scholarly journals The sodium current underlying action potentials in guinea pig hippocampal CA1 neurons.

1988 ◽  
Vol 91 (3) ◽  
pp. 373-398 ◽  
Author(s):  
P Sah ◽  
A J Gibb ◽  
P W Gage
Keyword(s):  
Action Potentials ◽  
Time Course ◽  
Sodium Current ◽  
Hippocampal Slices ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Sodium Currents ◽  
Time To Peak ◽  
Ca1 Region ◽  
Inward Currents

Neurons were acutely dissociated from the CA1 region of hippocampal slices from guinea pigs. Whole-cell recording techniques were used to record and control membrane potential. When the electrode contained KF, the average resting potential was about -40 mV and action potentials in cells at -80 mV (current-clamped) had an amplitude greater than 100 mV. Cells were voltage-clamped at 22-24 degrees C with electrodes containing CsF. Inward currents generated with depolarizing voltage pulses reversed close to the sodium equilibrium potential and could be completely blocked with tetrodotoxin (1 microM). The amplitude of these sodium currents was maximal at about -20 mV and the amplitude of the tail currents was linear with potential, which indicates that the channels were ohmic. The sodium conductance increased with depolarization in a range from -60 to 0 mV with an average half-maximum at about -40 mV. The decay of the currents was not exponential at potentials more positive than -20 mV. The time to peak and half-decay time of the currents varied with potential and temperature. Half of the channels were inactivated at a potential of -75 mV and inactivation was essentially complete at -40 to -30 mV. Recovery from inactivation was not exponential and the rate varied with potential. At lower temperatures, the amplitude of sodium currents decreased, their time course became longer, and half-maximal inactivation shifted to more negative potentials. In a small fraction of cells studied, sodium currents were much more rapid but the voltage dependence of activation and inactivation was very similar.

Pharmacology of a Slowly Inactivating Outward Current in Hippocampal CA3 Pyramidal Neurons

2006 ◽  
Vol 96 (3) ◽  
pp. 1116-1123 ◽  
Author(s):  
Riccardo Bianchi ◽  
Shih-Chieh Chuang ◽  
Robert K. S. Wong
Keyword(s):  
Time Course ◽  
Pyramidal Neurons ◽  
Hippocampal Slices ◽  
Reversal Potential ◽  
Outward Current ◽  
Pyramidal Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Transient Outward Current ◽  
Activation Threshold

The pharmacology of a slowly inactivating outward current was examined using whole cell patch-clamp recordings in CA3 pyramidal cells of guinea pig hippocampal slices. The current had a low activation threshold (about −60 mV) and inactivated slowly (time constant of 3.4 ± 0.5 s at −50 mV) and completely at membrane voltages depolarized to −50 mV. The slowly inactivating outward current was mainly mediated by K+ with a reversal potential close to the equilibrium potential for K+. The slowly inactivating outward current had distinct pharmacological properties: its time course was not affected by extracellular Cs+ (1 mM) or 4-AP (1–5 mM)—broad spectrum inhibitors of K+ currents and of inactivating K+ currents, respectively. The presence of extracellular Mn2+ (0.5–1 mM), which suppresses several Ca2+-dependent K+ currents, also did not affect the slowly inactivating outward current. The current was partially suppressed by TEA (50 mM) and was blocked by intracellular Cs+ (134 mM). In addition, intracellular QX-314 (5 mM), a local anesthetic derivative, inhibited this current. The slowly inactivating outward current with its low activation threshold should be operational at the resting potential. Our results suggest that the transient outward current activated at subthreshold membrane potentials in hippocampal pyramidal cells consists of at least three components. In addition to the well-described A- and D-currents, the slowest decaying component reflects the time course of a distinct current, suppressible by QX-314.

scholarly journals Slow sodium inactivation in nerve after exposure to sulhydryl blocking reagents.

1977 ◽  
Vol 69 (2) ◽  
pp. 183-202 ◽  
Author(s):  
P Shrager
Keyword(s):  
Sodium Current ◽  
Potassium Conductance ◽  
Kinetic Studies ◽  
High Specificity ◽  
Resting Potential ◽  
Dependent Manner ◽  
Sodium Currents ◽  
Time To Peak ◽  
Sodium Inactivation ◽  
Protein Sulfhydryl Groups

Exposure to N-ethylmaleimide (NEM), a reagent that binds covalently to protein sulfhydryl groups, results in a specific reduction in sodium conductance in crayfish axons. Resting potential, the delayed rise in potassium conductance, and the selectivity of the sodium channel are unaffected. Sodium currents are only slightly increased by hyperpolarizing prepulses of up to 50 ms duration, but can be restored to about 70% of their value before treatment if this duration is increased to 300-800 ms. The time to peak sodium current and the time constant of decay of sodium tail currents are unaffected by NEM, suggesting that the sodium activation system remains unaltered. Kinetic studies suggest that NEM reacts with a "slow" sodium inactivation system that is present in normal axons and that may be seen after depolarization produced by lowered the holding potential or increasing the external potassium concentration. NEM also perturbs the fast h inactivation system, and in a potential-dependent manner. At small depolarizations tauh is decreased, while at strong depolarizations it is increased over control values. Experiments with structural analogs of NEM suggest that sulfhydryl block is involved, but do not rule out an action similar to that of local anesthetics, p-Chloromercuriphenylsulfonic acid (PCMBS), another reagent with high specificity for SH groups, also blocks sodium currents, but restoration with prolonged hyperpolarizations is not possible.

Electrical properties and innervation of fibers in the orbital layer of rat extraocular muscles

1989 ◽  
Vol 61 (1) ◽  
pp. 116-125 ◽  
Author(s):  
J. Jacoby ◽  
D. J. Chiarandini ◽  
E. Stefani
Keyword(s):  
Electrical Properties ◽  
Nerve Stimulation ◽  
Action Potentials ◽  
Time Course ◽  
Lucifer Yellow ◽  
Extraocular Muscles ◽  
Resting Potential ◽  
Inferior Rectus ◽  
End Plate ◽  
Orbital Layer

1. The inferior rectus muscle of rat, one of the extraocular muscles, contains two populations of multiply innervated fibers (MIFs): orbital MIFs, located in the orbital layer of the muscle and global MIFs, found in the global layer. The electrical properties and the responses to nerve stimulation of orbital MIFs were studied with single intracellular electrodes and compared with those of twitch fibers of the orbital layer, MIFs of the global layer, and tonic fibers of the frog. 2. About 90% of the orbital MIFs did not produce overshooting action potentials. In these fibers the characteristics and time course of the responses to nerve stimulation varied along the length of the fibers. Within 2 mm of the end-plate band of the muscle, the responses consisted of several small end-plate potentials (EPPs) and a nonovershooting spike. Distal to 2 mm, the responses in most fibers consisted of large and small EPPs with no spiking response. Some fibers produced very small spikes surmounted on large EPPs. 3. Overshooting action potentials were observed in approximately 10% of the orbital MIFs recorded between the end-plate band and 2 mm distal. The presence or absence of action potentials was not related to the magnitude of the resting potential of the fibers. 4. The threshold of nerve stimulated responses in orbital MIFs was the same as that in orbital twitch fibers. A large number of orbital MIFs had latencies equal to those for the orbital twitch fibers recorded at the same distance from the end-plate band, but the average latency was greater in the MIFs. The latency of orbital MIFs was about one-half of that for the MIFs of the global layer. The values for the effective resistance and membrane time constant of orbital MIFs fell between those for orbital twitch fibers on the one hand, and global MIFs and frog tonic fibers on the other. 5. In order to compare electrical properties with innervation patterns, fibers identified electrophysiologically as orbital MIFs were injected with the fluorescent dye Lucifer yellow and then traced in Epon-embedded, serial transverse sections. In addition to numerous superficial endings distributed along the fibers, a single "en plaque" ending was also found in the end-plate band that resembled the end plates of the adjacent orbital twitch fibers. 6. From these results we conclude that the electrical activity of orbital MIFs varies along the length of the fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Posttetanic hyperpolarization produced by electrogenic Na(+)-K+ pump in lizard axons impaled near their motor terminals

1993 ◽  
Vol 70 (5) ◽  
pp. 1874-1884 ◽  
Author(s):  
K. Morita ◽  
G. David ◽  
J. N. Barrett ◽  
E. F. Barrett
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Input Resistance ◽  
Peak Amplitude ◽  
Resting Potential ◽  
Tetanic Stimulation ◽  
Train Duration ◽  
Consistent Change ◽  
Nodal Voltage

1. The hyperpolarization that follows tetanic stimulation was recorded intra-axonally from the internodal region of intramuscular myelinated motor axons. 2. The peak amplitude of the posttetanic hyperpolarization (PTH) that followed stimulation at 20-100 Hz for < or = 35 s increased with increasing train duration, reaching a maximum of 22 mV. PTH decayed over a time course that increased from tens to hundreds of seconds with increasing train duration. For a given frequency of stimulation the time integral of PTH was proportional to the number of stimuli in the train, averaging 3-4 mV.s per action potential. 3. Ouabain (0.1-1 mM) and cyanide (1 mM) depolarized the resting potential and abolished PTH. Tetanic stimulation in ouabain was followed by a slowly decaying depolarization (probably due to extra-axonal K+ accumulation) whose magnitude and duration increased as the duration of the train increased. 4. Axonal input resistance showed no consistent change during PTH in normal solution but increased during PTH in the presence of 3 mM Cs+ (which blocks axonal inward rectifier currents). 5. PTH was abolished when bath Na+ was replaced by Li+ or choline. PTH persisted after removal of bath Ca2+ and addition of 2 mM Mn2+. 6. Removal of bath K+ abolished the PTH recorded after brief stimulus trains and greatly reduced the duration of PTH recorded after longer stimulus trains. 7. A brief application of 10 mM K+, which normally depolarizes axons, produced a ouabain-sensitive hyperpolarization in axons bathed in K(+)-free solution. 8. These observations suggest that in these myelinated axons PTH is produced mainly by activation of an electrogenic Na(+)-K(+)-ATPase, rather than by changes in K+ permeability or transmembrane [K+] gradients. This conclusion is supported by calculations showing agreement between estimates of Na+ efflux/impulse based on PTH measurements and estimates of Na+ influx/impulse based on nodal voltage-clamp measurements. Pump activity also appears to contribute to the resting potential. 9. The stimulus intensity required to initiate a propagating action potential increased during PTH but decreased during the posttetanic depolarization recorded in ouabain. Thus changes in axonal excitability after tetanic stimulation correlate with changes in the posttetanic membrane potential. 10. Action potentials that propagated during PTH had a larger peak amplitude and were followed by a larger and longer depolarizing afterpotential than action potentials elicited at the resting potential. This enhancement of the depolarizing afterpotential is consistent with previous reports of an increased superexcitable period after action potentials evoked during PTH.

Activity-Dependent [Ca2+]i Changes in Guinea Pig Vagal Motoneurons: Relationship to the Slow Afterhyperpolarization

1997 ◽  
Vol 78 (2) ◽  
pp. 825-834 ◽  
Author(s):  
Nechama Lasser-Ross ◽  
William N. Ross ◽  
Yosef Yarom
Keyword(s):  
Guinea Pig ◽  
Time Constant ◽  
Recovery Time ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Cell Types ◽  
Time To Peak ◽  
Ca1 Region ◽  
Activity Dependent ◽  
Calcium Green

Lasser-Ross, Nechama, William N. Ross, and Yosef Yarom. Activity-dependent [Ca2+]i changes in guinea pig vagal motoneurons: relationship to the slow afterhyperpolarization. J. Neurophysiol. 78: 825–834, 1997. Vagal motoneurons in slices from the guinea-pig brain stem were injected with the fluorescent [Ca2+]i indicators fura-2, furaptra, or Calcium Green-1. Spike-induced fluorescence changes were measured in the soma and dendrites and simultaneously the long-lasting afterhyperpolarization was recorded with a sharp microelectrode in the soma. Na+ spikes or Ca2+ spikes increased [Ca2+]i (measured as a change in indicator fluorescence) in all locations in the soma and dendrites. Each spike in a train of action potentials caused a step increase in fluorescence of about equal amplitude when nonsaturating indicators were used. Peak changes at all locations occurred at the time of the last action potential. Transients measured with low concentrations of Calcium Green-1 or furaptra had a recovery time constant of ∼500–1,500 ms in the cell body. The recovery time course was faster in the dendrites than in the soma. The norepinephrine-sensitive, slow afterhyperpolarization (sAHP) had a time to peak of ∼800 ms and a recovery time constant of 2–5 s, much longer than the recovery time course of the fluorescence changes. Some of these experiments were repeated on pyramidal neurons from the CA1 region of the rat hippocampus with similar results. In both cell types, the data suggest that the time course of neither the rising phase nor the falling phase of the sAHP, nor the underlying conductance, directly reflects the time course of the [Ca2+]i change. The mechanism connecting the parameters remains unclear. One possibility is that an additional second messenger system is involved.

scholarly journals Two Components of the Cardiac Action Potential

1969 ◽  
Vol 54 (5) ◽  
pp. 607-635 ◽  
Author(s):  
Antonio Paes de Carvalho ◽  
Brian Francis Hoffman ◽  
Marilene de Paula Carvalho
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Slow Component ◽  
Slow Inward Current ◽  
Equilibrium Potential ◽  
Slow Phase ◽  
Positive Equilibrium ◽  
Cardiac Action

Transmembrane potentials recorded from the rabbit heart in vitro were displayed as voltage against time (V, t display), and dV/dt against voltage (V, V or phase-plane display). Acetylcholine was applied to the recording site by means of a hydraulic system. Results showed that (a) differences in time course of action potential upstroke can be explained in terms of the relative magnitude of fast and slow phases of depolarization; (b) acetylcholine is capable of depressing the slow phase of depolarization as well as the plateau of the action potential; and (c) action potentials from nodal (SA and AV) cells seem to lack the initial fast phase. These results were construed to support a two-component hypothesis for cardiac electrogenesis. The hypothesis states that cardiac action potentials are composed of two distinct and physiologically separable "components" which result from discrete mechanisms. An initial fast component is a sodium spike similar to that of squid nerve. The slow component, which accounts for both a slow depolarization during phase 0 and the plateau, probably is dependent on the properties of a slow inward current having a positive equilibrium potential, coupled to a decrease in the resting potassium conductance. According to the hypothesis, SA and AV nodal action potentials are due entirely or almost entirely to the slow component and can therefore be expected to exhibit unique electrophysiological and pharmacological properties.

scholarly journals The modulation of two motor behaviors by persistent sodium currents in Xenopus laevis tadpoles

2017 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Erik Svensson ◽  
Hugo Jeffreys ◽  
Wen-Chang Li
Keyword(s):  
Action Potentials ◽  
Sodium Current ◽  
Repetitive Firing ◽  
Sodium Currents ◽  
Spinal Neurons ◽  
Motor Behaviors ◽  
Low Concentrations ◽  
Descending Interneurons ◽  
Lateral Sclerosis

Persistent sodium currents ( INaP) are common in neuronal circuitries and have been implicated in several diseases, such as amyotrophic lateral sclerosis (ALS) and epilepsy. However, the role of INaP in the regulation of specific behaviors is still poorly understood. In this study we have characterized INaP and investigated its role in the swimming and struggling behavior of Xenopus tadpoles. INaP was identified in three groups of neurons, namely, sensory Rohon-Beard neurons (RB neurons), descending interneurons (dINs), and non-dINs (neurons rhythmically active in swimming). All groups of neurons expressed INaP, but the currents differed in decay time constants, amplitudes, and the membrane potential at which INaP peaked. Low concentrations (1 µM) of the INaP blocker riluzole blocked INaP ~30% and decreased the excitability of the three neuron groups without affecting spike amplitudes or cellular input resistances. Riluzole reduced the number of rebound spikes in dINs and depressed repetitive firing in RB neurons and non-dINs. At the behavior level, riluzole at 1 µM shortened fictive swimming episodes. It also reduced the number of action potentials neurons fired on each struggling cycle. The results show that INaP may play important modulatory roles in motor behaviors. NEW & NOTEWORTHY We have characterized persistent sodium currents in three groups of spinal neurons and their role in shaping spiking activity in the Xenopus tadpole. We then attempted to evaluate the role of persistent sodium currents in regulating tadpole swimming and struggling motor outputs by using low concentrations of the persistent sodium current antagonist riluzole.

scholarly journals On the effects of divalent cations and ethylene glycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetate on action potential duration in frog heart.

1978 ◽  
Vol 71 (1) ◽  
pp. 47-67 ◽  
Author(s):  
D J Miller ◽  
A Mörchen
Keyword(s):  
Ethylene Glycol ◽  
Action Potential ◽  
Calcium Ions ◽  
Action Potentials ◽  
Time Course ◽  
Divalent Cations ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Slow Inward Current ◽  
Frog Heart

Resting and action potentials were recorded from superfused strips of frog ventricle. Reducing the bathing calcium concentration ([Ca2+]0) with or without ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N'-tetraacetate (EGTA) prolongs the action potential (AP). The change in the duration of the AP extends over many minutes, but is rapidly reversed by restoring calcium ions. Other changes (e.g., in resting potential and overshoot) are, however, only more slowly reversed. Reducing [Ca2+]0 with 0.2, 2, or 5 mM EGTA produces progressively greater prolongation of AP; maximum values were well in excess of 1 min. This prolongation can be reversed by other divalent cations in EGTA (Mg2+, Sr2+) or Ca-free (Mn2+) solutions, or by acetylcholine. Barium ions increase AP duration in keeping with their known effect on potassium conductance. D600, which blocks the slow inward current in cardiac muscle, is without effect on the action potentials recorded in EGTA solutions, or on the time course and extent of the recovery to normal duration upon restoring calcium ions. It is concluded that divalent cations exert an influence on membrane potassium conductance extracellularly in frog heart. The cell membrane does not become excessively "leaky" in EGTA solutions.

Ionic Composition of Haemolymph and Nervous Function in the Cockroach, Periplaneta Americana L

1968 ◽  
Vol 49 (1) ◽  
pp. 31-38
Author(s):  
Y. PICHON ◽  
J. BOISTEL
Keyword(s):  
Action Potentials ◽  
Periplaneta Americana ◽  
Extracellular Fluid ◽  
Sodium Concentration ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Unequal Distribution ◽  
High Sodium ◽  
Giant Axons ◽  
Nerve Cords

1. Resting and action potentials have been recorded in giant axons of the cockroach when the intact nerve cord was bathed in the insect's own haemolymph. 2. Low resting potentials (43.0±4.8 mV.) and large action potentials (105.1±6.8 mV.) were obtained in these preparations as compared with those recorded in de-sheathed nerve cords. 3. Recordings of the maximum rates of rise and fall have shown that the shape of the action potential was essentially similar in de-sheathed preparations and in intact nerve cords. 4. These results have been discussed in terms of the unequal distribution of ions between the haemolymph, the extracellular fluid and the axoplasm of the giant axons. 5. The low measured resting potential agrees with a K+ concentration in the haemolymph of about 20 mM./l., a value which is only slightly lower than the measured one (Pichon, 1963). 6.The occurrence of large action potentials in these apparently depolarized axons may be related to the stabilizing action of divalent cations such as Ca2+ which are contained in the extracellular fluid in relatively large amounts. 7. The very large recorded overshoots (62.1±7.0 mV.) may be linked with a low sodium concentration in the axoplasm and a high sodium concentration in the extracellular fluid of the giant axons of intact nerve cords, thus resulting in a high sodium equilibrium potential, ENa.

Recurrent Inhibition in the Giant-Fibre System of the Crayfish and Its Effect on the Excitability of the Escape Response

1968 ◽  
Vol 48 (3) ◽  
pp. 545-567
Author(s):  
ALAN ROBERTS
Keyword(s):  
Escape Response ◽  
Time Course ◽  
Excitatory Input ◽  
Recurrent Inhibition ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Giant Fibre ◽  
Impulse Generation ◽  
Giant Axons ◽  
Slow Potentials

1. A single impulse in any one of the central giant fibres of the crayfish is sufficient to evoke a full escape response. 2. Following such a single impulse a search was made for inhibitory processes of similar duration to the driving movement of the escape response. 3. There is no inhibition of flexor motoneurones or muscles to prevent response to impulses in the central giant axons during the escape response. However, following an impulse in any central giant, intracellular recording showed that there is inhibition of excitatory input to the lateral giants in the abdomen. This inhibition suppresses impulse generation for the duration of the escape response. 4. The inhibition coincides with slow, depolarizing potentials in the lateral giants. These have an equilibrium potential between the normal resting potential and the threshold for spike initiation in the lateral giants. During these slow potentials there is a postsynaptic resistance decrease coinciding very closely in time course with the inhibition of excitatory input. The slow potentials are therefore identified as IPSPs (inhibitory postsynaptic potentials) because of their close association with a postsynaptic inhibitory process. This conclusion is endorsed: (a) by the absence of similar slow potentials in the abdominal medial giants which have no excitatory input at this location, and (b) by the diminution of the slow potentials by picrotoxin, a drug known to block inhibition at many crustacean synapses. 5. When evoked repetitively, even at low frequencies like 0.25 per sec, the IPSPs decrease in amplitude. No other ‘after effects’ of repeated activity were found. 6. Attempts to localize the inhibitory synapses are frustrated by the large space constant of the lateral giants. However, the evidence is compatible with the notion that inhibition originates within each abdominal ganglion. There is occlusion and crossed response decrement between the central giant axons evoking lateral giant inhibition. This suggests that the different presynaptic fibres excite some common inhibitory pathway in each ganglion. Further experiments showed that pathways producing inhibition in one ganglion can be excited in others. Interneuronal arrangements to explain properties of the inhibitory pathways are discussed. 7. Two functions are suggested for the recurrent inhibition in the crayfish lateral giants. First, it may limit the number of impulses that are evoked by a single afferent excitatory volley. Secondly, it may coordinate successive escape responses by suppressing impulse generation in the lateral giants during such responses.

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