scholarly journals Putative synaptic mechanisms of inhibition in Limulus lateral eye.

1976 ◽  
Vol 67 (4) ◽  
pp. 417-431 ◽  
Author(s):  
A R Adolph
Keyword(s):  
Receptor Potential ◽  
Cell Receptor ◽  
Ion Concentration ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Extracellular Potassium ◽  
Retinular Cell ◽  
Generator Potential ◽  
Iontophoretic Application ◽  
Lateral Eye

Serotonin (5-HT) perfusion of a thin section of Limulus lateral eye hyperpolarizes retinular and eccentric cell membrane potential, and blocks spike action potentials fired by the eccenteric cell. The indoleamine does not directly affect retinular cell receptor potential or eccenteric cell generator potential in response to light stimuli. LSD perfusion blocks both this inhibitory action of 5-HT and light-evoked, synaptically mediated, lateral inhibition. Iontophoretic application of 5-HT to the synaptic neuropil produces shorter latency and duration and larger amplitude of inhibition than does the perfusion technique. This inhibition is dose dependent; the accompanying inhibitory postsynaptic potential (IPSP) appears to have an equilibrium potential more hyperpolarized than normal resting potential levels of ca. -50 mV. IPSP amplitude is sensitive to extracellular potassium ion concentration: it increases with decreased [K+]0 and decreases with increased [K+]0. LSD blocks the inhibition produced by iontophoretic application of 5-HT. Interaction between light-evoked, natural synaptic transmitter-mediated IPSP's and 5-HT IPSP's suggests a common postsynaptic receptor or transmitter-receptor-permeability change mechanism.

scholarly journals FURTHER STUDY OF SOMA, DENDRITE, AND AXON EXCITATION IN SINGLE NEURONS

1955 ◽  
Vol 39 (1) ◽  
pp. 121-153 ◽  
Author(s):  
Carlos Eyzaguirre ◽  
Stephen W. Kuffler
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Recovery Period ◽  
Local Potential ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Cell Soma ◽  
Generator Potential ◽  
Wide Range ◽  
Set Up

The present investigation continues a previous study in which the soma-dendrite system of sensory neurons was excited by stretch deformation of the peripheral dendrite portions. Recording was done with intracellular leads which were inserted into the cell soma while the neuron was activated orthodromically or antidromically. The analysis was also extended to axon conduction. Crayfish, Procambarus alleni (Faxon) and Orconectes virilis (Hagen), were used. 1. The size and time course of action potentials recorded from the soma-dendrite complex vary greatly with the level of the cell's membrane potential. The latter can be changed over a wide range by stretch deformation which sets up a "generator potential" in the distal portions of the dendrites. If a cell is at its resting unstretched equilibrium potential, antidromic stimulation through the axon causes an impulse which normally overshoots the resting potential and decays into an afternegativity of 15 to 20 msec. duration. The postspike negativity is not followed by an appreciable hyperpolarization (positive) phase. If the membrane potential is reduced to a new steady level a postspike positivity appears and increases linearly over a depolarization range of 12 to 20 mv. in various cells. At those levels the firing threshold of the cell for orthodromic discharges is generally reached. 2. The safety factor for conduction between axon and cell soma is reduced under three unrelated conditions, (a) During the recovery period (2 to 3 msec.) immediately following an impulse which has conducted fully over the cell soma, a second impulse may be delayed, may invade the soma partially, or may be blocked completely. (b) If progressive depolarization is produced by stretch, it leads to a reduction of impulse height and eventually to complete block of antidromic soma invasion, resembling cathodal block, (c) In some cells, when the normal membrane potential is within several millivolts of the relaxed resting state, an antidromic impulse may be blocked and may set up within the soma a local potential only. The local potential can sum with a second one or it may sum with potential changes set up in the dendrites, leading to complete invasion of the soma. Such antidromic invasion block can always be relieved by appropriate stretch which shifts the membrane potential out of the "blocking range" nearer to the soma firing level. During the afterpositivity of an impulse in a stretched cell the membrane potential may fall below or near the blocking range. During that period another impulse may be delayed or blocked. 3. Information regarding activity and conduction in dendrites has been obtained indirectly, mainly by analyzing the generator action under various conditions of stretch. The following conclusions have been reached: The large dendrite branches have similar properties to the cell body from which they arise and carry the same kind of impulses. In the finer distal filaments of even lightly depolarized dendrites, however, no axon type all-or-none conduction occurs since the generator potential persists to a varying degree during antidromic invasion of the cell. With the membrane potential at its resting level the dendrite terminals contribute to the prolonged impulse afternegativity of the soma. 4. Action potentials in impaled axons and in cell bodies have been compared. It is thought that normally the over-all duration of axon impulses is shorter. Local activity during reduction of the safety margin for conduction was studied. 5. An analysis was made of high frequency grouped discharges which occasionally arise in cells. They differ in many essential aspects from the regular discharges set up by the generator action. It is proposed that grouped discharges occur only when invasion of dendrites is not synchronous, due to a delay in excitation spread between soma and dendrites. Each impulse in a group is assumed to be caused by an impulse in at least one of the large dendrite branches. Depolarization of dendrites abolishes the grouped activity by facilitating invasion of the large dendrite branches.

scholarly journals Effects of the rod receptor potential upon retinal extracellular potassium concentration.

1979 ◽  
Vol 74 (6) ◽  
pp. 713-737 ◽  
Author(s):  
B Oakley ◽  
D G Flaming ◽  
K T Brown
Keyword(s):  
Time Course ◽  
Potassium Concentration ◽  
Receptor Potential ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Photoreceptor Layer ◽  
Extracellular Potassium Concentration ◽  
Wide Range ◽  
The Relationship ◽  
Toad Bufo

It has been hypothesized that the light-evoked rod hyperpolarization (the receptor potential) initiates the light-evoked decrease in extracellular potassium ion concentration, [K+]o, in the distal retina. The hypothesis was tested using the isolated, superfused retina of the toad, Bufo marinus; the receptor potential was recorded intracellularly from red rods, and [K+]o was measured in the photoreceptor layer with K+-specific microelectrodes. In support of the hypothesis, variations in stimulus irradiance or duration, or in retinal temperature, produced qualitatively similar effects on both the receptor potential and the decrease in [K+]o. A mechanism for the relationship between the receptor potential and the decrease in [K+]o was suggested by Matsuura et al. (1978. Vision Res. 18:767-775). In the dark, the passive efflux of K+ out of the rod is balanced by an equal influx of K+ fromthe Na+/K+ pump. The light-evoked rod hyperpolarization is assumed to reduce the passive efflux, with little effect on the pump. Thus, the influx will exceed the efflux, and [K+]o will decrease. Consistent with this mechanism, the largest and most rapid decrease in [K+]o was measured adjacent to the rod inner segments, where the Na+/K+ pump is most likely located; in addition, inhibition of the pump with ouabain abolished the decrease in [K]o more rapidly than the rod hyperpolarization. Based upon this mechanism, Matsuura et al. (1978) developed a mathematical model: over a wide range of stimulus irradiance, this model successfully predicts the time-course of the decrease in [K+]o, given only the time-course of the rod hyperpolarization.

Effect of elevated potassium on the ion content of mouse astrocytes and neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S263-S268 ◽  
Author(s):  
H. Steve White ◽  
Sien Yao Chow ◽  
Y. C. Yen-Chow ◽  
Dixon M. Woodbury
Keyword(s):  
Cortical Neurons ◽  
Cell Types ◽  
Mouse Cell ◽  
Ion Concentration ◽  
Cellular Heterogeneity ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Individual Response ◽  
Extracellular Potassium Concentration ◽  
The Brain

Potassium is tightly regulated within the extracellular compartment of the brain. Nonetheless, it can increase 3- to 4-fold during periods of intense seizure activity and 10- to 20-fold under certain pathological conditions such as spreading depression. Within the central nervous system, neurons and astrocytes are both affected by shifts in the extracellular concentration of potassium. Elevated potassium can lead to a redistribution of other ions (e.g., calcium, sodium, chloride, hydrogen, etc.) within the cellular compartment of the brain. Small shifts in the extracellular potassium concentration can markedly affect acid–base homeostasis, energy metabolism, and volume regulation of these two brain cells. Since normal neuronal function is tightly coupled to the ability of the surrounding glial cells to regulate ionic shifts within the brain and since both cell types can be affected by shifts in the extracellular potassium, it is important to characterize their individual response to an elevation of this ion. This review describes the results of side-by-side studies conducted on cortical neurons and astrocytes, which assessed the effect of elevated potassium on their resting membrane potential, intracellular volume, and their intracellular concentration of potassium, sodium, and chloride. The results obtained from these studies suggest that there exists a marked cellular heterogeneity between neurons and astrocytes in their response to an elevation in the extracellular potassium concentration.Key words: astrocytes, neurons, ion concentration, neuronal–glial interactions, mouse, cell culture.

Synaptic transmission and its duplication by focally applied acetylcholine in parasympathetic neurons in the heart of the frog

1971 ◽  
Vol 177 (1049) ◽  
pp. 509-539 ◽  
Keyword(s):  
Synaptic Transmission ◽  
Ganglion Cells ◽  
Postsynaptic Membrane ◽  
Equilibrium Potential ◽  
Neuronal Membrane ◽  
Excitatory Postsynaptic Potential ◽  
Parasympathetic Nerve ◽  
Iontophoretic Application ◽  
Synaptic Boutons ◽  
Synaptic Transmitter

Synaptic transmission has been analysed in parasympathetic nerve cells that lie in the transparent interatrial septum of the heart of the frog. Using Nomarski interference optics, one can see much cellular detail, including synaptic boutons in living preparations. 1. On each ganglion cell, the 10 to 20 synaptic boutons are usually derived from a single vagal nerve fibre. These fibres branch extensively to innervate a number of septal ganglion cells. 2. The chemical transmitter, acetylcholine (ACh), liberated by a presynaptic impulse survives for up to 40 ms, setting up an excitatory postsynaptic potential (e.p.s.p.) which triggers one and sometimes two action potentials in the postsynaptic cell. The e.p.s.p. is made up of quantal components, as at the neuromuscular junction. 3. Nerve-evoked e.p.s.p.s can be well matched in amplitude and time course by iontophoretic application of ACh to selected areas of the neuronal membrane. In particular, the miniature e.p.s.p., which is due to the focal release of a small quantity of transmitter, was accurately mimicked by iontophoretic application of ACh. By grading the amount of ACh released from an electrode one could also duplicate the wide variety of nerve-evoked postsynaptic discharges of ganglion cells. 4. The permeability changes initiated in the postsynaptic membrane by applied ACh and the synaptic transmitter appear identical, since the ionic fluxes for both responses have the same equilibrium potential. Also, the receptors which react with the synaptic transmitter are desensitized by applied ACh. 5. Cholinesterase inhibitors (Tensilon and Eserine) have a variable action on different cells, with respect both to nerve-evoked and Ach evoked potentials. The reasons for this variation are unclear, and need further study. 6. Miniature e.p.s.p.s resemble analogous potentials at nerve-muscle junctions and other synapses. A significant proportion of the min e.p.s.p.s is released as multiple units. This proportion is increased in high Ca2+, while single units alone occur in a low Ca2+-high Mg2+ environment. 7. The experiments provide information about the release of ACh from nerve terminals and its action on the postsynaptic membrane of neurons. They are in good agreement with analogous studies on skeletal neuromuscular junctions

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Evolution of Endolymph Secretion and Endolymphatic Potential Generation in the Vertebrate Inner Ear

2018 ◽  
Vol 92 (1-2) ◽  
pp. 1-31 ◽  
Author(s):  
Christine Köppl ◽  
Viviane Wilms ◽  
Ian John Russell ◽  
Hans Gerd Nothwang
Keyword(s):  
Inner Ear ◽  
Lateral Line ◽  
Vestibular System ◽  
Molecular Mechanisms ◽  
Receptor Potential ◽  
Cell Types ◽  
Cell Receptor ◽  
Striking Difference ◽  
High K ◽  
Endolymphatic Potential

The ear of extant vertebrates reflects multiple independent evolutionary trajectories. Examples include the middle ear or the unique specializations of the mammalian cochlea. Another striking difference between vertebrate inner ears concerns the differences in the magnitude of the endolymphatic potential. This differs both between the vestibular and auditory part of the inner ear as well as between the auditory periphery in different vertebrates. Here we provide a comparison of the cellular and molecular mechanisms in different endorgans across vertebrates. We begin with the lateral line and vestibular systems, as they likely represent plesiomorphic conditions, then review the situation in different vertebrate auditory endorgans. All three systems harbor hair cells bathed in a high (K+) environment. Superficial lateral line neuromasts are bathed in an electrogenically maintained high (K+) microenvironment provided by the complex gelatinous cupula. This is associated with a positive endocupular potential. Whether this is a special or a universal feature of lateral line and possibly vestibular cupulae remains to be discovered. The vestibular system represents a closed system with an endolymph that is characterized by an enhanced (K+) relative to the perilymph. Yet only in land vertebrates does (K+) exceed (Na+). The endolymphatic potential ranges from +1 to +11 mV, albeit we note intriguing reports of substantially higher potentials of up to +70 mV in the cupula of ampullae of the semicircular canals. Similarly, in the auditory system, a high (K+) is observed. However, in contrast to the vestibular system, the positive endolymphatic potential varies more substantially between vertebrates, ranging from near zero mV to approximately +100 mV. The tissues generating endolymph in the inner ear show considerable differences in cell types and location. So-called dark cells and the possibly homologous ionocytes in fish appear to be the common elements, but there is always at least one additional cell type present. To inspire research in this field, we propose a classification for these cell types and discuss potential evolutionary relationships. Their molecular repertoire is largely unknown and provides further fertile ground for future investigation. Finally, we propose that the ultimate selective pressure for an increased endolymphatic potential, as observed in mammals and to a lesser extent in birds, is specifically to maintain the AC component of the hair-cell receptor potential at high frequencies. In summary, we identify intriguing questions for future directions of research into the molecular and cellular basis of the endolymph in the different compartments of the inner ear. The answers will provide important insights into evolutionary and developmental processes in a sensory organ essential to many species, including humans.

Hyperpolarization-Activated Inward Current in Neurons of the Rat's Dorsal Nucleus of the Lateral Lemniscus In Vitro

1997 ◽  
Vol 78 (5) ◽  
pp. 2235-2245 ◽  
Author(s):  
Xiao Wen Fu ◽  
Borys L. Brezden ◽  
Shu Hui Wu
Keyword(s):  
Membrane Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Extracellular Potassium ◽  
Current Clamp ◽  
Lateral Lemniscus ◽  
Inward Current ◽  
Dorsal Nucleus ◽  
Maximal Activation

Fu, Xiao Wen, Borys L. Brezden, and Shu Hui Wu. Hyperpolarization-activated inward current in neurons of the rat's dorsal nucleus of the lateral lemniscus in vitro. J. Neurophysiol. 78: 2235–2245, 1997. The hyperpolarization-activated current ( I h) underlying inward rectification in neurons of the rat's dorsal nucleus of the lateral lemniscus (DNLL) was investigated using whole cell patch-clamp techniques. Patch recordings were made from DNLL neurons of young rats (21–30 days old) in 400 μm tissue slices. Under current clamp, injection of negative current produced a graded hyperpolarization of the cell membrane, often with a gradual sag in the membrane potential toward the resting value. The rate and magnitude of the sag depended on the amount of hyperpolarizing current. Larger current resulted in a larger and faster decay of the voltage. Under voltage clamp, hyperpolarizing voltage steps elicited a slowly activating inward current that was presumably responsible for the sag observed in the voltage response to a steady hyperpolarizing current recorded under current clamp. Activation of the inward current ( I h) was voltage and time dependent. The current just was seen at a membrane potential of −70 mV and was activated fully at −140 mV. The voltage value of half-maximal activation of I h was −78.0 ± 6.0 (SE) mV. The rate of I h activation was best approximated by a single exponential function with a time constant that was voltage dependent, ranging from 276 ± 27 ms at −100 mV to 186 ± 11 ms at −140 mV. Reversal potential ( E h) of I h current was more positive than the resting potential. Raising the extracellular potassium concentration shifted E h to a more depolarized value, whereas lowering the extracellular sodium concentration shifted E h in a more negative direction. I h was sensitive to extracellular cesium but relatively insensitive to extracellular barium. The current amplitude near maximal-activation (about −140 mV) was reduced to 40% of control by 1 mM cesium but was reduced to only 71% of control by 2 mM barium. When the membrane potential was near the resting potential (about −60 mV), cesium had no effect on the membrane potential, current-evoked firing rate and input resistance but reduced the spontaneous firing. When the membrane potential was more negative than −70 mV, cesium hyperpolarized the cell, decreased current-evoked firing and increased the input resistance. I h in DNLL neurons does not contribute to the normal resting potential but may enhance the extent of excitation, thereby making the DNLL a consistently powerful inhibitory source to upper levels of the auditory system.

scholarly journals Timing of Ca2+ Release from Intracellular Stores and the Electrical Response of Limulus Ventral Photoreceptors to Dim Flashes

2000 ◽  
Vol 115 (6) ◽  
pp. 735-748 ◽  
Author(s):  
Richard Payne ◽  
James Demas
Keyword(s):  
Latent Period ◽  
Electrical Response ◽  
Cyclopiazonic Acid ◽  
Receptor Potential ◽  
Ion Concentration ◽  
Free Calcium ◽  
Flash Intensity ◽  
Stochastic Variation ◽  
Highly Correlated ◽  
Indicator Dyes

Light-induced release of Ca2+ from stores in Limulus ventral photoreceptors was studied using confocal fluorescence microscopy and the Ca2+ indicator dyes, Oregon green-5N and fluo-4. Fluorescence was collected from a spot within 4 μm of the microvillar membrane. A dual-flash protocol was used to reconstruct transient elevations of intracellular free calcium ion concentration (Cai) after flashes delivering between 10 and 5 × 105 effective photons. Peak Cai increased with flash intensity to 138 ± 76 μM after flashes delivering ∼104 effective photons, while the latent period of the elevation of Cai fell from ∼140 to 21 ms. The onset of the light-induced elevation of Cai was always highly correlated with that of the receptor potential. The time for Cai to exceed 2 μM was approximately equal to that for the receptor potential to exceed 8 mV (mean difference; 2.2 ± 6.4 ms). Cai was also measured during steps of light delivering ∼105 effective photons/s to photoreceptors that had been bleached with hydroxylamine so as to reduce their quantum efficiency. Elevations of Cai were detected at the earliest times of the electrical response to the steps of light, when a significant receptor potential had yet to develop. Successive responses exhibited stochastic variation in their latency of up to 20 ms, but the elevation of Cai and the receptor potential still rose at approximately the same time, indicating a shared process generating the latent period. Light-induced elevations of Cai resulted from Ca2+ release from intracellular stores, being abolished by cyclopiazonic acid (CPA), an inhibitor of endoplasmic reticulum Ca2+ pumps, but not by removal of extracellular Ca2+ ions. CPA also greatly diminished and slowed the receptor potential elicited by dim flashes. The results demonstrate a rapid release of Ca2+ ions that appears necessary for a highly amplified electrical response to dim flashes.

scholarly journals The Ventral Photoreceptor Cells of Limulus

1969 ◽  
Vol 54 (3) ◽  
pp. 310-330 ◽  
Author(s):  
Ronald Millecchia ◽  
Alexander Mauro
Keyword(s):  
Receptor Potential ◽  
Photoreceptor Cells ◽  
Regenerative Process ◽  
Resting Potential ◽  
Transient Phase ◽  
External Concentration ◽  
Slow Potential ◽  
Retinular Cells ◽  
Convenient Model ◽  
State Component

The ventral photoreceptors of Limulus polyphemus are unipolar cells with large, ellipsoidal somas located long both "lateral olfactory nerves." As a consequence of their size and location, the cells are easily impaled with microelectrodes. The cells have an average resting potential of -48 mv. The resting potential is a function of the external concentration of K. When the cell is illuminated, it gives rise to the typical "receptor potential" seen in most invertebrate photoreceptors which consists of a transient phase followed by a maintained phase of depolarization. The amplitude of the transient phase depends on both the state of adaptation of the cell and the intensity of the illumination, while the amplitude of the maintained phase depends only on the intensity of the illumination. The over-all size of the receptor potential depends on the external concentration of Na, e.g. in sodium-free seawater the receptor potential is markedly reduced, but not abolished. On the other hand lowering the Ca concentration produces a marked enhancement of both components of the response, but predominantly of the steady-state component. Slow potential fluctuations are seen in the dark-adapted cell when it is illuminated with a low intensity light. A spike-like regenerative process can be evoked by either the receptor potential or a current applied via a microelectrode. No evidence of impulse activity has been found in the axons of these cells. The ventral photoreceptor cell has many properties in common with a variety of retinular cells and therefore should serve as a convenient model of the primary receptor cell in many invertebrate eyes.

scholarly journals In Vivo Neocortical [K]o Modulation by Targeted Stimulation of Astrocytes

2021 ◽  
Vol 22 (16) ◽  
pp. 8658
Author(s):  
Azin EbrahimAmini ◽  
Shanthini Mylvaganam ◽  
Paolo Bazzigaluppi ◽  
Mohamad Khazaei ◽  
Alexander Velumian ◽  
...  
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Potassium Ion ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Spreading Depolarization ◽  
Potential Tool ◽  
Stimulation Of

A normally functioning nervous system requires normal extracellular potassium ion concentration ([K]o). Throughout the nervous system, several processes, including those of an astrocytic nature, are involved in [K]o regulation. In this study we investigated the effect of astrocytic photostimulation on [K]o. We hypothesized that in vivo photostimulation of eNpHR-expressing astrocytes leads to a decreased [K]o. Using optogenetic and electrophysiological techniques we showed that stimulation of eNpHR-expressing astrocytes resulted in a significantly decreased resting [K]o and evoked K responses. The amplitude of the concomitant spreading depolarization-like events also decreased. Our results imply that astrocytic membrane potential modification could be a potential tool for adjusting the [K]o.

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