Differences between steady-state and transient post-synaptic potentials elicited by stimulation of the sural nerve

1992 ◽  
Vol 91 (1) ◽  
Author(s):  
C.J. Heckman ◽  
J.F. Miller ◽  
M. Munson ◽  
W.Z. Rymer
Keyword(s):  
Steady State ◽  
Sural Nerve ◽  
Synaptic Potentials ◽  
Stimulation Of

scholarly journals Receptor-operated Ca2+ channels in gastric parietal cells: gastrin and carbachol induce Ca2+ influx in depleting intracellular Ca2+ stores

1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous
Keyword(s):  
Steady State ◽  
Receptor Activation ◽  
Parietal Cells ◽  
The Other ◽  
Bivalent Cation ◽  
Gtp Binding ◽  
Gastric Parietal Cells ◽  
Type Receptor ◽  
Ca2 Channels ◽  
Stimulation Of

The mechanism whereby gastrin-type receptor and muscarinic M3-type receptor regulate free intracellular Ca2+ concentration ([Ca2+]i) was studied in rabbit gastric parietal cells stimulated by either gastrin or carbachol. Both agonists induced a biphasic [Ca2+]i response: a transient [Ca2+]i rise, followed by a sustained steady state depending on extracellular Ca2+. Gastrin and carbachol also caused a rapid and transient increase in Mn2+ influx (a tracer for bivalent-cation entry). Pre-stimulation of cells with one agonist drastically decreased both [Ca2+]i increase and Mn2+ influx induced by the other. Neither diltiazem nor pertussistoxin treatment had any effect on agonist-stimulated Mn2+ entry. Thapsigargin, a Ca(2+)-pump inhibitor, induced a biphasic [Ca2+]i increase, and enhanced the rate of Mn2+ entry. Preincubation of cells with thapsigargin inhibits the [Ca2+]i increase as well as Mn2+ entry stimulated by gastrin or by carbachol. Thapsigargin induced a weak but significant increase in Ins(1,4,5)P3 content, but this agent had no effect on the agonist-evoked Ins(1,4,5)P3 response. In permeabilized parietal cells, Ins(1,4,5)P3 and caffeine caused an immediate Ca2+ release from intracellular pools, followed by a reloading of Ca2+ pools which can be prevented in the presence of thapsigargin. We conclude that (i) gastrin and carbachol mobilize common Ca2+ intracellular stores, (ii) Ca2+ permeability secondary to receptor activation involves neither a voltage-sensitive Ca2+ channel nor a GTP-binding protein from the G1 family, and (iii) agonists regulate common Ca2+ channels in depleting intracellular Ca2+ stores.

The synaptic organization of optic afferents in the amphibian tectum

1974 ◽  
Vol 187 (1089) ◽  
pp. 421-447 ◽  
Keyword(s):  
Optic Nerve ◽  
Cell Layer ◽  
Maximum Amplitude ◽  
Synaptic Organization ◽  
Nerve Fibres ◽  
Synaptic Potentials ◽  
Postsynaptic Cell ◽  
Optic Fibre ◽  
Stimulation Of

Potentials in the amphibian tectum, evoked by stimulation of the optic nerve, were recorded extracellularly. Four discrete potentials, referred to as the m 1 , m 2 , u 1 and u 2 waves, occur at different latencies after stimulation. We have shown that these waves represent summed post-synaptic potentials generated by synchronous activation of four different groups of optic nerve fibres. The m 1 and m 2 waves are generated by two classes of myelinated optic nerve fibres, previously characterized as ‘dimming’ and ‘event’ fibres. The maximum amplitude of the m 2 wave occurs just below, and of the m 2 wave just above, cell layer 8 of P. Ramón. The u 1 and u 2 waves are generated by ‘edge’ and ‘convexity’ fibres, respectively. The maximum amplitude of the u 1 wave occurs near the surface of the tectum, and of the u 2 wave some 100 μm below it. Postsynaptic cell bodies for all four classes of optic fibre are located in layer 8.

Mormyromast electroreceptor organs and their afferent fibers in mormyrid fish. II. Intra-axonal recordings show initial stages of central processing

1990 ◽  
Vol 63 (2) ◽  
pp. 303-318 ◽  
Author(s):  
C. C. Bell
Keyword(s):  
Lateral Line ◽  
Electric Organ Discharge ◽  
Electric Organ ◽  
Direct Stimulation ◽  
Postsynaptic Potentials ◽  
Central Processing ◽  
Refractory Periods ◽  
Synaptic Potentials ◽  
Afferent Fibers ◽  
Stimulation Of

1. Physiologically and morphologically identified primary afferent fibers from mormyromast electroreceptor organs were recorded intracellularly. The fiber recordings were made from the nerve root of the posterior lateral line nerve, where the fibers enter the brain, and from the electrosensory lateral line lobe (ELL), near the central terminals of the fibers. 2. The intracellular recordings reveal a variety of potentials, synaptic and nonsynaptic, in addition to the large orthodromic action potentials from the periphery. The goal of the present study was to describe and interpret these various potentials in mormyromast afferent fibers as a first step in understanding the processing of electrosensory information in ELL. 3. Three types of synaptic potentials were recorded inside mormyromast afferent fibers: 1) electric organ corollary discharge (EOCD) excitatory postsynaptic potentials (EPSPs), driven by the motor command that elicits the electric organ discharge (EOD); 2) EPSPs evoked by electrosensory stimulation of electroreceptors in the skin near the electroreceptor from which the recorded fiber originates or by direct stimulation of an electrosensory nerve; and 3) inhibitory postsynaptic potentials (IPSPs) evoked by electrosensory stimulation of more distant electroreceptors. These synaptic potentials can be attributed to synaptic input to postsynaptic cells in ELL that is observed inside the afferent fibers because of electrical synapses between the fibers and the postsynaptic cells. 4. The peripherally evoked EPSPs could frequently be shown to be unitary. The unitary EPSPs were identical to the orthodromic spikes in originating from a single electroreceptor, in threshold, and in latency shift with increasing stimulus intensity. These similarities suggest that the unitary EPSPs are electrotonic EPSPs caused by impulses in other mormyromast afferent fibers that terminate on some of the same postsynaptic cells as the recorded fiber. The peripherally evoked IPSPs had a longer latency than the EPSPs or orthodromic spikes, requiring the presence of an inhibitory interneuron. 5. The peripherally evoked EPSPs, both unitary and nonunitary, show absolute refractory periods of 3-8 ms, followed by relative refractory periods of approximately 8 ms, when tested with two identical stimuli to a nerve. These refractory periods are interpreted as because of refractoriness in the fine preterminal branches of the axonal arbor. 6. A depolarizing afterpotential is commonly associated with the orthodromic spike and probably results from the successful propagation of the spike into the entire terminal arbor. The depolarizing afterpotential has a refractory period that is similar to that of the peripherally evoked EPSPs and that is also interpreted as refractoriness in the fine preterminal branches.(ABSTRACT TRUNCATED AT 400 WORDS)

Tetanic hyperpolarization of single medullated nerve fibers in sodium and lithium

1976 ◽  
Vol 231 (4) ◽  
pp. 1033-1038 ◽  
Author(s):  
GM Schoepfle
Keyword(s):  
Steady State ◽  
Interspike Interval ◽  
Nerve Fibers ◽  
Repetitive Stimulation ◽  
Time Dependent ◽  
Potassium Ions ◽  
Current Densities ◽  
Medullated Nerve Fiber ◽  
Sodium And Potassium ◽  
Stimulation Of

Repetitive stimulation of a single medullated nerve fiber of Xenopus yields a succession of postspike voltage-time curves which are nearly coincident until attainment of a voltage that corresponds to that of the maximum attained by the normal postspike undershoot. Initially the interspike potential returns toward a resting level after this brief phase of hyperpolarization. However, as tetanization proceeds, a pattern of hyperpolarization develops with the result that, in the tetanic steady state, there exists a progressive hyperpolarization throughout each interspike interval. Extent of postspike hyperpolarization in terms of a deviation deltaVm from the resting level of membrane potential is approximated by the variation deltaVm = delta[MNa + MK]/[GNa + GK] where MNa and MK are current densities associated with active pumping of sodium and potassium ions and GNa and GK are corresponding time-dependent leak conductances. Tetanic hyperpolarization is reversibly abolished by cyanide and by exposure to lithium Ringer. Eventual reappearance of tetanic hyperpolarization in the presence of lithium Ringer suggests lithium pumping.

Human intracranially-recorded cortical responses evoked by painful electrical stimulation of the sural nerve

NeuroImage ◽  
2007 ◽  
Vol 34 (2) ◽  
pp. 743-763 ◽  
Author(s):  
R. Dowman ◽  
T. Darcey ◽  
H. Barkan ◽  
V. Thadani ◽  
D. Roberts
Keyword(s):  
Electrical Stimulation ◽  
Sural Nerve ◽  
Cortical Responses ◽  
Stimulation Of

scholarly journals The "late" Ca channel in squid axons.

1981 ◽  
Vol 78 (6) ◽  
pp. 683-700 ◽  
Author(s):  
L J Mullins ◽  
J Requena
Keyword(s):  
Steady State ◽  
Repetitive Stimulation ◽  
Test Solution ◽  
Ca Channel ◽  
Normal Concentration ◽  
Giant Axons ◽  
Light Production ◽  
High K ◽  
K Response ◽  
Stimulation Of

Squid giant axons were injected with aequorin and then treated with seawater containing 50 mM Ca and 100-465 mM K+. Measurements of light production suggested a phasic entry of Ca as well as an enhanced steady-state aequorin glow. After a test K+ depolarization, the aequorin-injected axon was stimulated for 30 min in Li seawater that was Ca-free, a procedure known to reduce [Na]i to about one-half the normal concentration. Reapplication of the elevated K+ test solution now showed that the Ca entry was virtually abolished by this stimulation in Li. A subsequent stimulation of the axon in Na seawater for 30 min resulted in recovery of the response to depolarization by high K+ noted in a normal fresh axon. In axons first tested for a high K+ response and then stimulated in Na seawater for 30 min (where [Na]i increases approximately 30%), there was approximately eight fold enhancement in this response to a test polarization. Axons depolarized with 465 mM K seawater in the absence of external Ca for several minutes were still capable of producing a large phasic entry of Ca when [Ca]0 was made 50 mM, which suggests that it is Ca entry itself rather than membrane depolarization that produced inactivation. Responses to stimulation at 60 pulses/s in Na seawater containing 50 mM Ca are at best only 5% of those measured with high K solutions. The response to repetitive stimulation is not measurable if [Ca]o is made 1 mM, whereas the response to steady depolarization is scarcely affected.

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