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.

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.

scholarly journals Current Separations in Myxicola Giant Axons

1969 ◽  
Vol 54 (6) ◽  
pp. 741-754 ◽  
Author(s):  
L. Goldman ◽  
L. Binstock
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Reversal Potential ◽  
Transient Current ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Concentration Data ◽  
Giant Axons ◽  
Current Reversal

The effect of reducing the external sodium concentration, [Na]o, on resting potential, action potential, membrane current, and transient current reversal potential in Myxicola giant axons was studied. Tris chloride was used as a substitute for NaCl. Preliminary experiments were carried out to insure that the effect of Tris substitution could be attributed entirely to the reduction in [Na]o. Both choline and tetramethylammonium chloride were found to have additional effects on the membrane. The transient current is carried largely by Na, while the delayed current seems to be independent of [Na]o. Transient current reversal potential behaves much like a pure Nernst equilibrium potential for sodium. Small deviations from this behavior are consistent with the possibility of some small nonsodium component in the transient current. An exact PNa/PK for the transient current channels could not be computed from these data, but is certainly well greater than unity and possibly quite large. The peak of the action potential varied with [Na]o as expected for a sodium action potential with some substantial potassium permeability at the time of peak. Resting membrane potential is independent of [Na]o. This finding is inconsistent with the view that the resting membrane potential is determined only by the distribution of K and Na, and PNa/PK. It is suggested that PNa/PK's obtained from resting membrane potential-potassium concentration data do not always have the physical meaning generally attributed to them.

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.

scholarly journals Time Course of TEA+-Induced Anomalous Rectification in Squid Giant Axons

1966 ◽  
Vol 50 (2) ◽  
pp. 491-503 ◽  
Author(s):  
Clay M. Armstrong
Keyword(s):  
Time Course ◽  
Sea Water ◽  
Resting Potential ◽  
Tetraethylammonium Chloride ◽  
Giant Axons ◽  
Interesting Conclusion ◽  
Simple Kinetic Model ◽  
K Current ◽  
Current Record ◽  
External K

Changes in the voltage clamp currents of squid giant axons wrought by low axoplasmic TEA+ (tetraethylammonium chloride) concentrations (0.3 mM and above) are described. They are: (a) For positive steps from the resting potential in sea water, the K+ current increases, decreases, then increases, instead of increasing monotonically. (b) For positive steps from the resting potential in 440 mM external K+, the current has an exponentially decaying component, whose decay rate increases with axoplasmic [TEA+]. The control currents increase monotonically. (c) For negative steps from the resting potential in 440 mM external K+, the current record has a peak followed by a decay that is slow relative to the control. The control record decreases monotonically. Qualitatively these findings can be described by a simple kinetic model, from which, with one assumption, it is possible to calculate the rate at which K+ ions move through the K+ channels. An interesting conclusion from (c) is that the channels cannot be closed by the normal voltage-sensitive mechanism (described by Hodgkin and Huxley) until they are free of TEA+.

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.

Relative contributions of passive equilibrium and active transport to the distribution of chloride in mammalian cortical neurons

1988 ◽  
Vol 60 (1) ◽  
pp. 105-124 ◽  
Author(s):  
S. M. Thompson ◽  
R. A. Deisz ◽  
D. A. Prince
Keyword(s):  
Time Constant ◽  
Cortical Neurons ◽  
Time Course ◽  
Chloride Concentration ◽  
Reversal Potential ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Gamma Aminobutyric Acid ◽  
The Mean ◽  
Mean Time

1. Active and passive factors affecting the chloride gradient of cortical neurons were assessed using intracellular recordings from neurons in slices of cingulate cortex maintained in vitro. The chloride equilibrium potential (ECl-) was estimated indirectly from the reversal potentials of responses to perisomatic gamma-aminobutyric acid (GABA) application and the Cl(-)-dependent inhibitory postsynaptic potential (IPSP). Under control conditions the mean resting potential (Vm; -69.7 mV) was not significantly different than the mean IPSP reversal potential (EIPSP; -70.1 mV). 2. Increasing the external potassium concentration ([K+]o) from 1 to 10 mM shifted the mean EIPSP from -80.4 to -61.8 mV. The mean EIPSP was approximately equal to the mean Vm at all [K+]oS. The conditions of Donnan equilibrium are not met in [K+]o less than 10 mM. 3. Polarization of Vm up to 20 mV away from EIPSP for 4 min with maintained current injection had no significant effect on EIPSP. 4. The GABA reversal potential was maintained 37-52 mV less negative than Vm after equilibration in saline in which the external chloride concentration had been reduced from 133 to 5 mM by substitution with isethionate. Vm and input resistance were not significantly different from control values in cells recorded under these conditions. 5. We conclude that Cl- is not passively distributed in cortical neurons, perhaps due to a low resting Cl- permeability. 6. Impalement with electrodes containing 2 M KCl resulted in a rapid 10 mV depolarizing shift in EIPSP that then remained relatively constant. Intracellular iontophoresis of Cl- resulted in a further depolarizing shift of EIPSP of 5-10 mV that returned to control in less than 1 min. The time course of recovery of IPSP amplitude could be fit with a single exponential having a mean time constant of 6.9 +/- 1.5 s and was independent of the amount of Cl- injected or stimulation frequency. 7. Reductions in temperature from 37 to 32 degrees C significantly increased the mean time constant of IPSP recovery from Cl- injection to 11.1 +/- 3.3 s, corresponding to Q10 = 2.6.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Activation-inactivation of potassium channels and development of the potassium-channel spike in internally perfused squid giant axons.

1981 ◽  
Vol 78 (1) ◽  
pp. 43-61 ◽  
Author(s):  
I Inoue
Keyword(s):  
Potassium Channels ◽  
Potassium Channel ◽  
Voltage Clamp ◽  
Time Constant ◽  
Equilibrium Potential ◽  
Giant Axons ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Time Courses ◽  
Calcium Permeability

A spike that is the result of calcium permeability through potassium channels was separated from the action potential is squid giant axons internally perfused with a 30 mM NaF solution and bathed in a 100 mM CaCl2 solution by blocking sodium channels with tetrodotoxin. Currents through potassium channels were studied under voltage clamp. The records showed a clear voltage-dependent inactivation of the currents. The inactivation was composed of at least two components; one relatively fast, having a time constant of 20--30 ms, and the other very slow, having a time constant of 5--10 s. Voltage clamp was carried out with a variety of salt compositions in both the internal and external solutions. A similar voltage-dependent inactivation, also composed of the two components, was recognized in all the current through potassium channels. Although the direction and intensity of current strongly depended on the salt composition of the solutions, the time-courses of these currents at corresponding voltages were very similar. These results strongly suggest that the inactivation of the currents in attributable to an essential, dynamic property of potassium channels themselves. Thus, the generation of a potassium-channel spike can be understood as an event that occurs when the equilibrium potential across the potassium channel becomes positive.

Is cyclic guanosine monophosphate the internal 'second messenger' for cholinergic actions on central neurons?

1976 ◽  
Vol 54 (2) ◽  
pp. 172-176 ◽  
Author(s):  
K. Krnjević ◽  
E. Puil ◽  
R. Werman
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Resting Potential ◽  
Electrical Excitability ◽  
Spinal Motoneurons ◽  
Central Neurons ◽  
Intracellular Cgmp ◽  
Post Synaptic Potential

The most consistent effects produced by intracellular injections of guanosine 3′,5′-cyclic monophosphate (cGMP) (but not 5′-guanosine 5′-monophosphate in spinal motoneurons of cats are a rise in membrane conductance, acceleration in time course of spike potentials, and accentuation of the post-spike hyperpolarization. Associated changes in resting potential are smaller, less constant, and more often in the depolarizing than hyperpolarizing direction. cGMP tends to increase electrical excitability but reduces excitatory post-synaptic potential amplitudes. Most of the effects of intracellular cGMP are quite different from, or indeed opposite to, those of either extra- or intracellular applications of acetylcholine and therefore not consistent with the proposal that cGMP is the internal mediator of muscarinic actions.

Inward rectification in rat nucleus accumbens neurons

1989 ◽  
Vol 62 (6) ◽  
pp. 1280-1286 ◽  
Author(s):  
N. Uchimura ◽  
E. Cherubini ◽  
R. A. North
Keyword(s):  
Steady State ◽  
Nucleus Accumbens ◽  
Time Course ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Potential Range ◽  
Inward Current ◽  
Rat Nucleus Accumbens

1. Intracellular recordings were made from neurons in slices cut from the rat nucleus accumbens septi. Membrane currents were measured with a single-electrode voltage-clamp amplifier in the potential range -50 to -140 mV. 2. In control conditions (2.5 mM potassium), the resting membrane potential of the neurons was -83.4 +/- 1.1 (SE) mV (n = 157). Steady state membrane conductance was voltage dependent, being 34.8 +/- 1.7 nS (n = 25) at -100 mV and 8.0 +/- 0.7 nS (n = 25) at -60 mV. 3. Barium (1 microM) markedly reduced the inward rectification and caused a small inward current (40.6 +/- 8.7 pA, n = 8) at the resting potential. These effects became larger with higher barium concentrations, and, in 100 microM barium, the current-voltage relation was straight. 4. The block of the inward current by barium (at -130 mV) occurred with an exponential time course; the time constant was approximately 1 s at 1 microM barium and less than 90 ms with 100 microM. Strontium had effects similar to those of barium, but 1000-fold higher concentrations were required. Cesium chloride (2 mM) and rubidium chloride (2 mM) also blocked the inward rectification; their action reached steady state within 50 ms. 5. It is concluded that the nucleus accumbens neurons have a potassium conductance with many features of a typical inward rectifier and that this contributes to the potassium conductance at the resting potential.

A delayed rectifier conductance in type I hair cells of the mouse utricle

1996 ◽  
Vol 76 (2) ◽  
pp. 995-1004 ◽  
Author(s):  
A. Rusch ◽  
R. A. Eatock
Keyword(s):  
Hair Cells ◽  
Time Course ◽  
Dissociation Constants ◽  
Resting Potential ◽  
Delayed Rectifier ◽  
Type I ◽  
Type Ii ◽  
Voltage Range ◽  
Average Maximum

1. Membrane currents of hair cells in acutely excised or cultured mouse utricles were recorded with the whole cell voltage-clamp method at temperatures between 23 and 36 degrees C. 2. Type I and II hair cells both had delayed rectifier conductances that activated positive to -55 mV. 3. Type I, but not type II, hair cells had an additional delayed rectifier conductance (gK,L) with an activation range that was unusually negative and variable. At 23-25 degrees C, V(1/2) values ranged from -88 to -62 mV in 57 cells. 4. gK,L was very large. At 23-25 degrees C, the average maximum chord conductance was 75 +/- 65 nS (mean +/- SD, n = 57; measured at -54 mV), or approximately 21 nS/pF of cell capacitance. 5. gK,L was highly selective for K+ over Na+ (permeability ratio PNa+/PK+:0.006), but unlike other delayed rectifiers, gK,L was significantly permeable to Cs+ (PCs+/PK+:0.31). gK,L was independent of extracellular Ca2+. 6. At -64 mV, Ba2+ and 4-aminopyridine blocked gK,L with apparent dissociation constants of 2.0 mM and 43 microM, respectively. Extracellular Cs+ (5 mM) blocked gK,L by 50% at -124 mV. Apamin (100 nM) and dendrotoxin (10 nM) has no effect. 7. The kinetic data of gK,L are consistent with a sequential gating model with at least two closed states and one open state. The slow activation kinetics (principal time constants at 23-25 degrees C:600-200 ms) had a thermal Q10 of 2.1. Inactivation (Q10:2.7) was partial at all temperatures. Deactivation followed a double-exponential time course and had a Q10 of 2.0. 8. At 23-25 degrees C, gK,L was appreciably activated at the mean resting potential of type I hair cells (-77 +/- 3.1 mV, n = 62), so that input conductances were often more than an order of magnitude larger than those of type II cells. If these conditions hold in vivo, type I cells would produce unusually small receptor potentials. Warming the cells to 36 degrees C produced parallel shifts in gK,L's activation range (0.8 +/- 0.3 mV/degrees C, n = 8), and in the resting potential (0.6 +/- 0.3 mV/degrees C, n = 4). Thus the high input conductances were not an artifact of unphysiological temperatures but remained high near body temperature. It remains possible that in vivo gK,L's activation range is less negative and input conductances are lower; the large variance in the voltage range of activation suggests that it may be subject to modulation.

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