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+).

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.

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 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.

Development of glycine- and GABA-gated currents in rat spinal motoneurons

1995 ◽  
Vol 74 (1) ◽  
pp. 113-121 ◽  
Author(s):  
B. X. Gao ◽  
L. Ziskind-Conhaim
Keyword(s):  
Amino Acids ◽  
Membrane Conductance ◽  
Gamma Aminobutyric Acid ◽  
Spinal Motoneurons ◽  
Cell Recording ◽  
Inward Currents ◽  
Conductance Changes ◽  
Conductance Increase ◽  
Best Fit ◽  
Reversal Potentials

1. Developmental changes in glycine- and gamma-aminobutyric acid (GABA)-activated currents were studied in spinal motoneurons of embryonic and neonatal rats with the use of whole cell recording techniques. 2. Pressure ejection of glycine or GABA onto motoneuron somata produced Cl(-)-mediated inward currents and membrane depolarizations. During embryonic development, the average amplitude of GABA-gated currents was threefold larger than that of glycine-gated currents, but as a result of a large eightfold postnatal increase in glycine-activated currents, similar currents were produced by both amino acids after birth. 3. At all ages the decay of glycine- and GABA-gated currents best fit one-exponential curve, and their time constants were similar. The average decay time constant decreased by twofold after birth. 4. The ionic specificity of glycine- and GABA-gated channels was studied to determine whether the large amplitude of GABA-activated currents in embryonic motoneurons resulted from the contribution of an outward HCO-3 movement. Manipulations of Cl- and HCO-3 concentrations produced changes in the reversal potentials of glycine and GABA that were similar to the calculated changes in the equilibrium potentials of Cl-. This suggested that glycine- and GABA-gated currents were Cl- specific, and HCO-3 movement did not contribute more to the current generated by GABA than that produced by glycine. 5. Glycine- and GABA-gated currents were associated with severalfold increases in membrane conductance. The conductance increase generated by GABA in embryonic motoneurons was sevenfold larger than that generated by glycine, but similar conductance changes were produced by both amino acids after birth.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

BICUCULLINE/BACLOFEN-INSENSITIVE GABA RESPONSE IN CRUSTACEAN NEURONES IN CULTURE

1994 ◽  
Vol 191 (1) ◽  
pp. 167-193
Author(s):  
C Jackel ◽  
W Krenz ◽  
F Nagy
Keyword(s):  
Reversal Potential ◽  
Membrane Conductance ◽  
Gamma Aminobutyric Acid ◽  
Action Potential Firing ◽  
Patch Clamp Technique ◽  
Conformationally Restricted ◽  
Whole Cell Patch Clamp ◽  
Gabac Receptor ◽  
Potential Firing ◽  
Sr 95531

Neurones were dissociated from thoracic ganglia of embryonic and adult lobsters and kept in primary culture. When gamma-aminobutyric acid (GABA) was applied by pressure ejection, depolarizing or hyperpolarizing responses were produced, depending on the membrane potential. They were accompanied by an increase in membrane conductance. When they were present, action potential firing was inhibited. The pharmacological profile and ionic mechanism of GABA-evoked current were investigated under voltage-clamp with the whole-cell patch-clamp technique. The reversal potential of GABA-evoked current depended on the intracellular and extracellular Cl- concentration but not on extracellular Na+ and K+. Blockade of Ca2+ channels by Mn2+ was also without effect. The GABA-evoked current was mimicked by application of the GABAA agonists muscimol and isoguvacine with an order of potency muscimol>GABA>isoguvacine. cis-4-aminocrotonic acid (CACA), a folded and conformationally restricted GABA analogue, supposed to be diagnostic for the vertebrate GABAC receptor, also induced a bicuculline-resistant chloride current, although with a potency about 10 times lower than that of GABA. The GABA-evoked current was largely blocked by picrotoxin, but was insensitive to the GABAA antagonists bicuculline, bicuculline methiodide and SR 95531 at concentrations of up to 100 µmol l-1. Diazepam and phenobarbital did not exert modulatory effects. The GABAB antagonist phaclophen did not affect the GABA-induced current, while the GABAB agonists baclophen and 3-aminopropylphosphonic acid (3-APA) never evoked any response. Our results suggest that lobster thoracic neurones in culture express a chloride-conducting GABA-receptor channel which conforms to neither the GABAA nor the GABAB types of vertebrates but shows a pharmacology close to that of the novel GABAC receptor described in the vertebrate retina.

GABA responses in rat dentate granule neurons are mediated by chloride

1988 ◽  
Vol 66 (5) ◽  
pp. 637-642 ◽  
Author(s):  
Timothy J. Blaxter ◽  
Peter L. Carlen
Keyword(s):  
Granule Cells ◽  
Hippocampal Slices ◽  
Reversal Potential ◽  
Chloride Ion ◽  
Chloride Ions ◽  
Ion Concentration ◽  
Aminobutyric Acid ◽  
Granule Neurons ◽  
Nernst Equation ◽  
Central Neurons

The dendrites of granule cells in hippocampal slices responded to γ-aminobutyric acid (GABA) with a depolarization. The response was blocked by picrotoxin in a noncompetitive manner. Reductions in the extracellular chloride ion concentration changed the reversal potential of the response by an amount predicted from the Nernst equation for chloride ion. Chloride-dependent hyperpolarizing responses were sometimes also found in the cell body of the granule cells. Since the reversal potential followed that predicted from the Nernst equation for chloride, we conclude that the response was mediated by chloride ions alone with no contribution from other ions. This has not previously been shown for the depolarizing response to GABA in central neurons.

Hodgkin–Huxley neurons with defective and blocked ion channels

2015 ◽  
Vol 26 (10) ◽  
pp. 1550112 ◽  
Author(s):  
James Christopher S. Pang ◽  
Johnrob Y. Bantang
Keyword(s):  
Ion Channels ◽  
Action Potentials ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Potassium Ions ◽  
Temporal Response ◽  
Constant Input ◽  
Control Drug ◽  
Channel Control ◽  
Sodium And Potassium

We utilize the original Hodgkin–Huxley (HH) model to consider the effects of defective ion channels to the temporal response of neurons. Statistics of firing rate and inter-spike interval (ISI) reveal that production of action potentials (APs) in neurons is not sensitive to changes in membrane conductance for sodium and potassium ions, as well as to the reversal potential for sodium ions, as long as the relevant parameters do not exceed 13% from their normal levels. We also found that blockage of a critical fraction of either sodium or potassium channels (dependent on constant input current) respectively limits the firing activity or increases spontaneous spiking activity of neurons. Our model may be used to guide experiment designs related to ion channel control drug development.

A Novel Gaba Receptor on Central Neurones

1980 ◽  
Vol 25 (4) ◽  
pp. S3-S11 ◽  
Author(s):  
N. G. Bowery ◽  
A. Doble ◽  
D. R. Hill ◽  
A. L. Hudson ◽  
J. Shaw ◽  
...  
Keyword(s):  
Peripheral Nerve ◽  
Ligand Binding ◽  
Gaba Receptor ◽  
Membrane Conductance ◽  
Chloride Ions ◽  
Aminobutyric Acid ◽  
The Novel ◽  
Inhibitory Neurotransmitter ◽  
Gaba Analogues ◽  
Potent Agonist

The features of γ-aminobutyric acid (GABA) as an inhibitory neurotransmitter are described, together with those of its receptor as defined by both iontophoretic and radiolabelled ligand binding techniques. Evidence is presented supporting the existence of a second GABA receptor at both peripheral nerve endings and within the CNS. At the classical receptor, GABA can produce a depolarisation of the ganglion cell body or mediate hyperpolarisation within the CNS by increasing membrane conductance to chloride ions. At this second receptor GABA acts in a bicuculline-insensitive manner to reduce neurotransmitter outflow. Many GABA analogues active at the classical receptor are inactive at the second receptor but by contrast baclofen which is inactive at the classical receptor is a potent agonist at the novel site.

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+.

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