulation, in CA3 by hilar stimulation. 2. In slices from adults, EPSPs in CA1 were depressed by 90% after 2 min of anoxia, and postanoxic recovery was relatively slow (one-half recovery times 4.0 +/- 0.23 min, mean +/- SE). EPSPs in CA3 were consistently more resistant, especially those generated by mossy fibers; after 2 min of anoxia, these were reduced by only 14.7 +/- 5.4%. 3. In newborn animals (PN1-4), both intra- and extracellular EPSPs (but no population spikes) could be recorded in CA1. Although smaller and more fatigable than in the adult, they were much more resistant to anoxia, after 2 min being reduced by only 44.1 +/- 8.8%; and they were not abolished even after 6-7 min. On the other hand, postanoxic recovery was very rapid, being one-half complete in 2.4 +/- 0.48 min. Only large and very prolonged (giant) depolarizing PSPs [probably inhibitory postsynaptic potentials (IPSPs)] could be recorded in CA3 neurons; they were rapidly blocked by anoxia. 4. In older pups (PN6-21), the CA1 EPSPs became progressively more sensitive to anoxia. At the end of the second week, they were as rapidly blocked as in slices from adults; but postanoxic recovery remained quicker throughout this period. In CA3, EPSPs could now be evoked that were as resistant to anoxia as in adult slices. 5. In both CA1 and CA3 neurons from adult rats, anoxia (for 2-3 min) reduced the input resistance (RN) by 45.7 +/- 6.25%. In CA1 neurons, there was most often some hyperpolarization (-7.2 +/- 1.8 mV), which was less consistent in CA3 cells. The return of O2 typically led to a second (postanoxic) phase of hyperpolarization (-7.9 +/- 1.93 mV). 6. At PN1-4, the resting potential (Vm) of most cells had to be maintained by current injection; the input resistance (RN) of CA1 neurons was 70% higher than in mature cells, and there was little time-dependent inward rectification. Anoxia produced no regular changes in Vm, and reductions in RN were very small (by only 9.6 +/- 5.0%). A postanoxic hyperpolarization was seen in only 2 neurons out of 11.(ABSTRACT TRUNCATED AT 400 WORDS)

A COMPARISON OF FREE ADRENAL CORTICAL STEROIDS IN THE BLOOD OF A HIBERNATING AND NON-HIBERNATING MAMMAL

1960 ◽  
Vol 38 (1) ◽  
pp. 1479-1487 ◽  
Author(s):  
Arliss Denyes ◽  
Robert H. Horwood
Keyword(s):  
Adrenal Glands ◽  
Slow Component ◽  
Cortical Activity ◽  
Fast Component ◽  
Intermediary Metabolism ◽  
Adrenal Weight ◽  
Reliable Index ◽  
Ion Balance ◽  
White Rats ◽  
Alarm Reaction

White rats and hamsters were fasted and exposed to cold (6 ± 1 °C) for various periods of time. The adrenal glands were weighed and adrenal cortical steroids were extracted from the blood for separation by paper chromatography.The adrenal weight was not a reliable index of adrenal cortical activity as measured by the quantities of circulating hormones. Two steroid fractions were separated from rat and hamster blood. The fast component was identified as corticosterone and the slow component as an amorphous fraction.The adrenal cortical response to cold is different in rats and hamsters. The hamster does not have the typical alarm reaction and only trace quantities of hormones are found in the hibernating animal. Within 6 hours of arousal the concentrations of circulating adrenal cortical hormones have increased to or beyond those of the control animals. The changes in circulating adrenal cortical hormones of hamsters exposed to cold for varying periods of time can be correlated with changes in their intermediary metabolism and ion balance.

Quantitative changes in permeability of rat lung epithelium in lung edema

1978 ◽  
Vol 44 (4) ◽  
pp. 576-580 ◽  
Author(s):  
T. H. Gardiner
Keyword(s):  
Slow Component ◽  
Fast Component ◽  
Lung Edema ◽  
Pulmonary Absorption ◽  
Rat Lung ◽  
Lung Epithelium ◽  
Order Component ◽  
First Order ◽  
Quantitative Changes

The pulmonary absorption of 14C-labeled urea, mannitol, inulin, and dextran was measured in vivo in anesthetized rats with alpha-naphthylthiourea (ANTU)-induced (5 mg/kg, ip) lung edema. At 1 h after ANTU treatment, the absorption of mannitol was significantly increased; in 4-h ANTU-treated animals, the absorption of urea was unchanged, whereas the absorption of mannitol, inulin and dextran was increased markedly compared to controls. Although disappearance of each solute from control lungs could be described by a single, first-order rate, absorption time curves for mannitol and inulin showed at least two components in edematous lungs: a fast component(s) and a slower, first-order component; fast-component rates for the two saccharides appeared to be similar; the slow-component rate for each compound was not significantly different from its control rate. The results suggest that fast-component absorption in ANTU-treated rats represents a fraction of instilled solute which entered damaged areas of lung where the porosity of the absorbing membranes was markedly increased, whereas slow-component absorption occurred from normal areas of lung.

Tachykinin-mediated modulation of sensory neurons, interneurons, and synaptic transmission in the lamprey spinal cord

1996 ◽  
Vol 76 (6) ◽  
pp. 4031-4039 ◽  
Author(s):  
D. Parker ◽  
S. Grillner
Keyword(s):  
Spinal Cord ◽  
Substance P ◽  
Synaptic Transmission ◽  
Dorsal Root ◽  
Input Resistance ◽  
Dorsal Column ◽  
Giant Interneurons ◽  
Potassium Conductances ◽  
Dorsal Cells ◽  
Measurable Change

1. Tachykinin-like immunoreactivity is found in the dorsal roots, dorsal horn, and dorsal column of the lamprey. The effect of tachykinins on sensory processing was examined by recording intracellularly from primary sensory dorsal cells and second-order spinobulbar giant interneurons. Modulation of synaptic transmission was examined by making paired recordings from dorsal cells and giant interneurons, or by eliciting compound depolarizations in the giant interneurons by stimulating the dorsal root or dorsal column. 2. Bath application of tachykinins depolarized the dorsal cells. This effect was mimicked by stimulation of the dorsal root, suggesting that dorsal root afferents may be a source of endogenous tachykinin input to the spinal cord. The depolarization was reduced by removal of sodium or calcium from the Ringer, or when potassium conductances were blocked, and was not associated with a measurable change in input resistance. Dorsal root stimulation also caused a depolarization in the dorsal cells, and this effect and that of bath-applied substance P, was blocked by the tachykinin antagonist spantide. 3. The tachykinin substance P could reduce inward and outward rectification in the dorsal cells, the effect on outward rectification only being seen when potassium conductances were blocked by tetraethylammonium (TEA). 4. Substance P increased the excitability of the dorsal cells and giant interneurons, shown by the increased spiking in response to depolarizing current pulses. The increased excitability was blocked by the tachykinin antagonist spantide. 5. Substance P modulated the dorsal cell action potential, by increasing the spike duration and reducing the amplitude of the afterhyperpolarization. The spike amplitude was not consistently affected. 6. Stimulation of the dorsal column resulted in either depolarizing or hyperpolarizing potentials in the giant interneurons. The amplitude of the depolarization was increased by substance P, whereas the amplitude of the hyperpolarization was reduced. These effects occurred independently of a measurable change in postsynaptic input resistance, suggesting that the modulation occurred presynaptically. Paired recordings from dorsal cells and giant interneurons failed to reveal an effect of substance P on dorsal cell-evoked excitatory postsynaptic potentials (EPSPs), suggesting that the potentiation of the dorsal column-evoked depolarization was due to an effect on other axons in the dorsal column. Dorsal root-evoked potentials could also be increased in the presence of substance P, although this effect was less consistent than the effect on dorsal column stimulation. 7. These results suggest that tachykinins modulate sensory input to the lamprey spinal cord by increasing the excitability of primary afferents and second-order giant interneurons, and also by modulating synaptic transmission. Tachykinins may result in potentiation of local spinal reflexes and also modulation of descending reticulospinal inputs to the spinal locomotor network as a result of potentiation of spinobulbar inputs.

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