scholarly journals Simultaneous changes in the equilibrium potential and potassium conductance in voltage clamped Ranvier node in the frog.

1981 ◽  
Vol 318 (1) ◽  
pp. 279-295 ◽  
Author(s):  
J M Dubois
Keyword(s):  
Potassium Conductance ◽  
Equilibrium Potential ◽  
Ranvier Node

Effect of substance P on C1 and other bulbospinal cells of the RVLM in neonatal rats

1997 ◽  
Vol 273 (2) ◽  
pp. R805-R813 ◽  
Author(s):  
Y. W. Li ◽  
P. G. Guyenet
Keyword(s):  
Substance P ◽  
Discharge Rate ◽  
Potassium Conductance ◽  
Input Resistance ◽  
Ventrolateral Medulla ◽  
Equilibrium Potential ◽  
Neonatal Rats ◽  
Spontaneous Firing Rate ◽  
Sympathetic Vasomotor Tone

Sixty-two bulbospinal neurons were recorded in the rostral ventrolateral medulla (RVLM) of neonatal rats using patch electrodes. Sixty-one percent of the recorded neurons identified by histology contained tyrosine-hydroxylase (C1 cells). Substance P increased the spontaneous firing rate of all recorded cells but had no effect on spike configuration. The peptide depolarized neurons that were silenced by injection of hyperpolarizing current and increased their input resistance. All cells (n = 12) were activated by a neurokinin (NK)1 receptor agonist but most were unaffected by an NK2- or an NK2-selective compound. In voltage clamp, substance P produced a current that was linearly related to the membrane voltage. This current reversed polarity close to the potassium equilibrium potential in 11 of 23 cells. It reversed at more hyperpolarized potentials or not at all in the rest of the cells. In conclusion, substance P upregulates the intrinsic discharge rate of C1 and other putative sympathoexcitatory cells in neonatal rats. This effect is mediated via NK1 receptors. The depolarization is mediated by a reduction in resting potassium conductance and possibly by an additional cationic conductance. These results support the possibility that substance P could play a role "in vivo" in setting the basal level of discharge of the vasomotor cells of RVLM and therefore in regulating sympathetic vasomotor tone.

Analysis of decreased conductance serotonergic response in Aplysia ink motor neurons

1985 ◽  
Vol 53 (2) ◽  
pp. 590-602 ◽  
Author(s):  
J. P. Walsh ◽  
J. H. Byrne
Keyword(s):  
Cell Body ◽  
Motor Neurons ◽  
Potassium Conductance ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Slow Inward Current ◽  
Equilibrium Potential ◽  
Voltage Sensitivity ◽  
Inward Current ◽  
Bath Application

Micropressure ejection of serotonin (5-hydroxytryptamine, 5-HT) produced excitatory responses in the L14 ink motor neurons of Aplysia that depended on the site of application. Ejection of 5-HT onto the cell body produced a slow response that showed variability in voltage sensitivity between preparations. In contrast, ejection of 5-HT onto the neuropil underneath the cell body produced a response whose amplitude was consistently a linear function of the holding potential, reversing near the predicted potassium equilibrium potential. Subsequent analyses focused on this second response. The neuropil response induced by 5-HT had a linear current-voltage relationship (reversing at ca. -80 mV), was associated with a decrease in input conductance, and was sensitive to changes in the concentration of extracellular K+. Serotonin application in artificial seawater (ASW) containing 30 mM K+ produced a response that reversed close to the altered Nernst potential for K+. The 5-HT response did not appear to be due to secondary activation of interneurons or to depend primarily on extracellular Ca2+, since ejection of 5-HT onto cells bathed in ASW containing 30 mM Co2+ produced responses comparable to, although somewhat attenuated from, those observed in ASW. Serotonin responses similar to those produced in ASW were obtained after perfusing the ganglion with ASW containing Co2+, 4-aminopyridine (4-AP), and tetraethylammonium (TEA). This suggests that the 5-HT-sensitive current is separate from the Ca2+-activated, fast, and delayed rectifying K+ currents. The 5-HT response appeared to be mediated by changes in levels of cAMP. Bath application of the phosphodiesterase inhibitors IBMX (3-isobutyl-1-methylxanthine) or Ro 20-1724, or the adenylate cyclase activator forskolin mimicked the 5-HT response by producing a slow inward current associated with a decrease in membrane conductance. Alteration of cellular cAMP metabolism modulated the response to 5-HT. Exposure of the ganglion to low concentrations of either Ro 20-1724 or forskolin potentiated the 5-HT response. Higher concentrations of these agents largely blocked the response to subsequent 5-HT applications. Bath application of the 8-bromo derivative of either cAMP or cGMP produced a slow inward current associated with a decrease in membrane conductance in cells voltage clamped at the resting potential. Responses to 5-HT were blocked, however, after exposure to 8-bromo-cAMP, but not to 8-bromo-cGMP. These results suggest that 5-HT produces a voltage-independent decrease in a steady-state potassium conductance that may be mediated by cAMP.(ABSTRACT TRUNCATED AT 400 WORDS)

Pre- and Postsynaptic Inhibitory Actions of Methionine-Enkephalin on Identified Bulbospinal Neurons of the Rat RVL

1998 ◽  
Vol 80 (4) ◽  
pp. 2003-2014 ◽  
Author(s):  
Abdallah Hayar ◽  
Patrice G. Guyenet
Keyword(s):  
Decay Time ◽  
Potassium Conductance ◽  
Outward Current ◽  
Cardiovascular Effects ◽  
Ventrolateral Medulla ◽  
Equilibrium Potential ◽  
Cellular Mechanisms ◽  
Patch Clamp Technique ◽  
Methionine Enkephalin ◽  
Postsynaptic Currents

Hayar, Abdallah and Patrice G. Guyenet. Pre- and postsynaptic inhibitory actions of methionine-enkephalin on identified bulbospinal neurons of the rat RVL. J. Neurophysiol. 80: 2003–2014, 1998. The effects of methionine-enkephalin (ME) on visualized bulbospinal neurons of the rostral ventrolateral medulla (RVL) were characterized in thin slices at 32°C using the whole cell patch-clamp technique. Thirty-five percent of the recorded neurons were found to be tyrosine hydroxylase immunoreactive (C1 neurons). In voltage-clamp recordings, ME (3 μM) induced an outward current in 66% of RVL bulbospinal neurons. A similar percentage of C1 and non-C1 neurons were opioid sensitive. The current induced by ME was inwardly rectifying, reversed close to the potassium equilibrium potential, and was blocked by barium. Most spontaneous postsynaptic currents recorded in these neurons were tetrodotoxin (TTX)-resistant miniature postsynaptic currents (mPSCs). Approximately, 75% of mPSCs had rapid kinetics (decay time = 4.7 ms) and were glutamatergic [miniature excitatory postsynaptic currents (mEPSCs)] because they were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM). The remaining mPSCs had much slower kinetics (decay time = 19.6 ms) and were GABAergic [miniature inhibitory postsynaptic currents (mIPSCs)] as they were blocked by gabazine (3 μM) but not by strychnine (3–10 μM). ME decreased the frequency of mEPSCs and mIPSCs by 69 and 43%, respectively. The inhibitory effects of ME were mimicked by the selective μ-opioid receptor agonist endomorphin-1 (EM, 3 μM) and were blocked by naloxone (1 μM). In the absence of TTX, excitatory PSCs evoked by focal electrical stimulation were isolated by application of gabazine and strychnine. EM reduced the amplitude of the evoked EPSCs by 41% without changing their decay time. We conclude that opioids inhibit the majority of RVL C1 and non-C1 bulbospinal neurons by activating a potassium conductance postsynaptically and by decreasing the presynaptic release of glutamate. These cellular mechanisms could explain the depressive cardiovascular effects and the sympathoinhibition produced by opioid transmitters in the RVL, in particular during hypotensive hemorrhage.

scholarly journals Using lectures to identify student misconceptions: a study on the paradoxical effects of hyperkalemia on vascular smooth muscle

2020 ◽  
Vol 44 (1) ◽  
pp. 15-20
Author(s):  
Stephen J. Bordes ◽  
Jason Gandhi ◽  
Blake Bauer ◽  
Matthew Protas ◽  
Nadia Solomon ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Smooth Muscle ◽  
Medical Students ◽  
Potassium Conductance ◽  
Equilibrium Potential ◽  
Control Mechanisms ◽  
Student Misconceptions ◽  
Clinical Scenarios ◽  
Paradoxical Effects ◽  
Muscle Types

Medical students have difficulty understanding the mechanisms underlying hyperkalemia-mediated local control of blood flow. Such control mechanisms are crucial in the brain, kidney, and skeletal muscle vasculature. We aimed to identify medical students’ misconceptions via assessment of students’ in-class knowledge and, subsequently, improve future teaching of this concept. In-class polling was performed with the TurningPoint clicker response system ( n = 860) to gauge students’ understanding of three physiological concepts related to hyperkalemia: membrane potential ( Vm), conductance, and smooth muscle response. Vm includes the concepts of equilibrium potential ( Veq) for specific ions, as well as driving force (DF =  Vm − Veq). Students understood the concept of DF (~70% answered correctly), suggesting their understanding of Vm. However, students misunderstood that hyperkalemia results in depolarization (~52% answered correctly) and leads to an increase in potassium conductance (~31% answered correctly). Clarification of the type of smooth muscle as vascular increased the percentage of correct responses (~51 to 73%). The data indicate that students lacked knowledge of specific potassium conductance in various muscle types, resulting in divergent responses, such as the canonical depolarization in skeletal muscle versus hyperpolarization in smooth muscle cells during hyperkalemia. Misunderstanding of this crucial concept of conductance is directly related to the students’ performance. Furthermore, we connected the paradoxical effect of hyperkalemia to pathological acute and chronic hyperkalemia clinical scenarios.

scholarly journals Increased Chloride Conductance As the Proximate Cause of Hydrogen Ion Concentration Effects in Aplysia Neurons

1970 ◽  
Vol 56 (5) ◽  
pp. 559-582 ◽  
Author(s):  
A. M. Brown ◽  
J. L. Walker ◽  
R. B. Sutton
Keyword(s):  
Organic Liquid ◽  
Potassium Conductance ◽  
Giant Cells ◽  
Ion Exchanger ◽  
Chloride Conductance ◽  
Ion Concentration ◽  
Equilibrium Potential ◽  
Concentration Effects ◽  
Hydrogen Ion Concentration ◽  
Hyperpolarizing Response

A fall in extracellular pH increased membrane conductance of the giant cell in the abdominal ganglion of Aplysia californica. Chloride conductance was trebled whereas potassium conductance was increased by 50%. Half the giant cells were hyperpolarized (2–8 mv) and half were depolarized (3–10 mv) by lowering the pH. The hyperpolarizing response always became a depolarizing response in half-chloride solutions. When internal chloride was increased electrophoretically, the hyperpolarization was either decreased or changed to depolarization. The depolarizing response was reduced or became a hyperpolarizing response after soaking the cell in 10.0 mM chloride, artificial seawater solution for 1 hr. Depolarization was unaffected when either external sodium, calcium, or magnesium was omitted. A glass micropipette having an organic liquid chloride ion exchanger in its tip was used to measure intracellular chloride activity in 14 giant cells; 7 had values of 27.7 ± 1.8 mM (SEM) and 7 others 40.7 ± 1.5 mM. Three of the first group were hyperpolarized when pH was lowered and three of the second group were depolarized. In all six cells, these changes of membrane potential were in the direction of the chloride equilibrium potential. Intracellular potassium activity was measured by means of a potassium ion exchanger microelectrode.

Adenosine inhibition of synaptic transmission in the substantia gelatinosa

1994 ◽  
Vol 72 (4) ◽  
pp. 1611-1621 ◽  
Author(s):  
J. Li ◽  
E. R. Perl
Keyword(s):  
Synaptic Transmission ◽  
Dorsal Root ◽  
Potassium Conductance ◽  
Outward Current ◽  
Postsynaptic Membrane ◽  
Substantia Gelatinosa ◽  
Equilibrium Potential ◽  
Primary Afferent ◽  
Primary Afferent Fibers ◽  
Sustained Outward Current

1. We studied adenosine's action on synaptic transmission from primary afferent fibers to neurons of the substantia gelatinosa (SG) using tight-seal whole cell recordings in transverse slices of hamster spinal cord. Adenosine had two actions, hyperpolarization of the postsynaptic membrane and depression of the excitatory postsynaptic currents (EPSCs) evoked by dorsal root stimulation. 2. Under voltage clamp adenosine elicited a sustained outward current at a holding potential of -70 mV. The outward current was blocked by a combination of intracellular cesium and tetraethylammonium, an effect characteristic of potassium channels. The adenosine-induced current reversed at -97 +/- 6 (SD) mV, close to the potassium equilibrium potential. These observations suggest that adenosine activates a potassium conductance in SG neurons so as to inhibit primary afferent synaptic transmission postsynaptically. 3. Adenosine reduced the miniature EPSC frequency without significantly changing the amplitude. In contrast, the glutamate receptor competitive antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) substantially reduced the amplitudes of miniature EPSCs while producing a much smaller effect on the miniature frequency than adenosine. In evoked EPSCs adenosine reduced unitary content without reducing unitary amplitude. The effects on both miniature and evoked EPSCs suggest that adenosine inhibits synaptic currents by suppressing presynaptic transmitter release. 4. EPSCs evoked by dorsal root stimuli were subdivided into monosynaptic and polysynaptic categories. Adenosine at superfusion concentrations of 20-300 microM suppressed all polysynaptic EPSCs. Less than half of monosynaptic EPSCs were inhibited, usually those evoked by the slowest-conducting primary afferents. These observations were interpreted to indicate that a principal action of adenosine in SG is on interneuronal communication.

Effect of procaine on electrical properties of squid axon membrane

1959 ◽  
Vol 196 (5) ◽  
pp. 1071-1078 ◽  
Author(s):  
Robert E. Taylor
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Squid Axon ◽  
Voltage Step ◽  
Axon Membrane ◽  
Rate Of Development

Procaine (0.025–0.1%; pH 7.9) caused a reduction in the amount and rate of development of the early transient (sodium) and late steady state (potassium) currents which occur during a depolarizing voltage step applied to the excised, voltage clamped squid axon. Consistent results were obtained by holding the membrane potential at a hyperpolarized value prior to the applied step. No effect was seen on the resting potential, on the sodium equilibrium potential, or on the proportion of the sodium carrying system which was ‘inactive’ at any membrane potential. The blocking action of procaine is a result of the inhibition by the drug of the sodium carrying system. The effect of procaine on the potassium conductance is such as to oppose the blocking action.

Inwardly rectifying potassium conductance can accelerate the hyperpolarizing response in retinal horizontal cells

1995 ◽  
Vol 74 (6) ◽  
pp. 2258-2265 ◽  
Author(s):  
C. J. Dong ◽  
F. S. Werblin
Keyword(s):  
Physiological Response ◽  
Potassium Conductance ◽  
Light Response ◽  
Horizontal Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Membrane Hyperpolarization ◽  
Response Range ◽  
Inwardly Rectifying ◽  
Onset Rate

1. We studied the activation properties and assessed the functional role of the inwardly rectifying potassium conductance (GK.IR) in acutely isolated retinal horizontal cells (HCs) with the use of the whole cell patch-clamp technique. 2. The potassium current mediated by GK.IR was isolated by the use of Cs+ or Ba2+ ions. This current was outward, although relatively small in amplitude, in the voltage range between the potassium equilibrium potential (EK) and 50-60 mV more positive. The current reversed its polarity at EK and became inward at potentials more negative than EK. When HCs were bathed in normal Ringer (EK = -90 mV), GK.IR began to active at about -30 mV, was 30-40% activated at the resting potential (-70 to -80 mV) and about fully activated at -130 mV. Thus a significant portion of the activation range of GK.IR overlaps the HC physiological response range (-20 to -80 mV). 3. GK.IR has a dramatic effect on the kinetics of membrane polarization. Blocking GK.IR with Cs+ or Ba2+ significantly slowed the rate of membrane hyperpolarization in response to a hyperpolarizing current ramp over the HC physiological response range. Blocking GK.IR also dramatically slowed the onset rate of a simulated light response generated by a brief break in a sustained glutamate puff. 4. These results suggest that GK.IR can enhance the temporal resolution of the HC by accelerating the onset rate of the hyperpolarizing light response.

scholarly journals Potassium flux ratio in voltage-clamped squid giant axons.

1980 ◽  
Vol 76 (1) ◽  
pp. 83-98 ◽  
Author(s):  
T Begenisich ◽  
P De Weer
Keyword(s):  
Simultaneous Measurement ◽  
Potassium Conductance ◽  
Flux Ratio ◽  
Giant Axon ◽  
Equilibrium Potential ◽  
Giant Axons ◽  
Average Value ◽  
Potassium Flux ◽  
K Current ◽  
Loligo Pealei

The potassium flux ratio across the axolemma of internally perfused, voltage-clamped giant axons of Loligo pealei has been evaluated at various membrane potentials and internal potassium concentrations ([K]i). Four different methods were used: (a) independent measurement of one-way influx and efflux of 42K; (b) simultaneous measurement of net K current (IK) and 42K influx; (c) simultaneous measurement of IK and 42K efflux; and (d) measurement of potassium conductance and 42K influx at the potassium equilibrium potential. The reliability of each of these methods is discussed. The average value of the exponent n' in the Hodgkin-Keynes equation ranged from 1.5 at -4mV and 200 mM [K]i to 3.3 at -38 mV and 350 mM [K]i and appeared to be a function of membrane potential and possibly of [K]i. It is concluded that the potassium channel of squid giant axon is a multi-ion, single-file pore with three or more sites.

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