Calcium-dependent potassium conductance in rat supraoptic nucleus neurosecretory neurons

1985 ◽  
Vol 54 (6) ◽  
pp. 1375-1382 ◽  
Author(s):  
C. W. Bourque ◽  
J. C. Randle ◽  
L. P. Renaud
Keyword(s):  
Time Constant ◽  
Action Potentials ◽  
Supraoptic Nucleus ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Input Resistance ◽  
Mean Amplitude ◽  
Progressive Increase ◽  
Calcium Dependent ◽  
Neurosecretory Neurons

Intracellular recordings of rat supraoptic nucleus neurons were obtained from perfused hypothalamic explants. Individual action potentials were followed by hyperpolarizing afterpotentials (HAPs) having a mean amplitude of -7.4 +/- 0.8 mV (SD). The decay of the HAP was approximated by a single exponential function having a mean time constant of 17.5 +/- 6.1 ms. This considerably exceeded the cell time constant of the same neurons (9.5 +/- 0.8 ms), thus indicating that the ionic conductance underlying the HAP persisted briefly after each spike. The HAP had a reversal potential of -85 mV and was unaffected by intracellular Cl- ionophoresis of during exposure to elevated extracellular concentrations of Mg2+. In contrast, the peak amplitude of the HAP was proportional to the extracellular Ca2+ concentration and could be reversibly eliminated by replacing Ca2+ with Co2+, Mn2+, or EGTA in the perfusion fluid. During depolarizing current pulses, evoked action potential trains demonstrated a progressive increase in interspike intervals associated with a potentiation of successive HAPs. This spike frequency adaptation was reversibly abolished by replacing Ca2+ with Co2+, Mn2+, or EGTA. Bursts of action potentials were followed by a more prolonged afterhyperpolarization (AHP) whose magnitude was proportional to the number of impulses elicited (greater than 20 Hz) during a burst. Current injection revealed that the AHP was associated with a 20-60% decrease in input resistance and showed little voltage dependence in the range of -70 to -120 mV. The reversal potential of the AHP shifted with the extracellular concentration of K+ [( K+]o) with a mean slope of -50 mV/log[K+]o.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Action Potentials in Rhodnius Oocytes: Repolarization is Sensitive to Potassium Channel Blockers

1986 ◽  
Vol 126 (1) ◽  
pp. 119-132
Author(s):  
M. J. O'DONNELL
Keyword(s):  
Potassium Channel ◽  
Action Potentials ◽  
Potassium Conductance ◽  
Channel Blockers ◽  
Calcium Dependent ◽  
Outward Rectification ◽  
Current Voltage ◽  
Potassium Channel Blockers ◽  
Potassium Conductances ◽  
Voltage Dependent

Depolarization of Rhodnius oocytes evokes action potentials (APs) whose rising phase is calcium-dependent. The ionic basis for the repolarizing (i.e. falling) phase of the AP was examined. Addition of potassium channel blockers (tetraethylammonium, tetrabutylammonium, 4-aminopyridine, atropine) to the bathing saline increased the duration and overshoot of APs. Intracellular injection of tetraethyl ammonium had similar effects. These results suggest that a voltage-dependent potassium conductance normally contributes to repolarization. Repolarization does not require a chloride influx, because substitution of impermeant anions for chloride did not increase AP duration. AP duration and overshoot actually decreased progressively when chloride levels were reduced. Current/voltage curves show inward and outward rectification, properties often associated with potassium conductances. Outward rectification was largely blocked by external tetraethylammonium. Possible functions of the rectifying properties of the oocyte membrane are discussed.

Effects of Octopamine on Calcium Action Potentials in Insect Oocytes

1989 ◽  
Vol 142 (1) ◽  
pp. 115-124
Author(s):  
M. J. O'DONNELL ◽  
B. SINGH
Keyword(s):  
Action Potentials ◽  
Rank Order ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Threshold Concentration ◽  
Resting Potential ◽  
Calcium Dependent ◽  
Octopamine Receptors ◽  
Voltage Dependent ◽  
Maximum Rate Of Rise

Our experiments show that octopamine receptors are present on the developing follicles of an insect, Rhodnius prolixus. Application of D,L-octopamine decreased the duration and overshoot of calcium-dependent action potentials (APs), and increased the intrafollicular concentration of cyclic AMP. The threshold concentration of D,L-octopamine for the reduction in electrical excitability was between 1 and 5×10−7moll−1, and maximal effects of a 40–50% reduction in AP overshoot and duration were apparent at 10−4moll−1. At concentrations above 10−5moll−1, a small (<10%) hyperpolarization of the resting potential was also apparent. Effects of D,L-octopamine on oocyte excitability were independent of these small shifts in resting potential. Current injection experiments, in which calcium entry was blocked by cobalt, demonstrated that D,L-octopamine reduced membrane resistance at both hyperpolarizing and depolarizing potentials. Octopamine did not affect the maximum rate of rise of the AP, dV/dtmax, which is an indicator of inward calcium current. It is suggested that octopamine may mediate its effects on excitability through an increase in a voltage-dependent potassium conductance. Application of other phenolamines indicated a rank order of potency of D, Loctopamine > D,L-synephrine > tyramine. The α-adrenergic agonists clonidine, naphazoline and tolazoline were without significant effect at 10−5-10−3moll−1. Reduction of excitability by D,L-octopamine was effectively blocked by phentolamine and metoclopramide. Yohimbine and gramine were less effective as antagonists. Possible functions of octopamine receptors in insect follicles are discussed.

Input Resistance, Time Constants, and Spike Initiation

1998 ◽  
Author(s):  
Christof Koch
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Action Potentials ◽  
Input Resistance ◽  
Current Injection ◽  
Membrane Conductances ◽  
Voltage Dependent ◽  
Dc Component ◽  
Definition Of ◽  
A Current

This chapter represents somewhat of a tephnical interlude. Having introduced the reader to both simplified and more complex compartmental single neuron models, we need to revisit terrain with which we are already somewhat familiar. In the following pages we reevaluate two important concepts we defined in the first few chapters: the somatic input resistance and the neuronal time constant. For passive systems, both are simple enough variables: Rin is the change in somatic membrane potential in response to a small sustained current injection divided by the amplitude of the current injection, while τm is the slowest time constant associated with the exponential charging or discharging of the neuronal membrane in response to a current pulse or step. However, because neurons express nonstationary and nonlinear membrane conductances, the measurement and interpretation of these two variables in active structures is not as straightforward as before. Having obtained a more sophisticated understanding of these issues, we will turn toward the question of the existence of a current, voltage, or charge threshold at which a biophysical faithful model of a cell triggers action potentials. We conclude with recent work that suggests how concepts from the subthreshold domain, like the input resistance or the average membrane potential, could be extended to the case in which the cell is discharging a stream of action potentials. This chapter is mainly for the cognoscendi or for those of us that need to make sense of experimental data by comparing therp to theoretical models that usually fail to reflect reality adequately. In Sec. 3.4, we defined Kii (f) for passive cable structures as the voltage change at location i in response to a sinusoidal current injection of frequency f at the same location. Its dc component is also referred to as input resistance or Rin. Three difficulties render this definition of input resistance problematic in real cells: (1) most membranes, in particular at the soma, show voltage-dependent nonlinearities, (2) the associated ionic membrane conductances are time dependent and (3) instrumental aspects, such as the effect of the impedance of the recording electrode on Rin, add uncertainty to the measuring process.

A role for a background sodium current in spontaneous action potentials and secretion from rat lactotrophs

1996 ◽  
Vol 271 (6) ◽  
pp. C1927-C1934 ◽  
Author(s):  
S. Sankaranarayanan ◽  
S. M. Simasko
Keyword(s):  
Action Potentials ◽  
Sodium Current ◽  
Plaque Assay ◽  
Input Resistance ◽  
Cytosolic Calcium ◽  
Calcium Dependent ◽  
Whole Cell Patch Clamp ◽  
Spontaneous Action ◽  
Spontaneous Action Potentials ◽  
Spontaneous Secretion

We have used the perforated-patch variation of whole cell patch-clamp techniques, measurements of cytosolic calcium with use of fura 2, and secretion measurements with use of the reverse-hemolytic plaque assay to address the role of depolarizing background currents in maintaining spontaneous action potentials and spontaneous secretion from rat lactotrophs in primary culture. Replacement of bath sodium with tris(hydroxymethyl)aminomethane or N-methyl-D-glucamine caused a dramatic hyperpolarization of the cells, a cessation of spontaneous action potentials, and an increase in input resistance of cells. Tetrodotoxin had no effect on spontaneous action potentials, and removal of bath calcium stopped spiking but did not hyperpolarize the cells. The hyperpolarization in response to removal of bath sodium was associated with a decrease in cytosolic calcium levels. Finally, removal of bath sodium caused a decrease in spontaneous secretion of prolactin from lactotrophs. These data suggest that a background sodium current is essential to drive the membrane to threshold for firing spontaneous calcium-dependent action potentials in lactotrophs. This, in turn, results in elevated intracellular calcium, which supports spontaneous secretion of prolactin from these cells.

Cholecystokinin-8s excites identified rat pancreatic-projecting vagal motoneurons

2007 ◽  
Vol 293 (2) ◽  
pp. G484-G492 ◽  
Author(s):  
Shuxia Wan ◽  
F. Holly Coleman ◽  
R. Alberto Travagli
Keyword(s):  
Brain Stem ◽  
Pancreatic Polypeptide ◽  
Potassium Conductance ◽  
Input Resistance ◽  
Exocrine Secretion ◽  
Motor Nucleus ◽  
Pancreatic Exocrine Secretion ◽  
Calcium Dependent ◽  
Synaptic Circuits ◽  
Pancreatic Exocrine

It is known that cholecystokinin (CCK) acts in a paracrine fashion to increase pancreatic exocrine secretion via vagal circuits. Recent evidence, however, suggests that CCK-8s actions are not restricted to afferent vagal fibers, but also affect brain stem structures directly. Within the brain stem, preganglionic neurons of the dorsal motor nucleus of the vagus (DMV) send efferent fibers to subdiaphragmatic viscera, including the pancreas. Our aims were to investigate whether DMV neurons responded to exogenously applied CCK-8s and, if so, the mechanism of action. Using whole cell patch-clamp recordings we show that perfusion with CCK-8s induced a concentration-dependent excitation in ∼60% of identified pancreas-projecting DMV neurons. The depolarization was significantly reduced by tetrodotoxin, suggesting both direct (on the DMV membrane) and indirect (on local synaptic circuits) effects. Indeed, CCK-8s increased the frequency of miniature excitatory currents onto DMV neurons. The CCK-A antagonist, lorglumide, prevented the CCK-8s-mediated excitation whereas the CCK-B preferring agonist, CCK-nonsulfated, had no effect, suggesting the involvement of CCK-A receptors only. In voltage clamp, the CCK-8s-induced inward current reversed at −106 ± 3 mV and the input resistance increased by 150 ± 15%, suggesting an effect mediated by the closure of a potassium conductance. Indeed, CCK-8s reduced both the amplitude and the time constant of decay of a calcium-dependent potassium conductance. When tested with pancreatic polypeptide (which reduces pancreatic exocrine secretion), cells that responded to CCK-8s with an excitation were, instead, inhibited by pancreatic polypeptide. These data indicate that CCK-8s may control pancreas-exocrine secretion also via an effect on pancreas-projecting DMV neurons.

Mechanism of long-lasting synaptic inhibition in Aplysia neuron R15

1980 ◽  
Vol 44 (6) ◽  
pp. 1148-1160 ◽  
Author(s):  
W. B. Adams ◽  
I. Parnas ◽  
I. B. Levitan
Keyword(s):  
Action Potentials ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Short Exposure ◽  
Ion Conductance ◽  
Current Voltage ◽  
Voltage Dependent ◽  
Aplysia Neuron ◽  
Reversible Component ◽  
Stimulation Of

1. Long-lasting inhibition is a synaptically mediated response found in certain molluscan nerve cells that fire action potentials in bursts. It is elicited by repetitive stimulation of a presynaptic nerve and may last for minutes or hours after stimulation. 2. Voltage-clamp techniques were employed to measure the voltage dependence of the synaptically elicited current. Current-voltage curves were obtained by stepping or sweeping the voltage over the range -40 to -120 mV. 3. Long-lasting inhibition was found to be mediated by two separate conductance mechanisms. A component that reverses near -80 mV is most prominent at times up to 5 min following stimulation. A component with no reversal potential between -40 and -120 mV predominates at later times. 4. The reversible component is attenuated by reducing the intensity of stimulation of the presynaptic nerve, by injection of TEA into the postsynaptic cell, or by activation of a potassium conductance with serotonin prior to stimulation of the nerve. Thus, the reversible component appears to be mediated by an increase in potassium conductance. 5. The effects of the nonreversible component measured in the soma appear to be too large to attribute it to a conductance change that is electrically "distant" from the soma. It is attenuated by turning off a resting inward ion conductance with dopamine prior to stimulation of the nerve. It is not affected by short exposure to ouabain, but is attenuated by longer exposures that reduce the sodium and calcium gradients. Thus, the nonreversible component may be mediated by a decrease in voltage-dependent inward current flow carried by sodium or calcium.

Posttetanic potentiation of group Ia EPSPs: possible mechanisms for differential distribution among medial gastrocnemius motoneurons

1983 ◽  
Vol 50 (2) ◽  
pp. 379-398 ◽  
Author(s):  
A. Lev-Tov ◽  
M. J. Pinter ◽  
R. E. Burke
Keyword(s):  
Negative Correlation ◽  
Action Potentials ◽  
Input Resistance ◽  
Mean Amplitude ◽  
Synaptic Depression ◽  
Medial Gastrocnemius ◽  
Posttetanic Potentiation ◽  
Differential Distribution ◽  
Strong Negative Correlation ◽  
Statistical Probability

We have reinvestigated the phenomenon of posttetanic potentiation (PTP) of group Ia monosynaptic excitatory postsynaptic potentials (EPSPs) in medial gastrocnemius (MG) alpha-motoneurons of pentobarbital-anesthetized cats. The results generally confirm earlier reports by Luscher and colleagues (43, 44) of a negative correlation between the maximum percentage potentiation of Ia EPSP amplitude (Pmax) and 1) the mean amplitude of the pretetanic control EPSP in the same cell and 2) the input resistance of the postsynaptic motoneuron. These negative correlations, which we will refer to as "differential distribution of PTP" within the MG motor pool, were less strong in the present work than reported by Luscher et al. (43, 44). We also found a relatively strong negative correlation between posttetanic EPSP depression, assessed by the amplitude of the first posttetanic EPSP, and the level of Pmax subsequently attained. We found no evidence that posttetanic depression is caused by failure of presynaptic action potentials. We investigated a second type of depression, referred to as "specific" synaptic depression, in which the second EPSP of paired responses (interval 250 ms) is, on average, smaller in peak amplitude than the first EPSP. This phenomenon appears to reflect decreases in the probability of transmitter release from previously activated synapses. Specific synaptic depression was consistently increased when paired responses were conditioned by a high-frequency tetanus. This is most easily explained by postulating that PTP results, at least in part, from an increase in the statistical probability of transmitter liberation from group Ia synapses that are activated (i.e., presumably invaded by action potentials) both before and after afferent tetanization. On the basis of the present results and other available evidence, we conclude that the differential distribution of PTP can be explained by two main factors: 1) the nonlinear relation between conductance and voltage changes inherent in all chemical synapses and 2) systematic variations in the properties of group Ia synapses that innervated different motoneurons, which remain to be clarified.

Electrical properties of neurons recorded from the rat supraoptic nucleus in vitro

1983 ◽  
Vol 217 (1207) ◽  
pp. 141-161 ◽  
Keyword(s):  
Membrane Potential ◽  
Electrical Properties ◽  
Time Constant ◽  
Synaptic Input ◽  
Action Potentials ◽  
Supraoptic Nucleus ◽  
Synaptic Activity ◽  
Intracellular Recordings ◽  
Average Cell ◽  
Spike Threshold

The electrical properties of neurons in the supraoptic nucleus (so.n.) have been studied in the hypothalamic slice preparation by intracellular and extracellular recording techniques, with Lucifer Yellow CH dye injection to mark the recording site as being the so. n. Intracellular recordings from so. n. neurons revealed them to have an average membrane potential of ─ 67±0.8 mV (mean±s. e. m.), membrane resistance of 145±9 MΩ with linear current–voltage relations from 40 mV in the hyperpolarizing direction to the level of spike threshold in the depolarizing direction. Average cell time constant was 14±2.2 ms. So. n. action potentials ranged in amplitude from 55 to 95 mV, with a mean of 76±2 mV, and a spike width of 2.6±0.5 ms at 30% of maximal spike height. Both single spikes and trains of spikes were followed by a strong, long-lasting hyperpolarization with a decay fitted by a single exponential having a time constant of 8.6±1.8 ms. Action potentials could be blocked by 10 -6 m tetrodotoxin. Spontaneously active so. n. neurons were characterized by synaptic input in the form of excitatory and inhibitory postsynaptic potentials, the latter being apparently blocked when 4 m KCI electrodes were used. Both forms of synaptic activity were blocked by application of divalent cations such as Mg 2+ , Mn 2+ or Co 2+ . 74% of so. n. neurons fired spontaneously at rates exceeding 0.1 spikes per second, with a mean for all cells of 2.9±0.2 s -1 . Of these cells, 21% fired slowly and continuously at 0.1─1.0 s -1 , 45 % fired continuously at greater than 1 Hz, and the remaining 34% fired phasically in bursts of activity followed by silence or low frequency firing. Spontaneously firing phasic cells showed a mean burst length of 16.7± 4.5 s and a silent period of 28.2±4.2 s. Intracellular recordings revealed the presence of slow variations in membrane potential which modified the neuron’s proximity to spike threshold, and controlled phasic firing. Variations in synaptic input were not observed to influence firing in phasic cells.

Angiotensin II receptor activation depolarizes rat supraoptic neurons in vitro

1992 ◽  
Vol 263 (6) ◽  
pp. R1333-R1338 ◽  
Author(s):  
C. R. Yang ◽  
M. I. Phillips ◽  
L. P. Renaud
Keyword(s):  
Angiotensin Ii ◽  
Supraoptic Nucleus ◽  
Reversal Potential ◽  
Input Resistance ◽  
Receptor Activation ◽  
Induced Response ◽  
Angiotensin Ii Receptor ◽  
Functional Studies

Functional studies indicate that hypothalamic magnocellular neurosecretory neurons are a target for angiotensin. The present investigation used intracellular recordings to characterize the nature and type of angiotensin II receptors on rat supraoptic nucleus neurons maintained in superfused hypothalamic explants. Of 68 cells transiently exposed to either Val5- or Ile5-angiotensin II (maximum peak concentration 1-25 microM), 34 responded with a gradual membrane depolarization (1-15 mV) that peaked in 2.2 +/- 0.4 (SD) min and was accompanied by a 17.6 +/- 4.8% reduction of input resistance. Responses persisted (and were actually enhanced) in media containing tetrodotoxin (0.5-1.0 microM) and/or nominally zero calcium, indicating a direct postsynaptic action. In 19 responsive cells, the mean reversal potential for the angiotensin-induced response was -26.4 +/- 2 mV. Bath application of the nonpeptide type-1 angiotensin receptor antagonist DuP753 (5-20 microM) reversibly blocked the angiotensin-induced depolarization in all of 11 cells tested. By contrast, equimolar applications of the type-2 antagonist PD123177 were ineffective in all seven angiotensin-responsive cells tested. These observations provide novel evidence for the existence of functional type-1 receptors on rat supraoptic nucleus neurons. The reversal potential for the angiotensin-induced response suggests mediation through a nonselective cationic conductance.

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