Mechanisms of depolarizing inhibition at the crayfish giant motor synapse. II. Quantitative reconstruction

1990 ◽  
Vol 64 (2) ◽  
pp. 541-550 ◽  
Author(s):  
D. H. Edwards
Keyword(s):  
Potassium Current ◽  
Sodium Current ◽  
Outward Current ◽  
Resting Potential ◽  
Excitatory Postsynaptic Potential ◽  
Inhibitory Effects ◽  
Inward Current ◽  
Postsynaptic Potential ◽  
Parameter Values ◽  
Outward Potassium Current

1. The relative strengths of four mechanisms of depolarizing synaptic inhibition described in the previous paper were evaluated with an electrical model of the giant motor synapse (GMS) and postsynaptic region of the motor giant motoneuron (MoG). 2. The model consists of one compartment that represents the presynaptic region of the medial giant (MG) interneuron and three compartments that represent the postsynaptic region and proximal axon of the MoG. The presynaptic MG compartment is linked to a postsynaptic MoG compartment by a rectifying conductance that represents the GMS. Each compartment consists of parallel paths to ground for active and/or passive membrane currents. 3. Parameter values of the model were set so the MG compartment would replicate an MG impulse and the MoG compartments would replicate the current-clamp, voltage-clamp, and synaptic responses of a single MoG neuron described in the previous paper. The Hodgkin-Huxley equations described voltage-sensitive sodium and potassium currents. 4. Comparison of the MoG compartment currents that mediate an inhibited excitatory postsynaptic potential (EPSP) [triggered during a depolarizing inhibitory postsynaptic potential (d-IPSP)] with those of an uninhibited EPSP indicate that all four mechanisms have significant inhibitory effects. Reverse bias of the GMS by the d-IPSP reduced the GMS current by 65 nA (12%). The remaining inward current was further reduced by a 243-nA outward current through the inhibitory postsynaptic conductance. The d-IPSP inactivated sodium conductance so the inward sodium current evoked by the EPSP was reduced by 319 nA (-68%). The d-IPSP reduced the latency for potassium activation by the EPSP so that the outward potassium current coincided with the inward sodium current and reduced the net inward current by 100 nA. Together, these mechanisms reduced the EPSP amplitude by 69%. 5. The resting potential of MoG is normally 15 mV more positive than MG rest potential, but in some preparations this difference may be as much as 25 mV or as little as 0 mV. Corresponding differences in the rest potentials of the MoG and MG models have little effect on the amplitude of the model MoG EPSP because changes in the inward synaptic and sodium currents are balanced by corresponding changes in the outward potassium current.

Osmotic effects on the CA1 neuronal population in hippocampal slices with special reference to glucose

1991 ◽  
Vol 65 (5) ◽  
pp. 1055-1066 ◽  
Author(s):  
B. A. Ballyk ◽  
S. J. Quackenbush ◽  
R. D. Andrew
Keyword(s):  
Action Potential ◽  
Single Cell ◽  
Epileptiform Activity ◽  
Hippocampal Slices ◽  
Stratum Radiatum ◽  
Resting Potential ◽  
Excitatory Postsynaptic Potential ◽  
Stratum Pyramidale ◽  
Postsynaptic Potential ◽  
Axonal Excitability

1. Lowered osmolality promotes epileptiform activity both clinically and in the hippocampal slice preparation, but it is unclear how neurons are excited. We studied the effects of altered osmolality on the electrophysiological properties of CA1 pyramidal cells in hippocampal slices by the use of field and intracellular recordings. The excitability of these neurons under various osmotic conditions was gauged by population spike (PS) amplitude, single cell properties, and evoked synaptic input. 2. The orthodromic PS recorded in stratum pyramidale and the field excitatory postsynaptic potential (EPSP) in stratum radiatum were inversely proportional in amplitude to the artificial cerebrospinal fluid (ACSF) osmolality over a range of +/- 80 milliosmoles/kgH2O (mosM). The effect was osmotic because changes occurred within the time frame expected for cellular expansion or shrinkage and because permeable substances such as dimethyl sulfoxide or glycerol were without effect. Dilutional changes in ACSF constituents were experimentally ruled out as promoting excitability. 3. To test whether the field data resulted from a change in single-cell excitability, CA1 cells were intracellularly recorded during exposure to +/- 40 mosM ACSF over 15 min. There was no consistent effect upon CA1 resting potential, cell input resistance, or action potential threshold. 4. Osmotic alteration of orthodromic and antidromic field potentials might involve a change in axonal excitability. However, the evoked afferent volley recorded in CA1 stratum pyramidale or radiatum, which represents the compound action potential (CAP) generated in presynaptic axons, remained osmotically unresponsive with regard to amplitude, duration, or latency. This was also characteristic of CAPs evoked in isolated sciatic and vagus nerve preparations exposed to +/- 80 mosM. Therefore axonal excitability and associated extracellular current flow generated periaxonally are not significantly affected by osmotic shifts. 5. The osmotic effect on field potential amplitudes appeared to be independent of synaptic transmission because the inverse relationship with osmolality held for the antidromically evoked PS. Moreover, as recorded with respect to ground, the intracellular EPSP-inhibitory postsynaptic potential (IPSP) sequence (evoked from CA3 stratum radiatum) was not altered by osmolality. 6. The PS could occasionally be recorded intracellularly as a brief negativity interrupting the evoked EPSP. In hyposmotic ACSF, the amplitude increased and action potentials arose from the trough of the negativity as expected for a field effect. This is presumably the result of enhanced intracellular channeling of current caused by the increased extracellular resistance that accompanies cellular swelling.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Ionic Basis of Membrane Potential and of Acetylcholine-evduced Currents in the Cell Body of the Cockroach Fast Coxal Depressor Motor Neurone

1990 ◽  
Vol 151 (1) ◽  
pp. 21-39 ◽  
Author(s):  
JONATHAN A. DAVID ◽  
DAVID B. SATTELLE
Keyword(s):  
Cell Body ◽  
Outward Current ◽  
Motor Neurone ◽  
Resting Potential ◽  
Inward Current ◽  
Current Voltage ◽  
Low K ◽  
Current Voltage Relationship ◽  
Ionic Basis ◽  
Voltage Relationship

The ionic basis of the resting potential and of the response to acetylcholine (ACh) has been investigated in the cell body membrane of the fast coxal depressor motor neurone in the metathoracic ganglion of the cockroach Periplaneta americana. By means of ion-sensitive microelectrodes, intracellular concentrations of three ion species were estimated (mmoll−1): [K+]i, 1443; [Na+]i, 9±1; [Cl−], 7±1. The resting potential of continuously superfused cells was −75.6±1.9mV at 22° C. A change in resting potential of 42.0±2.5mV accompanied a decade change in [K+]o. Experiments with (10−4moll−1) ouabain, Na+ injection, low temperature (10°C) and non-superfused cells indicated the presence of an electrogenic sodium pump. Under current-clamp, the cell body membrane was depolarized by sequentially applied, ionophoretic pulses (500ms duration) of ACh. Under voltage-clamp, such doses of ACh resulted in an inward current which was abolished in low-Na+ saline. Ion-sensitive electrodes revealed an increase in [Na+]i but no change in [Cl−1]j in response to externally applied ACh. The ACh-induced current-voltage relationship was shifted in a negative direction by low-K+ saline. The AChinduced inward current was usually followed by a delayed outward current which reversed at Ek. Low-K+ saline had the same effect on this outward component as depolarizing the membrane. This suggests that the outward current component is carried by K+. The ACh-induced inward current and the delayed outward current were potentiated either when [Ca2+]i was lowered by injecting the calcium chelator BAPTA or by exposure of the cell to low-Ca2+ saline. High-Ca2+ saline reduced the inward component of the response and produced a negative shift in the AChinduced current-voltage relationship. The amplitude of the delayed outward

scholarly journals Membrane Currents in Mammalian Ventricular Heart Muscle Fibers Using a Voltage-Clamp Technique

1971 ◽  
Vol 57 (3) ◽  
pp. 290-296 ◽  
Author(s):  
Gerhard Giebisch ◽  
Silvio Weidmann
Keyword(s):  
Action Potential ◽  
Outward Current ◽  
Time Dependent ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Initial Amplitude ◽  
Inward Current ◽  
Gap Technique ◽  
Sucrose Gap

Bundles of sheep ventricular fibers were voltage-clamped utilizing a modified sucrose gap technique and intracellular voltage control. An action potential was fired off in the usual way, and the clamp circuit was switched on at preselected times during activity. Clamping the membrane back to its resting potential during the early part of an action potential resulted in a surge of inward current. The initial amplitude of this current surge decreased as the clamp was switched on progressively later during the action potential. Inward current decreasing as a function of time was also recorded if the membrane potential was clamped beyond the presumed K equilibrium potential (to -130 mv). Clamping the membrane to the inside positive range (+40 mv to +60 mv) at different times of an action potential resulted in a step of outward current which was not time-dependent. The results suggest that normal repolarization of sheep ventricle depends on a time-dependent decrease of inward current (Na, Ca) rather than on a time-dependent increase of outward current (K).

Two electrophysiologically distinct types of cultured pacemaker cells from rabbit sinoatrial node

1986 ◽  
Vol 250 (2) ◽  
pp. H325-H329 ◽  
Author(s):  
R. D. Nathan
Keyword(s):  
Sinoatrial Node ◽  
Sodium Current ◽  
Outward Current ◽  
Slow Inward Current ◽  
Transient Outward Current ◽  
Type I ◽  
Pacemaker Cells ◽  
Inward Current ◽  
Fast Transient

Previous investigations employing multicellular nodal preparations (i.e., mixtures of dominant and subsidiary pacemaker cells) have suggested that the fast transient inward sodium current (iNa) either is not present in dominant pacemaker cells or is present but inactivated at the depolarized take-off potentials that these cells exhibit. In the present study, this question was resolved by voltage clamp analysis of single pacemaker cells isolated from the sinoatrial node and maintained in vitro for 1-3 days. Two types of cells, each with a different morphology, exhibited two modes of electrophysiological behavior. Type I cells (presumably dominant pacemakers) displayed only a tetrodotoxin (TTX)-resistant (but cadmium-sensitive) slow inward current, whereas type II cells (presumably subsidiary pacemakers) exhibited two components of inward current, a TTX-sensitive, fast transient inward current and a TTX-resistant (but cadmium-sensitive) slow inward current. Three other voltage-gated currents, 1) a slowly developing inward current activated by hyperpolarization (if, ih, delta ip), 2) a transient outward current activated by strong depolarization (ito, iA), and 3) a delayed outward current, were recorded in both types of pacemaker cells.

Transient outward current contributes to Wenckebach-like rhythms in isolated rabbit ventricular cells

1997 ◽  
Vol 273 (1) ◽  
pp. H1-H11 ◽  
Author(s):  
A. R. Yehia ◽  
A. Shrier ◽  
K. C. Lo ◽  
M. R. Guevara
Keyword(s):  
Action Potential ◽  
Potassium Current ◽  
Phase 1 ◽  
Outward Current ◽  
Transient Outward Current ◽  
Ionic Model ◽  
Recovery Interval ◽  
Ventricular Cells ◽  
Outward Potassium Current ◽  
Phase Phase

Wenckebach-like rhythms in isolated rabbit ventricular cells are characterized by beat-to-beat increments in action potential duration (APD) and latency, giving rise to a beat-to-beat decrease in the recovery interval and culminating in a skipped beat. These systematic APD changes are associated with a beat-to-beat decrease in the slope of the early repolarizing phase (phase 1) of the action potential, which is partially controlled by the transient outward potassium current (Ito). When Ito is blocked with 4-aminopyridine, periodic Wenckebach rhythms are replaced by aperiodic Wenckebach rhythms, in which the beat-to-beat changes in the slope of phase 1 and in APD disappear but the beat-to-beat increase in latency remains. A beat-to-beat decrease in Ito, paralleling the beat-to-beat changes in the slope of phase 1 and in APD, is seen in action-potential clamp experiments with Wenckebach rhythms previously recorded in the same cell. Simulations with an ionic model of Ito show cyclical changes in Ito consistent with the experimental data. These results demonstrate a key role for Ito in the generation of maintained periodic Wenckebach rhythms in isolated rabbit ventricular cells.

Analysis of voltage-dependent membrane currents in spatially extended neurons from point-clamp data

1993 ◽  
Vol 69 (1) ◽  
pp. 241-247 ◽  
Author(s):  
W. Muller ◽  
H. D. Lux
Keyword(s):  
Voltage Dependence ◽  
Outward Current ◽  
Resting Potential ◽  
Inward Current ◽  
Outward Currents ◽  
Current Voltage ◽  
Voltage Dependent ◽  
Spatially Extended ◽  
Model Cell ◽  
Space Constant

1. Numerical methods were used to evaluate voltage space-clamp performance in the investigation of a voltage-dependent inward current similar to the noninactivating Ca current. In addition, the cell is equipped with a repolarizing system, represented by leak and outwardly rectifying outward conductances. The electrotonically compact model cell is represented by a cable with an electrotonic length of 1 space constant under control conditions, but that becomes effectively only 0.33 space constants during a 90% reduction of the leak and outward conductance. The cable is perfectly voltage clamped at one end. 2. The apparent voltage dependence, activation, and inactivation of the clamp current depend on the distribution of the membrane slope conductance along the cable; this depends on 1) the distribution of the inward current along the cable and 2) the amplitude of the inward current relative to the amplitudes of the leak and voltage-dependent outward currents. 3. Under control conditions, the membrane voltage decays steeply with distance from the command voltage at the clamp site to almost resting potential for most of the rest of the cable. This is because the leak and outward current are dominant over the inward current. The inward current is activated primarily at the clamped part of the cable. Clamp currents are activated instantaneously. The clamp-current current-voltage (I-V) relation is less steep with depolarization because the membrane potential for locations away from the clamp site lags behind the clamp potential. 4. When the conductances for leak and outward current are reduced by 90%, these conductances lose their dominance. The membrane slope conductance now has a range with negative values.(ABSTRACT TRUNCATED AT 250 WORDS)

Characterization of a muscarinic current that regulates excitability of an identified insect motoneuron

1994 ◽  
Vol 72 (4) ◽  
pp. 1862-1873 ◽  
Author(s):  
B. A. Trimmer
Keyword(s):  
Action Potentials ◽  
Acetylcholine Receptors ◽  
Divalent Cations ◽  
Muscarinic Acetylcholine Receptors ◽  
Resting Potential ◽  
Excitatory Postsynaptic Potential ◽  
Muscarinic Agonist ◽  
Complete Replacement ◽  
Inward Current ◽  
K Concentration

1. Application of the muscarinic agonist oxotremorine-M (oxo-M) to isolated abdominal ganglia of larval Manduca sexta excited an identified proleg retractor motoneuron called PPR. This excitation consisted of a persistent depolarization and an increased tendency to generate action potentials. Previous work has established that the action of oxo-M is probably mediated by muscarinic acetylcholine receptors (mAChRs) on PPR and that oxo-M mimics an afferent-induced long-lasting depolarization called the slow excitatory postsynaptic potential (sEPSP). 2. Action potentials in the ganglion could be blocked by applying tetrodotoxin (TTX) in the bath saline. Under these conditions all excitatory postsynaptic potentials in PPR were also blocked, but the depolarizing action of oxo-M was unaffected. In the absence of background activity PPR could be voltage clamped using a single-electrode switching clamp to study the currents underlying the response to oxo-M. 3. At a membrane potential of -50 mV, application of oxo-M to the ganglion in the bath saline (3-6 x 10(-7) M) or by brief (20–40 ms) pulses from a micropipette into the neuropil (1 x 10(-5) M) evoked an apparently inward current called Iox. The mean peak current change in response to pulses was -0.80 +/- 0.04 nA (n = 48 preparations). 4. The voltage dependence of Iox was determined by subtracting the current-voltage relationship for PPR in control saline from that during a response to oxo-M. Iox was maximal near the resting potential of PPR (-45 to -40 mV), decreasing slightly with hyperpolarization and strongly with depolarization. 5. Peak Iox was directly dependent on the bath Na+ concentration. Complete replacement of Na+ with N-methyl-D-glucamine in the saline blocked Iox. Changes in the bath K+ concentration (extracellular K+ concentration, [K+]o) had only a small effect on Iox. Reducing [Cl-]o from 140 to 74.5 mM had no significant effect on Iox during a 15-min exposure. Intracellular injections of Cl- from a KCl-containing electrode also had no measurable effect on Iox. 6. Changes in the bath Ca2+ concentration above or below 2 mM inhibited Iox. Furthermore, the divalent cations Ni2+, Co2+, Mg2+, and Ba2+ at millimolar concentrations and the Ca2+ channel blocking agents nifedipine and Cd2+ at micromolar concentrations inhibited Iox. 7. These results suggest that mAChRs on PPR activate an inward current that is persistent, TTX insensitive, voltage dependent and carried predominantly by Na+. However, the results cannot eliminate the possibility that changes in K+ or Cl- conductances might also be involved.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Synaptic and voltage-gated currents in interplexiform cells of the tiger salamander retina.

1990 ◽  
Vol 95 (4) ◽  
pp. 755-770 ◽  
Author(s):  
G Maguire ◽  
P Lukasiewicz ◽  
F Werblin
Keyword(s):  
Potassium Current ◽  
Lucifer Yellow ◽  
Sodium Current ◽  
Plexiform Layer ◽  
Membrane Properties ◽  
Inner Plexiform Layer ◽  
Synaptic Inputs ◽  
Voltage Gated ◽  
Whole Cell Patch Clamp ◽  
Outward Potassium Current

We have correlated the membrane properties and synaptic inputs of interplexiform cells (IPCs) with their morphology using whole-cell patch-clamp and Lucifer yellow staining in retinal slices. Three morphological types were identified: (a) a bistratified IPC with descending processes ramifying in both sublaminas a and b of the inner plexiform layer (IPL), and an ascending process that branched in the outer plexiform layer (OPL) and originated from the soma, (b) another bistratified IPC with descending processes ramifying in both sublaminas a and b, and an ascending process that branched in the OPL and originated directly from IPC processes in the IPL, and (c) a monostratified IPC with a descending process ramifying over large lateral extents within the most distal stratum of the IPL, and sending an ascending process to the OPL with little branching. Similar voltage-gated currents were measured in all three types including: (a) a transient inward sodium current, (b) an outward potassium current, and (c) an L-type calcium current. All cells generated multiple spikes with frequency increasing monotonically with the magnitude of injected current. The IPCs that send their descending processes into both sublaminas of the IPL (bistratified) receive excitatory synaptic inputs at both light ON and OFF that decay with a time constant of approximately 1.3 s. Slowly decaying excitation at both ON and OFF suggests that bistratified IPCs may spike continuously in the presence of a dynamic visual environment.

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