scholarly journals PROCESSES OF EXCITATION IN THE DENDRITES AND IN THE SOMA OF SINGLE ISOLATED SENSORY NERVE CELLS OF THE LOBSTER AND CRAYFISH

1955 ◽  
Vol 39 (1) ◽  
pp. 87-119 ◽  
Author(s):  
Carlos Eyzaguirre ◽  
Stephen W. Kuffler
Keyword(s):  
Membrane Potential ◽  
Cell Body ◽  
Action Potentials ◽  
Sensory Nerve ◽  
Resting Potential ◽  
Cell Soma ◽  
Appreciable Change ◽  
Generator Potential ◽  
Receptor Cells ◽  
Wide Range

The stretch receptor organs of Alexandrowicz in lobster and crayfish possess sensory neurons which have their cell bodies in the periphery. The cell bodies send dendrites into a fine nearby muscle strand and at the opposite pole they give rise to an axon running to the central nervous system. Mechanisms of excitation between dendrites, cell soma, and axon have been studied in completely isolated receptor structures with the cell components under visual observation. Two sensory neuron types were investigated, those which adapt rapidly to stretch, the fast cells, and those which adapt slowly, the slow cells. 1. Potentials recorded from the cell body of the neurons with intracellular leads gave resting potentials of 70 to 80 mv. and action potentials which in fresh preparations exceeded the resting potentials by about 10 to 20 mv. In some experiments chymotrypsin or trypsin was used to make cell impalement easier. They did not appreciably alter resting or action potentials. 2. It has been shown that normally excitation starts in the distal portion of dendrites which are depolarized by stretch deformation. The changed potential within the dendritic terminals can persist for the duration of stretch and is called the generator potential. Secondarily, by electrotonic spread, the generator potential reduces the resting potential of the nearby cell soma. This excitation spread between dendrites and soma is seen best during subthreshold excitation by relatively small stretches of normal cells. It is also seen during the whole range of receptor stretch in neurons in which nerve conduction has been blocked by an anesthetic. The electrotonic changes in the cells are graded, reflecting the magnitude and rate of rise of stretch, and presumably the changing levels of the generator potential. Thus in the present neurons the resting potential and the excitability level of the cell soma can be set and controlled over a wide range by local events within the dendrites. 3. Whenever stretch reduces the resting membrane potential, measured in the relaxed state in the cell body, by 8 to 12 mv. in slow cells and by 17 to 22 mv. in fast cells, conducted impulses are initiated. It is thought that in slow cells conducted impulses are initiated in the dendrites while in fast cells they arise in the cell body or near to it. In fresh preparations the speed of stretch does not appreciably influence the membrane threshold for discharges, while during developing fatigue the firing level is higher when extension is gradual. 4. Some of the specific neuron characteristics are: Fast receptor cells have a relatively high threshold to stretch. During prolonged stretch the depolarization of the cell soma is not well maintained, presumably due to a decline in the generator potential, resulting in cessation of discharges in less than a minute. This appears to be the basis of the relatively rapid adaptation. A residual subthreshold depolarization can persist for many minutes of stretch. Slow cells which resemble the sensory fibers of vertebrate spindles are excited by weak stretch. Their discharge rate remains remarkably constant for long periods. It is concluded that, once threshold excitation is reached, the generator potential within slow cell dendrites is well maintained for the duration of stretch. Possible reasons for differences in discharge properties between fast and slow cells are discussed. 5. If stretch of receptor cells is gradually continued above threshold, the discharge frequency first increases over a considerable range without an appreciable change in the firing level for discharges. Beyond that range the membrane threshold for conducted responses of the cell soma rises, the impulses become smaller, and partial conduction in the soma-axon boundary region occurs. At a critical depolarization level which may be maintained for many minutes, all conduction ceases. These overstretch phenomena are reversible and resemble cathodal block. 6. The following general scheme of excitation is proposed: stretch deformation of dendritic terminals → generator potential → electrotonic spread toward the cell soma (prepotential) → dendrite-soma impulse → axon impulse. 7. Following release of stretch a transient hyperpolarization of slow receptor cells was seen. This off effect is influenced by the speed of relaxation. 8. Membrane potential changes recorded in the cell bodies serve as very sensitive detectors of activity within the receptor muscle bundles, indicating the extent and time course of contractile events.

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.

Effects of pH on excitation and contraction in frog twitch muscle

1977 ◽  
Vol 55 (3) ◽  
pp. 709-723 ◽  
Author(s):  
J. G. Foulks ◽  
Florence A. Perry
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Time Course ◽  
Calcium Concentration ◽  
Divalent Cations ◽  
Ion Concentration ◽  
Resting Potential ◽  
Hydrogen Ion Concentration ◽  
Wide Range ◽  
Effects Of Ph

The electrical and mechanical behaviour of frog twitch muscle in response to changes in membrane potential has been examined over a wide range of hydrogen ion concentration (pH 3.0–11.0). The changes in resting and action potentials, twitches, and maximum potassium-induced contractures (K contractures) were remarkably small when the pH was varied between 5.0 and 10.0. The time course of action potentials generally displayed small graded changes with variation in pH, possibly as the result of changes in surface potential.The amplitude of twitches and maximum K contractures was substantially decreased when pH was reduced to 4.0 or raised to 11.0 without significant alteration in membrane resting potential or consistent suppression of excitation, but maximum caffeine-induced contractures were unchanged. Replacement of chloride with perchlorate promptly antagonized the depressant effects of pH extremes (4.0, 11.0) on both twitch amplitude and maximum K-contracture tension. Acid-induced reductions in maximum K-contracture tension also were partially antagonized by increased calcium concentration. The onset and recovery from the contraction-depressant effects of pH extremes were too slow to be explained by the titration of groups immediately accessible at the membrane surface but too rapid to be accounted for by changes in intracellular pH. Thus, excitation and contraction apparently were uncoupled by sufficient alteration in extracellular pH. Changes in external pH had little effect on the impairment of maximum K contractures by media lacking divalent cations, or on the restoration of such responses by perchlorate except at very alkaline pH (10.0–11.0).The threshold for K contractures was reduced at pH 11.0, but otherwise was little affected by variation in pH at normal concentrations of divalent cations. Altered pH did not modify the usual effects of increased calcium concentration on the relation between potassium concentration and K-contracture tension. When K contractures were maintained by perchlorate in the absence of divalent cations, hydrogen ions displayed calcium-like actions on the relation between external K concentration ([K]0) and K-contracture tension, and also on the time course of submaximum K contractures. These observations are compatible with similar effects of hydrogen and calcium ions on surface potential.The problem of identifying putative charged groups which might influence the linkage between contractile responses and changes in membrane potential is discussed.

scholarly journals SYNAPTIC INHIBITION IN AN ISOLATED NERVE CELL

1955 ◽  
Vol 39 (1) ◽  
pp. 155-184 ◽  
Author(s):  
Stephen W. Kuffler ◽  
Carlos Eyzaguirre
Keyword(s):  
Nerve Fiber ◽  
Cell Body ◽  
Inhibitory Action ◽  
Receptor Cell ◽  
Stretch Receptor ◽  
Synaptic Activity ◽  
Resting Potential ◽  
Generator Potential ◽  
Receptor Cells ◽  
Set Up

Following the preceding studies on the mechanisms of excitation in stretch receptor cells of crayfish, this investigation analyzes inhibitory activity in the synapses formed by two neurons. The cell body of the receptor neuron is located in the periphery and sends dendrites into a fine muscle strand. The dendrites receive innervation through an accessory nerve fiber which has now been established to be inhibitory. There exists a direct peripheral inhibitory control mechanism which can modulate the activity of the stretch receptor. The receptor cell which can be studied in isolation was stimulated by stretch deformation of its dendrites or by antidromic excitation and the effect of inhibitory impulses on its activity was analyzed. Recording was done mainly with intracellular leads inserted into the cell body. 1. Stimulation of the relatively slowly conducting inhibitory nerve fiber either decreases the afferent discharge rate or stops impulses altogether in stretched receptor cells. The inhibitory action is confined to the dendrites and acts on the generator mechanism which is set up by stretch deformation. By restricting depolarization of the dendrites above a certain level, inhibition prevents the generator potential from attaining the "firing level" of the cell. 2. The same inhibitory impulse may set up a postsynaptic polarization or a depolarization, depending on the resting potential level of the cell. The membrane potential at which the inhibitory synaptic potential reverses its polarity, the equilibrium level, may vary in different preparations. The inhibitory potentials increase as the resting potential is displaced in any direction from the inhibitory equilibrium. 3. The inhibitory potentials usually rise to a peak in about 2 msec. and decay in about 30 msec. After repetitive inhibitory stimulation a delayed secondary polarization phase has frequently been seen, prolonging the inhibitory action. Repetitive inhibitory excitation may also be followed by a period of facilitation. Some examples of "direct" excitation by the depolarizing action of inhibitory impulses are described. 4. The interaction between antidromic and inhibitory impulses was studied. The results support previous conclusions (a) that during stretch the dendrites provide a persisting "drive" for the more central portions of the receptor cell, and (b) that antidromic all-or-none impulses do not penetrate into the distal portions of stretch-depolarized dendrites. The "after-potentials" of antidromic impulses are modified by inhibition. 5. Evidence is presented that inhibitory synaptic activity increases the conductance of the dendrites. This effect may occur in the absence of inhibitory potential changes.

scholarly journals A chemical synapse between two motion detecting neurones in the locust brain

1984 ◽  
Vol 110 (1) ◽  
pp. 143-167 ◽  
Author(s):  
F. C. Rind
Keyword(s):  
Membrane Potential ◽  
Synaptic Transmission ◽  
Cell Body ◽  
Rise Time ◽  
Total Duration ◽  
Membrane Potentials ◽  
Resting Potential ◽  
Chemical Synapse ◽  
Half Time ◽  
Conductance Increase

The LGMD is the major source of visual input from the compound eye to the ipsilateral DCMD. Inactivating the LGMD or hyperpolarizing it, so it no longer spikes, abolishes the response of the DCMD to the visual stimulus. Synaptic transmission between the LGMD and DCMD neurones is chemical. A spike in the LGMD terminals induces a postsynaptic potential in the DCMD dendrites, with a transmission delay of 1 ms. There is a conductance increase in the DCMD during an LGMD-mediated PSP. The conductance increase occurs at membrane potentials when the current/voltage relationship of the DCMD membrane is linear, and at several different membrane potentials. The LGMD-mediated PSP within the dendritic region of the DCMD has a rise time of 1.3 ms, a half-time for decay of 2.2 ms and a total duration of 8.3 ms. In the cell body it has a rise time of 3.3 ms, a half-time for decay of 8 ms and a total duration of 21.3 ms. The amplitude of the LGMD-mediated PSP depends on the membrane potential of the DCMD. The PSP amplitude is increased by membrane hyperpolarization and decreased by membrane depolarizations. At a membrane potential 30 mV more positive than resting potential the extrapolated size of the PSP is zero. The synaptic efficiency of the LGMD-DCMD connection is usually 1.2. (formula; see text) There is a threshold of 13 mV in the LGMD before synaptic transmission occurs. Currents less than 13 mV are not transmitted in either direction across the synapse although they do reach the synaptic region if they are injected at the extremities of the neurones within the brain. Length constants for the LGMD are 0.36 mm between points c and d in the protocerebrum and 0.63 mm between point b in the optic lobe and point d in the protocerebrum. The length constant measured between the dendrite region of the DCMD and its cell body is 1.34 mm. DCMD spikes and PSPs follow spikes in the LGMD at a constant latency at frequencies up to 400 Hz. Usually a spike in the LGMD induces a spike in the DCMD.

Electrical Signaling in Neurons

The Neuron ◽  
2015 ◽  
pp. 41-62
Author(s):  
Irwin B. Levitan ◽  
Leonard K. Kaczmarek
Keyword(s):  
Plasma Membrane ◽  
Membrane Potential ◽  
Action Potentials ◽  
Sensory Information ◽  
External Stimulus ◽  
Resting Potential ◽  
Regular Pattern ◽  
Action Potential Firing ◽  
Potential Firing ◽  
Electrical Signaling

In neurons, information is carried from one part of the cell to another in the form of action potentials—large and rapidly reversible fluctuations in electrical voltage across the plasma membrane that propagate along the axon. Different neurons exhibit different patterns of action potential firing. Some neurons are normally silent; their membrane potential remains at the resting potential unless the firing of action potentials is triggered by some external stimulus, and they return to their non-firing state when the stimulus is no longer present. Many neurons exhibit more complex endogenous electrical activity, often firing action potentials in a regular pattern without an external stimulus. The electrical properties of a neuron are subject to modulation by input from the environment, including sensory information from the outside world, hormones released from other parts of the organism, and chemical and electrical signals from other neurons to which the neuron is functionally connected.

Helping students to understand that outward currents depolarize cells.

1999 ◽  
Vol 276 (6) ◽  
pp. S62
Author(s):  
M Stewart
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Building Blocks ◽  
Resting Potential ◽  
Potassium Ions ◽  
General Statement ◽  
Outward Currents ◽  
Excitable Membranes ◽  
A Cell

The physiology of excitable membranes is a fundamental topic in neuroscience and physiology courses at graduate and undergraduate levels. From the building blocks of ionic gradients and membrane channels whose permeability is selective and variable, we build the concepts of resting potential, action potential, and propagation in neurons and muscle fibers. Many students have an intuitive understanding of the movements of ions and the associated changes in membrane potential. For example, potassium ions leaving a cell through potassium-selective channels become unbalanced positive charges on the outside of the cell (and leave unbalanced negative charges on the inside), thus producing a potential across the membrane with the inside negative with respect to the outside. Later, when we discuss the local circuit currents that underlie propagation or the basis for extracellular stimulation, we make the general statement that "outward currents depolarize cells." Students respond with utter disbelief. Two simple additions to a discussion of membranes are suggested that permit the formulation of a consistent set of rules that apply to everything from the resting and action potentials of nerve and muscle through synaptic potentials and stimulation techniques.

Effects of estrogen and progesterone on single uterine muscle fibers in the rat

1959 ◽  
Vol 197 (4) ◽  
pp. 935-942 ◽  
Author(s):  
Jean M. Marshall
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Discharge Rate ◽  
Estradiol Benzoate ◽  
Resting Potential ◽  
Uterine Muscle ◽  
White Rats ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Ovariectomized white rats were treated as follows: group 1, 6.0 µg estradiol benzoate daily for 5 days; group 2, 6.0 µg estradiol for 3 days, then 1.6 µg estradiol plus 12 mg progesterone for 5 days; group 3, untreated controls. Membrane potentials were recorded from single uterine fibers, tension from the entire uterus. Untreated control fibers were quiescent, having a mean resting potential of 35.2 mv. Estrogen-dominated fibers were rhythmically contractile and had a mean resting potential of 57.6 mv. A train of action potentials accompanied and preceded each contraction of the muscle. In certain areas the fibers showed pacemaker-like characteristics, i.e. slow membrane depolarization between action potentials. Progesterone-dominated fibers had significantly higher resting potentials, mean 63.8 mv, but no localized pacemaker areas. Action potentials did not consistently precede or accompany contractions. In groups 1 and 2, acetylcholine stimulated contractions, lowered the membrane potential and increased the discharge rate of action potentials. Epinephrine diminished contractions, raised the membrane potential and abolished the action potential discharge.

scholarly journals Adenosine Triphosphate Activates a Noninactivating K+ Current in Adrenal Cortical Cells through Nonhydrolytic Binding

1997 ◽  
Vol 110 (6) ◽  
pp. 679-692 ◽  
Author(s):  
John J. Enyeart ◽  
Juan Carlos Gomora ◽  
Lin Xu ◽  
Judith A. Enyeart
Keyword(s):  
Membrane Potential ◽  
Resting Potential ◽  
K Channel ◽  
Atp Binding ◽  
Cortisol Secretion ◽  
Open Probability ◽  
Metabolic State ◽  
K Channels ◽  
Wide Range ◽  
K Current

Bovine adrenal zona fasciculata (AZF) cells express a noninactivating K+ current (IAC) that is inhibited by adrenocorticotropic hormone and angiotensin II at subnanomolar concentrations. Since IAC appears to set the membrane potential of AZF cells, these channels may function critically in coupling peptide receptors to membrane depolarization, Ca2+ entry, and cortisol secretion. IAC channel activity may be tightly linked to the metabolic state of the cell. In whole cell patch clamp recordings, MgATP applied intracellularly through the patch electrode at concentrations above 1 mM dramatically enhanced the expression of IAC K+ current. The maximum IAC current density varied from a low of 8.45 ± 2.74 pA/pF (n = 17) to a high of 109.2 ± 26.3 pA/pF (n = 6) at pipette MgATP concentrations of 0.1 and 10 mM, respectively. In the presence of 5 mM MgATP, IAC K+ channels were tonically active over a wide range of membrane potentials, and voltage-dependent open probability increased by only ∼30% between −40 and +40 mV. ATP (5 mM) in the absence of Mg2+ and the nonhydrolyzable ATP analog AMP-PNP (5 mM) were also effective at enhancing the expression of IAC, from a control value of 3.7 ± 0.1 pA/pF (n = 3) to maximum values of 48.5 ± 9.8 pA/pF (n = 11) and 67.3 ± 23.2 pA/pF (n = 6), respectively. At the single channel level, the unitary IAC current amplitude did not vary with the ATP concentration or substitution with AMP-PNP. In addition to ATP and AMP-PNP, a number of other nucleotides including GTP, UTP, GDP, and UDP all increased the outwardly rectifying IAC current with an apparent order of effectiveness: MgATP > ATP = AMP-PNP > GTP = UTP > ADP >> GDP > AMP and ATP-γ-S. Although ATP, GTP, and UTP all enhanced IAC amplitude with similar effectiveness, inhibition of IAC by ACTH (200 pM) occurred only in the presence of ATP. As little as 50 μM MgATP restored complete inhibition of IAC, which had been activated by 5 mM UTP. Although the opening of IAC channels may require only ATP binding, its inhibition by ACTH appears to involve a mechanism other than hydrolysis of this nucleotide. These findings describe a novel form of K+ channel modulation by which IAC channels are activated through the nonhydrolytic binding of ATP. Because they are activated rather than inhibited by ATP binding, IAC K+ channels may represent a distinctive new variety of K+ channel. The combined features of IAC channels that allow it to sense and respond to changing ATP levels and to set the resting potential of AZF cells, suggest a mechanism where membrane potential, Ca2+ entry, and cortisol secretion could be tightly coupled to the metabolic state of the cell through the activity of IAC K+ channels.

Whole cell recording from lobster olfactory receptor cells: responses to current and odor stimulation

1989 ◽  
Vol 61 (5) ◽  
pp. 994-1000 ◽  
Author(s):  
I. Schmiedel-Jakob ◽  
P. A. Anderson ◽  
B. W. Ache
Keyword(s):  
Membrane Potential ◽  
Electrical Properties ◽  
Olfactory Receptor ◽  
Action Potentials ◽  
Receptor Potential ◽  
Membrane Potentials ◽  
Patch Clamp Recording ◽  
Whole Cell ◽  
Olfactory Receptor Cells ◽  
Receptor Cells

1. The basic electrical properties of olfactory (antennule) receptor cells were studied in an in situ preparation of the spiny lobster using whole cell patch-clamp recording. 2. The current-voltage relationship of the cells was linear for membrane potentials between -150 and -40 mV and rectified at more positive membrane potentials. The input resistance at rest averaged 508 M omega. The cells displayed two time constants, with mean values of 29.8 and 8.2 ms. 3. Depolarizing current steps elicited fast, overshooting action potentials at a mean threshold of -32 mV from an imposed resting membrane potential of -65 mV. The action potentials were tetrodotoxin (TTX) and tetraethylammonium (TEA) sensitive, suggesting they are typical sodium/potassium action potentials. 4. Odor stimulation evoked slow, dose-dependent, depolarizing receptor potentials up to 50 mV in amplitude. In approximately 30% of cells tested, these led to repetitive spiking when the cells were depolarized beyond -45 to -30 mV. The amplitude of the receptor potential was graded as a linear function of the logarithm of the odor concentration. 5. The amplitude of the receptor potential varied linearly with the membrane potential between -70 and -30 mV. Extrapolated reversal potentials appeared to be normally distributed around a mean value of -3.6 mV. 6. The results collectively indicate that lobster olfactory receptor cells have electrical properties similar to, but not necessarily identical with, those currently envisaged for olfactory receptor cells in other species.

Mode of firing and rectifying properties of nucleus ovoidalis neurons in the avian auditory thalamus

1994 ◽  
Vol 71 (4) ◽  
pp. 1351-1360 ◽  
Author(s):  
B. Strohmann ◽  
D. W. Schwarz ◽  
E. Puil
Keyword(s):  
Action Potentials ◽  
Membrane Potentials ◽  
Resting Potential ◽  
Partial Result ◽  
Inward Rectification ◽  
Na Current ◽  
Stimulus Pulse ◽  
Current Pulses ◽  
Wide Range ◽  
Slow Potentials

1. We studied neurons of the nucleus ovoidalis, the principal auditory thalamic relay nucleus of the chicken, with tight-seal whole-cell recording techniques in in vitro slice preparations. Nucleus ovoidalis, marked by anterograde labeling of afferents from the inferior colliculus, consists of a clearly delineated group of densely packed, multipolar cells of approximately uniform diameter. We measured a wide range of non covarying resting potentials (-60 +/- 9 mV, mean +/- SD) and input resistances (277 +/- 168 M omega). All neurons discharged overshooting fast spikes. The observed electrophysiological properties may have a decisive role in the transfer of sensory signals. 2. We grouped neurons on the basis of their firing patterns, in response to intracellular injections of depolarizing current pulses from various membrane potentials. The majority of neurons (86%) displayed weakly adapting, tonic firing. A smaller group of neurons (14%) exhibited qualitative changes in firing modes. They fired repetitively when the stimulus pulse was superimposed on relatively depolarized levels, usually including the resting potential. DC-hyperpolarization led to burst responses consisting of fast action potentials on top of slow potentials. 3. In all neurons, application of 300 nM tetrodotoxin blocked the action potentials and reduced a depolarization-activated inward rectification, observed during 1-s current pulses in a range of membrane potentials depolarized from rest. This rectification is interpreted as a partial result of a persistent Na+ current. 4. During the applications of tetrodotoxin in neurons with burst firing capability, two other slow potentials were visible in isolation. Depolarizing current pulses evoked slow, transient depolarizations at the onset whereas rebound slow potentials occurred on termination of hyperpolarizing current pulses. The slow potentials were blocked by application of 0.5 mM Ni2+ and are likely a result of a low threshold Ca2+ current, such as a T-current. 5. A distinctive property of all ovoidalis neurons was a hyperpolarization-activated inward rectification. Application of Cs+ (3 mM) but not Ba2+ (3 mM), tetraethylammonium (10 mM), or 4-aminopyridine (4 mM) reversibly blocked the current that produced this rectification. The activation time constants for the current varied between approximately 50 and 400 ms and were voltage dependent in some neurons. Thus the hyperpolarization-activated current (IH), responsible for thalamic sleep mechanisms in mammals, also is present in a submammalian thalamus. 6. We suggest that the voltage and time dependencies of the persistent Na+ current and IH participate in generation of the sub- and suprathreshold temporal activity patterns in the neurons.(ABSTRACT TRUNCATED AT 400 WORDS)

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