Modification of Current Transmitted From Apical Dendrite to Soma by Blockade of Voltage- and Ca2+-Dependent Conductances in Rat Neocortical Pyramidal Neurons

1997 ◽  
Vol 78 (1) ◽  
pp. 187-198 ◽  
Author(s):  
Peter C. Schwindt ◽  
Wayne E. Crill
Keyword(s):  
Membrane Potential ◽  
Pyramidal Neurons ◽  
Reversal Potential ◽  
Apical Dendrite ◽  
Axial Current ◽  
Resting Potential ◽  
High Threshold ◽  
Voltage Gated ◽  
Distal Site ◽  
Neocortical Pyramidal Neurons

Schwindt, Peter C. and Wayne E. Crill. Modification of current transmitted from apical dendrite to soma by blockade of voltage- and Ca2+-dependent conductances in rat neocortical pyramidal neurons. J. Neurophysiol. 78: 187–198, 1997. The axial current transmitted to the soma during the long-lasting iontophoresis of glutamate at a distal site on the apical dendrite was measured by somatic voltage clamp of rat neocortical pyramidal neurons. Evidence for voltage- and Ca2+-gated channels in the apical dendrite was sought by examining the modification of this transmitted current resulting from the alteration of membrane potential and the application of channel-blocking agents. After N-methyl-d-aspartate receptor blockade, iontophoresis of glutamate on the soma evoked a current whose amplitude decreased linearly with depolarization to an extrapolated reversal potential near 0 mV. Under the same conditions, glutamate iontophoresis on the apical dendrite 241–537 μm from the soma resulted in a transmitted axial current that increased with depolarization over the same range of membrane potential (about −90 to −40 mV). Current transmitted from dendrite to soma was thus amplified during depolarization from resting potential (about −70 mV) and attenuated during hyperpolarization. After Ca2+ influx was blocked to eliminate Ca2+-dependent K+ currents, application of 10 mM tetraethylammonium chloride (TEA) altered the amplitude and voltage dependence of the transmitted current in a manner consistent with the reduction of dendritic voltage-gated K+ current. We conclude that dendritic, TEA-sensitive, voltage-gated K+ channels can be activated by tonic dendritic depolarization. The most prominent effects of blocking Ca2+ influx resembled those elicited by TEA application, suggesting that these effects were caused predominantly by blockade of a dendritic Ca2+-dependent K+ current. When cells were impaled with microelectrodes containing ethylene glycol-bis(β-amino-ethyl ether)- N,N′,N′-tetraacetic acid to prevent a rise in intracellular Ca2+ concentration, blockade of Ca2+ influx altered the tonic transmitted current in different manner consistent with the blockade of a inward dendritic current carried by high-threshold-activated Ca2+ channels. We conclude that the primary effect of Ca2+ influx during tonic dendritic depolarization is the activation of a dendritic Ca2+-dependent K+ current. The hyperpolarizing attenuation of transmitted current was unaffected by blocking all known voltage-gated inward currents except the hyperpolarization-activated cation current ( I h). Extracellular Cs+ (3 mM) reversibly abolished both the hyperpolarizing attenuation of transmitted current and I h measured at the soma. We conclude that activation of I h by hyperpolarization of the proximal apical dendrite would cause less axial current to arrive at the soma from a distal site than in a passive dendrite. Several functional implications of dendritic K+ and I h channels are discussed.

Local and Propagated Dendritic Action Potentials Evoked by Glutamate Iontophoresis on Rat Neocortical Pyramidal Neurons

1997 ◽  
Vol 77 (5) ◽  
pp. 2466-2483 ◽  
Author(s):  
Peter C. Schwindt ◽  
Wayne E. Crill
Keyword(s):  
Action Potentials ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Membrane Potentials ◽  
Current Injection ◽  
Resting Potential ◽  
Neural Input ◽  
Restricted Region ◽  
Low Threshold ◽  
Neocortical Pyramidal Neurons

Schwindt, Peter C. and Wayne E. Crill. Local and propagated dendritic action potentials evoked by glutamate iontophoresis on rat neocortical pyramidal neurons. J. Neurophysiol. 77: 2466–2483, 1997. Iontophoresis of glutamate at sites on the apical dendrite 278–555 μm from the somata of rat neocortical pyramidal neurons evoked low-threshold, small, slow spikes and/or large, fast spikes in 71% of recorded cells. The amplitude of the small, slow spikes recorded at the soma averaged 9.1 mV, and their apparent threshold was <10 mV positive to resting potential. Both their amplitude and their apparent threshold decreased as the iontophoretic site was moved farther from the soma. These spikes were not abolished by somatic hyperpolarization. When the somata of cells displaying these small spikes were voltage clamped at membrane potentials that prevented somatic or axonic firing, corresponding current spikes could be evoked all-or-none by dendritic depolarization, indicating that the small, slow spikes arose in the dendrite. Similar responses were not observed during somatic depolarization evoked by current pulses or glutamate iontophoresis. These small, slow spikes were abolished by blocking voltage-gated Ca2+ channels but not by blocking Na+ channels or N-methyl-d-aspartate receptors. We conclude that these Ca2+ spikes occurred in a spatially restricted region of the dendrite and were not actively propagated to the soma. In the presence of 10 mM tetraethylammonium chloride, the amplitudes of the iontophoretically evoked Ca2+ spikes were large, similar to those of the Ca2+ spikes evoked by somatic current injection, but their apparent thresholds were 63% lower. We conclude that dendritic K+ channels normally prevent the active propagation of Ca2+ spikes along the dendrite. In 36% of recorded cells dendritic glutamate iontophoresis evoked a Na+ spike with an apparent threshold 63% lower than those evoked by somatic current injection or somatic glutamate iontophoresis. Blockade of these low-threshold Na+ spikes by pharmacological or electrophysiological means often revealed underlying small dendritic Ca2+ spikes. When cells displaying the low-threshold Na+ spikes were voltage clamped at membrane potentials that prevented firing of the soma or axon, corresponding tetrodotoxin-sensitive current spikes could be evoked all-or-none by dendritic depolarization. We conclude that these low-threshold Na+ spikes were initiated in the dendrite, probably by local Ca2+ spikes, and subsequently propagated actively to the soma. Most cells displaying dendritic Na+ spikes fired multiple bursts of action potentials during tonic dendritic depolarization, whereas somatic depolarization of the same cells evoked only regular firing. We discuss the implications of dendritic Ca2+ and Na+ spikes for synaptic integration and neural input-output relations.

Equivalence of amplified current flowing from dendrite to soma measured by alteration of repetitive firing and by voltage clamp in layer 5 pyramidal neurons

1996 ◽  
Vol 76 (6) ◽  
pp. 3731-3739 ◽  
Author(s):  
P. Schwindt ◽  
W. Crill
Keyword(s):  
Voltage Clamp ◽  
Pyramidal Neurons ◽  
Network Models ◽  
Apical Dendrite ◽  
Axial Current ◽  
Resting Potential ◽  
Repetitive Firing ◽  
Active Dendrites ◽  
Parallel Shift ◽  
Curve Shift

1. Plots of steady firing rate versus injected current (f-I relations) were constructed from intrasomatic injected current pulses applied alone (control relations) and together with dendritic glutamate iontophoresis (test relations) at sites on the distal apical dendrite 185–555 microns from the soma in layer 5 pyramidal neurons from rat cortex studied in a brain slice. The test f-I relations exhibited a parallel shift along the current axis, and the slopes of the control and test relations differed by < 10% in most neurons. This behavior indicates that constant injected current and steady glutaminergic dendritic input evoke equivalent steady-state repetitive firing in a neuron with active dendrites. The parallel shift of the f-I curves allowed us to compute the amplitude of axial current arriving in the soma from the apical dendrite during repetitive firing. 2. We compared the transmitted current computed from the f-I curve shift with that measured by somatic voltage clamp during the same iontophoresis. When measured during voltage clamp at different somatic membrane potentials, the transmitted current increased with somatic depolarization (was amplified) in most cells, an observation inconsistent with passive dendrites. This larger-amplitude current closely predicted the transmitted current computed from the f-I curve shift, whereas the smaller transmitted current measured at resting potential did not. A set of control experiments indicated that these different predictions were well within the measurement error associated with computation of transmitted current based on f-I curve shifts. The action of blocking agents confirmed that the depolarizing amplification depended on tetrodotoxin (TTX)- and D-2-amino-5-phosphonopentoic acid (APV)-sensitive dendritic channels. 3. The agreement of two independent measurements (somatic voltage clamp and f-I curve shift) of the axial current transmitted from dendrite to soma indicates that the amplification of transmitted current observed in voltage clamp occurs physiologically. We discuss the usefulness of the effective current concept for determining synaptic weighting in network models of neurons with active dendrites.

Exposure to low temperature prepares the turtle brain to withstand anoxic environments during overwintering

2021 ◽  
Author(s):  
Ebrahim Lari ◽  
Leslie T. Buck
Keyword(s):  
Membrane Potential ◽  
Low Temperature ◽  
Action Potential ◽  
Pyramidal Neurons ◽  
Cellular Damage ◽  
Severe Hypoxia ◽  
Painted Turtle ◽  
Whole Cell ◽  
Voltage Gated ◽  
The Impact

In most vertebrates, anoxia drastically reduces the production of the essential adenosine triphosphate (ATP) to power its many necessary functions, and consequently, cell death occurs within minutes. However, some vertebrates, such as the painted turtle (Chrysemys picta bellii), have evolved the ability to survive months without oxygen by simultaneously decreasing ATP supply and demand, surviving the anoxic period without any apparent cellular damage. The impact of anoxia on the metabolic function of painted turtles has received a lot of attention. Still, the impact of low temperature has received less attention and the interactive effect of anoxia and temperature even less. In the present study, we investigated the interactive impacts of reduced temperature and severe hypoxia on the electrophysiological properties of pyramidal neurons in painted turtle cerebral cortex. Our results show that an acute reduction in temperature from 20 to 5°C decreases membrane potential, action potential width and amplitude, and whole-cell conductance. Importantly, acute exposure to 5°C considerably slows membrane repolarization by voltage-gated K+ channels. Exposing pyramidal cells to severe hypoxia in addition to an acute temperature change slightly depolarized membrane potential but did not alter action potential amplitude or width and whole-cell conductance. These results suggest that acclimation to low temperatures, preceding severe environmental hypoxia, induces cellular responses in pyramidal neurons that facilitate survival under low oxygen concentration. In particular, our results show that temperature acclimation invokes a change in voltage-gated K+ channel kinetics that overcomes the acute inhibition of the channel.

scholarly journals Effect of acetylcholine on postjunctional membrane permeability in eel electroplaque.

1977 ◽  
Vol 70 (1) ◽  
pp. 23-36 ◽  
Author(s):  
N L Lassignal ◽  
A R Martin
Keyword(s):  
Field Equation ◽  
Membrane Potential ◽  
Membrane Permeability ◽  
Ionic Composition ◽  
Reversal Potential ◽  
Resting Potential ◽  
Constant Field ◽  
Free Solution ◽  
Positive Direction ◽  
External K

Acetylcholine (ACh) was applied iontophoretically to the innervated face of isolated eel electroplaques while the membrane potential was being recorded intracellularly. At the resting potential (about -85 mV) application of the drug produced depolarizations (ACh potentials) of 20 mV or more which became smaller when the membrane was depolarized and reversed in polarity at about zero membrane potential. The reversal potential shifted in the negative direction when external Na+ was partially replaced by glucosamine. Increasing external K+ caused a shift of reversal potential in the positive direction. It was concluded that ACh increased the permeability of the postjunctional membrane to both ions. Replacement of Cl- by propionate had no effect on the reversal potential. In Na+-free solution containing glucosamine the reversal potential was positive to the resting potential, suggesting that ACh increased the permeability to glucosamine. Addition of Ca++ resulted in a still more positive reversal potential, indicating an increased permeability to Ca++ as well. Analysis of the results indicated that the increases in permeability of the postjunctional membrane to K+, Na+, Ca++, and glucosamine were in the ratios of approximately 1.0:0.9:0.7:0.2, respectively. With these permeability ratios, all of the observed shifts in reversal potential with changes in external ionic composition were predicted accurately by the constant field equation.

Control of intracellular calcium by membrane potential in human melanoma cells

1993 ◽  
Vol 265 (6) ◽  
pp. C1501-C1510 ◽  
Author(s):  
B. Nilius ◽  
G. Schwarz ◽  
G. Droogmans
Keyword(s):  
Cell Proliferation ◽  
Membrane Potential ◽  
Intracellular Calcium ◽  
Reversal Potential ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Human Melanoma Cells

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

Simulations of Intrinsically Bursting Neocortical Pyramidal Neurons

1994 ◽  
Vol 6 (6) ◽  
pp. 1086-1110 ◽  
Author(s):  
Paul A. Rhodes ◽  
Charles M. Gray
Keyword(s):  
Visual Cortex ◽  
Ion Channels ◽  
Pyramidal Neurons ◽  
Compartment Model ◽  
Morphological Data ◽  
High Threshold ◽  
Simulation Results ◽  
Dendritic Branches ◽  
Neocortical Pyramidal Neurons

Neocortical layer 5 intrinsically bursting (IB) pyramidal neurons were simulated using compartment model methods. Morphological data as well as target neurophysiological responses were taken from a series of published studies on the same set of rat visual cortex pyramidal neurons (Mason, A. and Larkman, A. J., 1990. J. Neurosci. 9,1440-1447; Larkman, A. J. 1991. J. Comp. Neurol. 306, 307-319). A dendritic distribution of ion channels was found that reproduced the range of in vitro responses of layer 5 IB pyramidal neurons, including the transition from repetitive bursting to the burst/tonic spiking mode seen in these neurons as input magnitude increases. In light of available data, the simulation results suggest that in these neurons bursts are driven by an inward flow of current during a high threshold Ca2+ spike extending throughout both the basal and apical dendritic branches.

scholarly journals Covariation of axon initial segment location and dendritic tree normalizes the somatic action potential

2016 ◽  
Vol 113 (51) ◽  
pp. 14841-14846 ◽  
Author(s):  
Mustafa S. Hamada ◽  
Sarah Goethals ◽  
Sharon I. de Vries ◽  
Romain Brette ◽  
Maarten H. P. Kole
Keyword(s):  
Action Potential ◽  
Initial Segment ◽  
Pyramidal Neurons ◽  
Dendritic Tree ◽  
Apical Dendrite ◽  
Axial Current ◽  
Axon Initial Segment ◽  
Output Code ◽  
The Face ◽  
Dendritic Complexity

In mammalian neurons, the axon initial segment (AIS) electrically connects the somatodendritic compartment with the axon and converts the incoming synaptic voltage changes into a temporally precise action potential (AP) output code. Although axons often emanate directly from the soma, they may also originate more distally from a dendrite, the implications of which are not well-understood. Here, we show that one-third of the thick-tufted layer 5 pyramidal neurons have an axon originating from a dendrite and are characterized by a reduced dendritic complexity and thinner main apical dendrite. Unexpectedly, the rising phase of somatic APs is electrically indistinguishable between neurons with a somatic or a dendritic axon origin. Cable analysis of the neurons indicated that the axonal axial current is inversely proportional to the AIS distance, denoting the path length between the soma and the start of the AIS, and to produce invariant somatic APs, it must scale with the local somatodendritic capacitance. In agreement, AIS distance inversely correlates with the apical dendrite diameter, and model simulations confirmed that the covariation suffices to normalize the somatic AP waveform. Therefore, in pyramidal neurons, the AIS location is finely tuned with the somatodendritic capacitive load, serving as a homeostatic regulation of the somatic AP in the face of diverse neuronal morphologies.

Electrical properties of frog motoneurons in the in situ spinal cord

1976 ◽  
Vol 39 (3) ◽  
pp. 459-473 ◽  
Author(s):  
P. C. Magherini ◽  
W. Precht
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Rana Temporaria ◽  
Reversal Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Spike Initiation

Electrical properties of the spinal motoneurons of Rana temporaria and R. esculenta were investigated in the in situ spinal cord at 20-22 degrees C by means of intracellular recording and current injection. Input resistance values depended on the method of measurement in a given cell but were generally inversely related to axon conduction velocity. The membrane-potential response to a subthreshold current pulse was composed of at least two exponentials with mean time constants of 2.5 and 20 ms. The membrance potential reached by the peak of a spike depended on the mode of spike initiation and membrane potential. Preceding a suprathreshold depolarization by a hyperpolarizing pulse could delay and eliminate spike initiation, similar to effects reported in certain invertebrate neurons. Antidromic invasion frequently failed in motoneurons of normal resting potential. Antidromic spike components (m,IS, SD) were similar to those of cat motoneurons. The delayed depolarization and the long afterhyperpolarization following an antidromic spike had many properties in common with the analogous afterpotentials of cat motoneurons. The reversal potential of the short afterhyperpolarization occurring immediately after the spike varied with resting potential and could not be used to determine potassium equilibrium potential. Sustained rhythmic firing could be evoked by continuous synaptic drive or long pulses of injected current. The plot of firing rate versus current strength had a substantial linear region. Both steady firing and adaptation properties varied markedly with motoneuron input resistance.

scholarly journals Small-conductance Ca2+-activated K+ channels modulate action potential-induced Ca2+ transients in hippocampal neurons

2013 ◽  
Vol 109 (6) ◽  
pp. 1514-1524 ◽  
Author(s):  
Raffaella Tonini ◽  
Teresa Ferraro ◽  
Marisol Sampedro-Castañeda ◽  
Anna Cavaccini ◽  
Martin Stocker ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Pyramidal Neurons ◽  
Apical Dendrite ◽  
Channel Blockers ◽  
Sk Channels ◽  
Hippocampal Pyramidal Neurons ◽  
Voltage Gated ◽  
Small Conductance

In hippocampal pyramidal neurons, voltage-gated Ca2+ channels open in response to action potentials. This results in elevations in the intracellular concentration of Ca2+ that are maximal in the proximal apical dendrites and decrease rapidly with distance from the soma. The control of these action potential-evoked Ca2+ elevations is critical for the regulation of hippocampal neuronal activity. As part of Ca2+ signaling microdomains, small-conductance Ca2+-activated K+ (SK) channels have been shown to modulate the amplitude and duration of intracellular Ca2+ signals by feedback regulation of synaptically activated Ca2+ sources in small distal dendrites and dendritic spines, thus affecting synaptic plasticity in the hippocampus. In this study, we investigated the effect of the activation of SK channels on Ca2+ transients specifically induced by action potentials in the proximal processes of hippocampal pyramidal neurons. Our results, obtained by using selective SK channel blockers and enhancers, show that SK channels act in a feedback loop, in which their activation by Ca2+ entering mainly through L-type voltage-gated Ca2+ channels leads to a reduction in the subsequent dendritic influx of Ca2+. This underscores a new role of SK channels in the proximal apical dendrite of hippocampal pyramidal neurons.

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