scholarly journals Ionic Mechanism of Thermoreception in Paramecium

1987 ◽  
Vol 127 (1) ◽  
pp. 95-103 ◽  
Author(s):  
YASUO NAKAOKA ◽  
TOHRU KUROTANI ◽  
HIROKAZU ITOH
Keyword(s):  
Transverse Section ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Constant Current ◽  
Transient Change ◽  
Calcium Dependent ◽  
Posterior Fragment ◽  
Ionic Basis ◽  
Reversal Potentials

The localization of thermoreceptors in Paramecium, and the ionic basis of thermoreception, was investigated in posterior and anterior fragments of cells. Transverse section of the animals was used to obtain these fragments, which sealed up and swam actively. In the anterior fragment, an increase in the frequency of directional changes in swimming and depolarization of the membrane was produced by cooling below the temperature of the culture. In the posterior fragment, these effects were produced by wanning above culture temperature. Reversal potentials of these effects were found by injection of constant current to change membrane potential. In the anterior fragment, the reversal potential of the response to cooling was more negative than the resting potential and was potassium-dependent (52 mV/log[K+]o). In the posterior fragment, the reversal potential of the warming response was above resting potential and was primarily calcium-dependent (28 mV/log[Ca2+]o). It is concluded that cooling results in changes in the frequency of directional changes in swimming of Paramecium by causing a transient change in the membrane conductance for potassium, whereas warming produces its effects by a transient change in calcium conductance.

Serotonin has different effects on two classes of Betz cells from the cat

1994 ◽  
Vol 72 (4) ◽  
pp. 1925-1937 ◽  
Author(s):  
W. J. Spain
Keyword(s):  
Firing Rate ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Constant Current ◽  
Repetitive Firing ◽  
Calcium Dependent ◽  
Constant Current Stimulation ◽  
Ionic Mechanisms ◽  
Betz Cells

1. Intracellular recording from cat Betz cells in vitro revealed a strong correlation between the dominant effect of serotonin (5-HT) and the Betz cell subtype in which it occurred. In large Betz cells that show posthyperpolarization excitation (termed PHE cells), 5-HT evoked a long-lasting membrane depolarization, whereas 5-HT evoked an initial hyperpolarization of variable duration in smaller Betz cells that show posthyperpolorization inhibition (termed PHI cells). 2. Voltage-clamp studies revealed that 5-HT caused a depolarizing shift of activation of the cation current Ih, which resulted in the depolarization in PHE cells, whereas the hyperpolarization in PHI cells is caused by an increase in a resting potassium conductance. 3. The effect of 5-HT on firing properties during constant current stimulation also differed consistently in the two types of Betz cells. In PHE cells the initial firing rate increased after 5-HT application, but the steady firing was unaffected. The depolarizing shift of Ih activation caused the increase of initial firing rate. 4. In PHI cells 5-HT caused a decrease in spike frequency adaptation. The decrease in adaptation was caused by a combination of two conductance changes. First, 5-HT caused a slow afterdepolarization in PHI cells that could trigger repetitive firing in the absence of further stimulation. The sADP depended on calcium entry through voltage-gated channels and was associated with a decrease in membrane conductance. Second, 5-HT caused reduction of a slow calcium-dependent potassium current that normally contributes to slow adaptation. 5. In conclusion, the effect of 5-HT on excitability differs systematically in Betz cell subtypes in part because they have different dominant ionic mechanisms that are modulated. If we assume that PHE cells and PHI cells represent fast and slow pyramidal tract (PT) neurons respectively, 5-HT will cause early recruitment of fast PT cells and delay recruitment of slow PT cells during low levels of synaptic excitation.

TRH-induced membrane hyperpolarization in rat clonal anterior pituitary cells

1985 ◽  
Vol 248 (1) ◽  
pp. E64-E69
Author(s):  
S. Ozawa
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Gh3 Cells ◽  
Ionophore A23187 ◽  
Pituitary Cells ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
The Relationship ◽  
Reversal Potentials

Thyrotropin-releasing hormone (TRH) induces biphasic membrane potential changes, a transient hyperpolarization followed by a prolonged enhancement of the generation of action potentials in the clonal GH3 pituitary cell. The nature of the TRH-induced hyperpolarization was studied in Cl--free solutions. Among various test substances, only TRH and its analogue, which stimulates the release of prolactin from the GH3 cells, were capable of inducing the transient membrane hyperpolarization. The Ca2+ ionophore A23187 also caused a transient hyperpolarization accompanied by an increase in the membrane conductance, although it failed to mimic the late facilitation of spike generation. The reversal potential of the TRH-induced hyperpolarization was identical with that induced by A23187. Reduction of the K+ concentration of the bathing medium caused a similar shift of both these reversal potentials toward a more hyperpolarized level. Injection of the Ca2+-chelator EGTA into the cell suppressed both TRH and Ca2+ ionophore-induced hyperpolarizations. These results suggest that TRH mobilizes the cellular-bound Ca, which in turn activates Ca2+-mediated K+ channels, thus causing the transient membrane hyperpolarization. The relationship between the membrane hyperpolarization and the TRH-stimulated hormone release is discussed.

K+-channel blockers do not decrease acetylcholine depolarizations in canine trachealis

1992 ◽  
Vol 70 (1) ◽  
pp. 43-52 ◽  
Author(s):  
E. E. Daniel ◽  
J. Jury ◽  
R. Serio ◽  
L. P. Jager
Keyword(s):  
Chloride Channels ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Resting Potential ◽  
K Channel ◽  
Channel Blockers ◽  
Membrane Effects ◽  
Sucrose Gap ◽  
Time Courses

Using the double sucrose gap, we have examined the role of K+ channels in the cholinergic depolarizations in response to field stimulation and acetylcholine (Ach) in canine trachealis. Acetylcholine-like depolarization per se decreased electrotonic potentials from hyperpolarizing currents. The net effect of acetylcholine (10−6 M) depolarization on membrane conductance was a small increase after the depolarization was compensated by current clamp. Reversal potentials for acetylcholine depolarization and for the excitatory junction potential (EJP) were determined by extrapolation to be 20–30 mV positive to the resting potential, previously shown to be approximately −55 mV. They were shifted positively by tetraethylammonium ion (TEA) at 20 mM or Ba2+ at 1 mM. TEA or Ba2+ initially depolarized the membrane and increased membrane resistance. Repolarization of the membrane restored any reductions in EJP amplitudes associated with depolarization. After 15 min, the membrane potential partially repolarized, and acetylcholine-induced depolarization and contractions were then increased by TEA. 4-Aminopyridine depolarized the membrane but decreased membrane resistance. Apamin (10−6 M), charybdotoxin (10−7 M), and glybenclamide (10−5 M) each failed to significantly depolarize membranes, increase membrane resistance, or reduce EJP amplitudes or depolarization to 10−6 M Ach. Glybenclamide reduced depolarizations to added acetylcholine slightly. TEA occasionally reduced the EJP markedly, but this was shown to be most likely a prejunctional effect mediated by norepinephrine release. TEA alone among K+-channel blockers slowed the onset and the time courses of the EJP as well as the acetylcholine-induced depolarization. K+-channel closure cannot be a complete explanation of acetylcholine-induced membrane effects on this tissue. Acetylcholine must have increased the conductance of an ion with a reversal potential positive to the resting potential in addition to any effect to close K+ channels.Key words: acetylcholine, tracheal smooth muscle, trachea, chloride channels, sucrose gap, potassium channels, tetraethylammonium, Ba2+.

scholarly journals The light-sensitive conductance of hyperpolarizing invertebrate photoreceptors: a patch-clamp study.

1994 ◽  
Vol 103 (6) ◽  
pp. 939-956 ◽  
Author(s):  
M P Gomez ◽  
E Nasi
Keyword(s):  
Single Channel ◽  
Light Stimulus ◽  
Divalent Cations ◽  
Reversal Potential ◽  
Outward Current ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Light Stimulation ◽  
Positive Direction ◽  
Single Channel Currents

Tight-seal recording was employed to investigate membrane currents in hyperpolarizing ciliary photoreceptors enzymatically isolated from the eyes of the file clam (Lima scabra) and the bay scallop (Pecten irradians). These two organisms are unusual in that their double retinas also possess a layer of depolarizing rhabdomeric cells. Ciliary photoreceptors from Lima have a rounded soma, 15-20 microns diam, and display a prominent bundle of fine processes up to 30 microns long. The cell body of scallop cells is similar in size, but the ciliary appendages are modified, forming small spherical structures that protrude from the cell. In both species light stimulation at a voltage near the resting potential gives rise to a graded outward current several hundred pA in amplitude, accompanied by an increase in membrane conductance. The reversal potential of the photocurrent is approximately -80 mV, and shifts in the positive direction by approximately 39 mV when the concentration of extracellular K is increased from 10 to 50 mM, consistent with the notion that light activates K-selective channels. The light-activated conductance increases with depolarization in the physiological range of membrane voltages (-30 to -70 mV). Such outward rectification is greatly reduced after removal of divalent cations from the superfusate. In Pecten, cell-attached recordings were also obtained; in some patches outwardly directed single-channel currents could be activated by light but not by voltage. The unitary conductance of these channels was approximately 26 pS. Solitary ciliary cells also gave evidence of the post stimulus rebound, which is presumably responsible for initiating the "off" discharge of action potentials at the termination of a light stimulus: in patches containing only voltage-dependent channels, light stimulation suppressed depolarization-induced activity, and was followed by a strong burst of openings, directly related to the intensity of the preceding photostimulation.

scholarly journals Light Response of a Giant Aplysia Neuron

1973 ◽  
Vol 62 (3) ◽  
pp. 239-254 ◽  
Author(s):  
Arthur M. Brown ◽  
H. Mack Brown
Keyword(s):  
Reversal Potential ◽  
Outward Current ◽  
Membrane Conductance ◽  
Light Response ◽  
Resting Potential ◽  
Neuronal Membrane ◽  
Giant Neuron ◽  
Membrane Hyperpolarization ◽  
Pressure Injection ◽  
External K

Illumination of an Aplysia giant neuron evokes a membrane hyperpolarization which is associated with a membrane conductance increase of 15%. The light response is best elicited at 490 nM: the neuron also has an absorption peak at this wavelength. At the resting potential (-50 to -60 mV) illumination evokes an outward current in a voltage-clamped cell. This current reverses sign very close to EK calculated from direct measurements of internal and external K+ activity. Increases in external K+ concentration shift the reversal potential of the light-evoked response by the same amount as the change in EK. Decreases in external Na+ or Cl- do not affect the response. Therefore, the response is attributed to an increase in K+ conductance. Pressure injection of Ca2+ into this neuron also hyperpolarizes the cell membrane. This effect is also due largely to an increase in K+ conductance. The light response after Ca2+ injection does not appear to be altered. Pressure injection of EGTA abolished or greatly reduced the light response. The effect was reversible. We suggest that light acts upon a single pigment in this neuron, releasing Ca2+ which in turn increases K+ conductance, thereby hyperpolarizing the neuronal membrane.

GABA and glycine actions on spinal motoneurons

1977 ◽  
Vol 55 (3) ◽  
pp. 658-669 ◽  
Author(s):  
K. Krnjević ◽  
E. Puil ◽  
R. Werman
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Aminobutyric Acid ◽  
Spinal Motoneurons ◽  
Peak Ratio ◽  
Positive Direction ◽  
Single Process ◽  
Site Of Action ◽  
Early Peak ◽  
Reversal Potentials

Applied microiontophoretically in the spinal cord of cats, glycine is consistently more powerful than γ-aminobutyric acid (GABA) in raising the membrane conductance of lumbosacral motoneurons (mean ratio of equipotent iontophoretic currents tested on same cells is 5.6:1). This is the reverse of the situation in cerebral cortex. The effect of glycine is well maintained during applications lasting about 1 min, but that of GABA, after an early peak, drops to a much lower plateau (mean plateau-over-peak ratio is 0.23). The reversal potentials for the action of GABA and glycine are initially similar but they behave differently during a prolonged application; that for glycine usually remains constant or becomes more negative whereas that for GABA tends to shift in the positive direction. Various explanations of these phenomena are considered. It is suggested that a single process, electrogenic uptake of GABA, may account for both desensitization (by removing GABA from its site of action) and the positive shift in GABA reversal potential (because uptake is probably associated with an influx of Na+).

scholarly journals Shunting Inhibition Does Not Have a Divisive Effect on Firing Rates

1997 ◽  
Vol 9 (5) ◽  
pp. 1001-1013 ◽  
Author(s):  
Gary R. Holt ◽  
Christof Koch
Keyword(s):  
Firing Rate ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Excitatory Postsynaptic Potential ◽  
Firing Rates ◽  
Shunting Inhibition ◽  
A Value ◽  
Inhibitory Conductance ◽  
Conductance Increase

Shunting inhibition, a conductance increase with a reversal potential close to the resting potential of the cell, has been shown to have a divisive effect on subthreshold excitatory postsynaptic potential amplitudes. It has therefore been assumed to have the same divisive effect on firing rates. We show that shunting inhibition actually has a subtractive effecton the firing rate in most circumstances. Averaged over several interspike intervals, the spiking mechanism effectively clamps the somatic membrane potential to a value significantly above the resting potential, so that the current through the shunting conductance is approximately independent of the firing rate. This leads to a subtractive rather than a divisive effect. In addition, at distal synapses, shunting inhibition will also have an approximately subtractive effect if the excitatory conductance is not small compared to the inhibitory conductance. Therefore regulating a cell's passive membrane conductance—for instance, via massive feedback—is not an adequate mechanism for normalizing or scaling its output.

The inactivating potassium currents of hair cells isolated from the crista ampullaris of the frog

1992 ◽  
Vol 68 (5) ◽  
pp. 1642-1653 ◽  
Author(s):  
C. H. Norris ◽  
A. J. Ricci ◽  
G. D. Housley ◽  
P. S. Guth
Keyword(s):  
Steady State ◽  
Hair Cells ◽  
Reversal Potential ◽  
Semicircular Canals ◽  
Cell Voltage ◽  
Leopard Frog ◽  
Resting Potential ◽  
Voltage Response ◽  
Calcium Dependent ◽  
Steady State Inactivation

1. A-type outward currents were studied in sensory hair cells isolated from the semicircular canals (SCC) of the leopard frog (Rana pipiens) with whole-cell voltage- and current-clamping techniques. 2. There appear to be two classes of A-type outward-conducting potassium channels based on steady-state, kinetic, pharmacological parameters, and reversal potential. 3. The two classes of A-type currents differ in their steady-state inactivation properties as well as in the kinetics of inactivation. The steady-state inactivation properties are such that a significant portion of the fast channels are available from near the resting potential. 4. The inactivating channels studied do not appear to be calcium dependent. 5. The A-channels in hair cells appear to subserve functions that are analogous to IA functions in neurons, that is, modulating spike latency and Q (the oscillatory damping function). The A-currents appear to temporally limit the hair cell voltage response to a current injection.

Properties of the hyperpolarization-activated current in rat hippocampal CA1 pyramidal cells

1993 ◽  
Vol 69 (6) ◽  
pp. 2129-2136 ◽  
Author(s):  
G. Maccaferri ◽  
M. Mangoni ◽  
A. Lazzari ◽  
D. DiFrancesco
Keyword(s):  
Membrane Conductance ◽  
Pyramidal Cells ◽  
Resting Potential ◽  
Constant Current ◽  
Patch Clamp Technique ◽  
Current Activation ◽  
Hyperpolarization Activated Current ◽  
K Concentration ◽  
Current Steps

1. Voltage and current clamp recordings were performed on CA1 rat hippocampal pyramidal cells using the patch clamp technique on "in vitro" slice preparations. 2. Hyperpolarizations from a holding potential of -35 mV elicited activation of the hyperpolarization-activated current (Ih) starting at voltages near -50 mV. 3. Ih recorded in voltage clamp conditions was blocked by external caesium (5 mM). 4. Raising the external K concentration from 4.35 to 24.35 mM sensibly increased the slope of the current-voltage (I/V) curve. Decreasing the external Na concentration from 133.5 to 33.5 mM depressed Ih without grossly altering the I/V slope. 5. The Ih fully activated I/V relation measured in the range -140 to -45 mV was linear with an extrapolated reversal at -17.0 +/- -1.6 (SE) mV. The current activation curve comprised the range between about -50 and -140 mV with a half-maximal activation at about -98 mV. 6. Perfusion of unclamped neurons with Cs (2 mM) hyperpolarized their resting potential by 3.8 +/- 0.2 mV and decreased the membrane conductance, as expected if Ih were activated at rest. Firing caused by depolarizing current steps was prevented by Cs-induced hyperpolarization, and could be restored by returning the membrane voltage to resting level by constant current injection. 7. The Cd-insensitive (medium-duration) afterhyperpolarization (AHP) elicited by a train of action potentials at -60 mV had an amplitude of 3.9 +/- 0.3 mV and was nearly fully abolished by 2 mM Cs (82.7 +/- 7.4%). Cs removed the depolarizing part of the afterhyperpolarization as expected if Ih activation was responsible for this phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Conductances evoked by light in the ON-β ganglion cell of cat retina

1994 ◽  
Vol 11 (2) ◽  
pp. 261-269 ◽  
Author(s):  
Michael A. Freed ◽  
Ralph Nelson
Keyword(s):  
Receptive Field ◽  
Ganglion Cell ◽  
Reversal Potential ◽  
Resting Potential ◽  
Β Cell ◽  
Cat Retina ◽  
Area Centralis ◽  
Conductance Increase ◽  
Reversal Potentials ◽  
Single Synapse

AbstractWhen a bar of light (215 x 5000 μm) illuminates the receptive field of an ON-β ganglion cell of cat retina, the cell depolarizes. Intracellular recording from the cat eyecup preparation shows that this depolarization is due to an increase in conductance (2.4 ± 0.6 nS). Different phases of this depolarization have different reversal potentials, but all of these reversal potentials are more positive than the cell’s resting potential in the dark. When the light is turned on, there is an initial transient depolarization; the reversal potential measured for this transient is positive (23 ± 11 mV). As the light is left on, the cell partially repolarizes to a sustained depolarization; the reversal potential measured for this sustained depolarization is close to zero (−1 ± 5 mV). When the light is turned off, the cell repolarizes further; the reversal potential measured for this repolarization is negative (−18 ± 7 mV), but still above the resting potential in the dark (−50 mV). To explain this variety of reversal potentials, at least two different synaptic conductances are required: one to ions which have a positive reversal potential and another to ions which have a negative reversal potential. Comparing the responses to broad and narrow bars suggests that these two conductances are associated with the center and surround, respectively. Finally, since an ON-β cell in the area centralis receives about 200 synapses, these results indicate that a single synapse produces an average conductance increase of about 15 pS during a near-maximal depolarization.

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