scholarly journals Quantitative Assessment of the Distributions of Membrane Conductances Involved in Action Potential Backpropagation Along Basal Dendrites

2009 ◽  
Vol 101 (3) ◽  
pp. 1524-1541 ◽  
Author(s):  
Corey D. Acker ◽  
Srdjan D. Antic
Keyword(s):  
Cortical Neurons ◽  
Action Potentials ◽  
Synaptic Integration ◽  
Membrane Properties ◽  
Delayed Rectifier ◽  
Published Data ◽  
Membrane Excitability ◽  
Voltage Gated ◽  
Prefrontal Cortical ◽  
Basal Dendrites

Basal dendrites of prefrontal cortical neurons receive strong synaptic drive from recurrent excitatory synaptic inputs. Synaptic integration within basal dendrites is therefore likely to play an important role in cortical information processing. Both synaptic integration and synaptic plasticity depend crucially on dendritic membrane excitability and the backpropagation of action potentials. We carried out multisite voltage-sensitive dye imaging of membrane potential transients from thin basal branches of prefrontal cortical pyramidal neurons before and after application of channel blockers. We found that backpropagating action potentials (bAPs) are predominantly controlled by voltage-gated sodium and A-type potassium channels. In contrast, pharmacologically blocking the delayed rectifier potassium, voltage-gated calcium, or Ih conductance had little effect on dendritic AP propagation. Optically recorded bAP waveforms were quantified and multicompartmental modeling was used to link the observed behavior with the underlying biophysical properties. The best-fit model included a nonuniform sodium channel distribution with decreasing conductance with distance from the soma, together with a nonuniform (increasing) A-type potassium conductance. AP amplitudes decline with distance in this model, but to a lesser extent than previously thought. We used this model to explore the mechanisms underlying two sets of published data involving high-frequency trains of APs and the local generation of sodium spikelets. We also explored the conditions under which IA down-regulation would produce branch strength potentiation in the proposed model. Finally, we discuss the hypothesis that a fraction of basal branches may have different membrane properties compared with sister branches in the same dendritic tree.

Resting and Active Properties of Pyramidal Neurons in Subiculum and CA1 of Rat Hippocampus

2000 ◽  
Vol 84 (5) ◽  
pp. 2398-2408 ◽  
Author(s):  
Nathan P. Staff ◽  
Hae-Yoon Jung ◽  
Tara Thiagarajan ◽  
Michael Yao ◽  
Nelson Spruston
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Current Injection ◽  
Synaptic Integration ◽  
Membrane Properties ◽  
Neuronal Membrane ◽  
Similar Action ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons

Action potentials are the end product of synaptic integration, a process influenced by resting and active neuronal membrane properties. Diversity in these properties contributes to specialized mechanisms of synaptic integration and action potential firing, which are likely to be of functional significance within neural circuits. In the hippocampus, the majority of subicular pyramidal neurons fire high-frequency bursts of action potentials, whereas CA1 pyramidal neurons exhibit regular spiking behavior when subjected to direct somatic current injection. Using patch-clamp recordings from morphologically identified neurons in hippocampal slices, we analyzed and compared the resting and active membrane properties of pyramidal neurons in the subiculum and CA1 regions of the hippocampus. In response to direct somatic current injection, three subicular firing types were identified (regular spiking, weak bursting, and strong bursting), while all CA1 neurons were regular spiking. Within subiculum strong bursting neurons were found preferentially further away from the CA1 subregion. Input resistance ( R N), membrane time constant (τm), and depolarizing “sag” in response to hyperpolarizing current pulses were similar in all subicular neurons, while R N and τm were significantly larger in CA1 neurons. The first spike of all subicular neurons exhibited similar action potential properties; CA1 action potentials exhibited faster rising rates, greater amplitudes, and wider half-widths than subicular action potentials. Therefore both the resting and active properties of CA1 pyramidal neurons are distinct from those of subicular neurons, which form a related class of neurons, differing in their propensity to burst. We also found that both regular spiking subicular and CA1 neurons could be transformed into a burst firing mode by application of a low concentration of 4-aminopyridine, suggesting that in both hippocampal subfields, firing properties are regulated by a slowly inactivating, D-type potassium current. The ability of all subicular pyramidal neurons to burst strengthens the notion that they form a single neuronal class, sharing a burst generating mechanism that is stronger in some cells than others.

Membrane properties and cell ultrastructure of taste receptor cells in Necturus lingual slices

1996 ◽  
Vol 75 (5) ◽  
pp. 1944-1956 ◽  
Author(s):  
A. Bigiani ◽  
D. J. Kim ◽  
S. D. Roper
Keyword(s):  
Action Potentials ◽  
Taste Receptor ◽  
Cell Ultrastructure ◽  
Membrane Properties ◽  
Dark Cells ◽  
Voltage Gated ◽  
Receptor Cells ◽  
Group 2 ◽  
K Currents ◽  
Group 1

1. Whole cell patch-clamp recordings and electron micrographs were obtained from cells in Necturus taste buds in lingual slices to study their membrane properties and to correlate these properties with cell ultrastructure. 2. Two different populations of taste receptor cells could be identified: one type possessed voltage-gated Na+ and K+ (noninactivating) currents (group 1 cells); the other type possessed only K+ (inactivating) currents (group 2 cells). 3. The zero-current ("resting") potential (Vo) and whole cell resistance (Ro) of these two types of taste cells differed significantly. For group 1 cells, on average, Vo = -75 mV and Ro = 24.6 G omega, and for group 2 cells, Vo = -49 mV and Ro = 48.9 G omega. The difference in Ro was not explained completely by differences in cell sizes, suggesting that intrinsic membrane properties differed between the populations. 4. Cells injected with biocytin were the electron microscope after tissues were reacted with majority (14 of 16) of cells with voltage-gated Na+ and K+ currents (group 1 cells) were characterized by abundant rough endoplasmic reticulum and dense granular packets in the apical process. These are features of dark cells. All the cells that only possessed K+ currents (group 2 cells) were characterize by well-developed smooth endoplasmic reticulum and an absence granular packets. These features characterize light cells. 5. These findings indicate that there is a good, although not exact, correlation between electrophysiological properties and cell morphotype in Necturus taste bud cells. All dark cells possessed Na+ and K+ currents and thus would be expected to be capable of generating action potentials. Most light cells only possessed outward K+ currents and thus would be incapable of generating action potentials.

Two Types of Voltage-Gated K+ Currents in Dissociated Heart Ventricular Muscle Cells of the Snail Lymnaea stagnalis

1999 ◽  
Vol 82 (5) ◽  
pp. 2415-2427 ◽  
Author(s):  
M. S. Yeoman ◽  
P. R. Benjamin
Keyword(s):  
Voltage Clamp ◽  
Action Potentials ◽  
Muscle Cells ◽  
Delayed Rectifier ◽  
Voltage Sensitivity ◽  
Ventricular Muscle ◽  
Current Time ◽  
Voltage Gated ◽  
Time To Peak ◽  
Voltage Dependent

We have used a combination of current-clamp and voltage-clamp techniques to characterize the electrophysiological properties of enzymatically dissociated Lymnaea heart ventricle cells. Dissociated ventricular muscle cells had average resting membrane potentials of −55 ± 5 mV. When hyperpolarized to potentials between −70 and −63 mV, ventricle cells were capable of firing repetitive action potentials (8.5 ± 1.2 spikes/min) that failed to overshoot 0 mV. The action potentials were either simple spikes or more complex spike/plateau events. The latter were always accompanied by strong contractions of the muscle cell. The waveform of the action potentials were shown to be dependent on the presence of extracellular Ca2+ and K+ ions. With the use of the single-electrode voltage-clamp technique, two types of voltage-gated K+ currents were identified that could be separated by differences in their voltage sensitivity and time-dependent kinetics. The first current activated between −50 and −40 mV. It was relatively fast to activate (time-to-peak; 13.7 ± 0.7 ms at +40 mV) and inactivated by 53.3 ± 4.9% during a maintained 200-ms depolarization. It was fully available for activation below −80 mV and was completely inactivated by holding potentials more positive than −40 mV. It was completely blocked by 5 mM 4-aminopyridine (4-AP) and by concentrations of tetraethylammonium chloride (TEA) >10 mM. These properties characterize this current as a member of the A-type family of voltage-dependent K+ currents. The second voltage-gated K+ current activated at more depolarized potentials (−30 to −20 mV). It activated slower than the A-type current (time-to-peak; 74.1 ± 3.9 ms at +40 mV) and showed little inactivation (6.2 ± 2.1%) during a maintained 200-ms depolarization. The current was fully available for activation below −80 mV with a proportion of the current still available for activation at potentials as positive as 0 mV. The current was completely blocked by 1–3 mM TEA. These properties characterize this current as a member of the delayed rectifier family of voltage-dependent K+ currents. The slow activation rates and relatively depolarized activation thresholds of the two K+ currents are suggestive that their main role is to contribute to the repolarization phase of the action potential.

scholarly journals Synergistic Inhibition of Delayed Rectifier K+ and Voltage-Gated Na+ Currents by Artemisinin in Pituitary Tumor (GH3) Cells

2017 ◽  
Vol 41 (5) ◽  
pp. 2053-2066 ◽  
Author(s):  
Edmund Cheung So ◽  
Sheng-Nan Wu ◽  
Ping-Ching Wu ◽  
Hui-Zhen  Chen ◽  
Chia-Jung Yang
Keyword(s):  
Pituitary Tumor ◽  
Ionic Currents ◽  
Neuroendocrine Cells ◽  
Endocrine Function ◽  
Gh3 Cells ◽  
Delayed Rectifier ◽  
Membrane Excitability ◽  
Inactivation Curve ◽  
Voltage Gated

Background: Artemisinin (ART) is an anti-malarial agent reported to influence endocrine function. Methods: Effects of ART on ionic currents and action potentials (APs) in pituitary tumor (GH3) cells were evaluated by patch clamp techniques. Results: ART inhibited the amplitude of delayed-rectifier K+ current (IK(DR)) in response to membrane depolarization and accelerated the process of current inactivation. It exerted an inhibitory effect on IK(DR) with an IC50 value of 11.2 µM and enhanced IK(DR) inactivation with a KD value of 14.7 µM. The steady-state inactivation curve of IK(DR) was shifted to hyperpolarization by 10 mV. Pretreatment of chlorotoxin (1 µM) or iloprost (100 nM) did not alter the magnitude of ART-induced inhibition of IK(DR) in GH3 cells. ART also decreased the peak amplitude of voltage-gated Na+ current (INa) with a concentration-dependent slowing in inactivation rate. Application of KMUP-1, an inhibitor of late INa, was effective at reversing ART-induced prolongation in inactivation time constant of INa. Under current-clamp recordings, ART alone reduced the amplitude of APs and prolonged the duration of APs. Conclusion: Under ART exposure, the inhibitory actions on both IK(DR) and INa could be a potential mechanisms through which this drug influences membrane excitability of endocrine or neuroendocrine cells appearing in vivo.

Dynamic Spatiotemporal Synaptic Integration in Cortical Neurons: Neuronal Gain, Revisited

2005 ◽  
Vol 94 (4) ◽  
pp. 2785-2796 ◽  
Author(s):  
Rony Azouz
Keyword(s):  
Firing Rate ◽  
Cortical Neurons ◽  
Temporal Integration ◽  
Synaptic Integration ◽  
Neuronal Membrane ◽  
Network Dynamic ◽  
Alternative Mechanism ◽  
Gain Modulation ◽  
Voltage Gated ◽  
The Relationship

Gain modulation is a ubiquitous phenomenon in cortical neurons, providing flexibility to operate under changing conditions. The prevailing view is that this modulation reflects a change in the relationship between mean input and output firing rate brought about by variation in neuronal membrane characteristics. An alternative mechanism is proposed for neuronal gain modulation that takes into account the capability of cortical neurons to process spatiotemporal synaptic correlations. Through the use of numerical simulations, it is shown that voltage-gated and leak conductances, membrane potential, noise, and input firing rate modify the sensitivity of cortical neurons to the degree of temporal correlation between their synaptic inputs. These changes are expressed in a change of the temporal window for synaptic integration and the range of input correlation over which response probability is graded. The study also demonstrates that temporal integration depends on the distance between the inputs and that this interplay of space and time is modulated by voltage-gated and leak conductances. Thus, gain modulation may reflect a change in the relationship between spatiotemporal synaptic correlations and output firing probability. It is further proposed that by acting synergistically with the network, dynamic spatiotemporal synaptic integration in cortical neurons may serve a functional role in the formation of dynamic cell assemblies.

scholarly journals Interaction of a dinoflagellate neurotoxin with voltage-activated ion channels in a marine diatom

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4533 ◽  
Author(s):  
Sheila A. Kitchen ◽  
Andrea J. Bourdelais ◽  
Alison R. Taylor
Keyword(s):  
Action Potential ◽  
Binding Site ◽  
Action Potentials ◽  
Harmful Algal Bloom ◽  
Single Domain ◽  
Marine Phytoplankton ◽  
Marine Diatom ◽  
Membrane Excitability ◽  
Voltage Gated ◽  
Kinetics Of

Background The potent neurotoxins produced by the harmful algal bloom species Karenia brevis are activators of sodium voltage-gated channels (VGC) in animals, resulting in altered channel kinetics and membrane hyperexcitability. Recent biophysical and genomic evidence supports widespread presence of homologous sodium (Na+) and calcium (Ca2+) permeable VGCs in unicellular algae, including marine phytoplankton. We therefore hypothesized that VGCs of these phytoplankton may be an allelopathic target for waterborne neurotoxins produced by K. brevis blooms that could lead to ion channel dysfunction and disruption of signaling in a similar manner to animal Na+ VGCs. Methods We examined the interaction of brevetoxin-3 (PbTx-3), a K. brevis neurotoxin, with the Na+/Ca2+ VGC of the non-toxic diatom Odontella sinensis using electrophysiology. Single electrode current- and voltage- clamp recordings from O. sinensis in the presence of PbTx-3 were used to examine the toxin’s effect on voltage gated Na+/Ca2+ currents. In silico analysis was used to identify the putative PbTx binding site in the diatoms. We identified Na+/Ca2+ VCG homologs from the transcriptomes and genomes of 12 diatoms, including three transcripts from O. sinensis and aligned them with site-5 of Na+ VGCs, previously identified as the PbTx binding site in animals. Results Up to 1 µM PbTx had no effect on diatom resting membrane potential or membrane excitability. The kinetics of fast inward Na+/Ca2+ currents that underlie diatom action potentials were also unaffected. However, the peak inward current was inhibited by 33%, delayed outward current was inhibited by 25%, and reversal potential of the currents shifted positive, indicating a change in permeability of the underlying channels. Sequence analysis showed a lack of conservation of the PbTx binding site in diatom VGC homologs, many of which share molecular features more similar to single-domain bacterial Na+/Ca2+ VGCs than the 4-domain eukaryote channels. Discussion Although membrane excitability and the kinetics of action potential currents were unaffected, the permeation of the channels underlying the diatom action potential was significantly altered in the presence of PbTx-3. However, at environmentally relevant concentrations the effects of PbTx- on diatom voltage activated currents and interference of cell signaling through this pathway may be limited. The relative insensitivity of phytoplankton VGCs may be due to divergence of site-5 (the putative PbTx binding site), and in some cases, such as O. sinensis, resistance to toxin effects may be because of evolutionary loss of the 4-domain eukaryote channel, while retaining a single domain bacterial-like VGC that can substitute in the generation of fast action potentials.

Differential contributions of voltage-gated potassium channel subunits in enhancing temporal coding in the bushy cells of the ventral cochlear nucleus

2021 ◽  
Author(s):  
Mingyu Fu ◽  
Lu Zhang ◽  
Xiao Xie ◽  
Ningqian Wang ◽  
Zhongju Xiao
Keyword(s):  
Cochlear Nucleus ◽  
Spike Timing ◽  
Temporal Coding ◽  
Membrane Properties ◽  
Membrane Excitability ◽  
Patch Clamp Recording ◽  
Voltage Gated ◽  
Ventral Cochlear Nucleus ◽  
Kv Channels ◽  
Bushy Cells

Temporal coding precision of bushy cells in the ventral cochlear nucleus (VCN), critical for sound localization and communication, depends on the generation of rapid and temporally precise action potentials (APs). Voltage-gated potassium (Kv) channels are critically involved in this. The bushy cells in rat VCN express Kv1.1, 1.2, 1.3, 1.6, 3.1, 4.2 and 4.3 subunits. The Kv1.1 subunit contributes to the generation of a temporally precise single AP. However, the understanding of the functions of other Kv subunits expressed in the bushy cells is limited. Here, we investigated the functional diversity of Kv subunits concerning their contributions to temporal coding. We characterized the electrophysiological properties of the Kv channels with different subunits using whole-cell patch-clamp recording and pharmacological methods. The neuronal firing pattern changed from single to multiple APs only when the Kv1.1 subunit was blocked. The Kv subunits, including the Kv1.1, 1.2, 1.6 or 3.1, were involved in enhancing temporal coding by lowering membrane excitability, shortening AP latencies, reducing jitter and regulating AP kinetics. Meanwhile, all the Kv subunits contributed to rapid repolarization and sharpening peaks by narrowing half-width and accelerating fall rate, while the Kv1.1 subunit also affected the depolarization of AP. The Kv1.1, 1.2 and 1.6 subunits endowed bushy cells with a rapid time constant and a low input resistance of membrane for enhancing spike timing precision. The present results indicate that the Kv channels differentially affect intrinsic membrane properties to optimize the generation of rapid and reliable APs for temporal coding.

Synaptic and intrinsic control of membrane excitability of neostriatal neurons. I. An in vivo analysis

1990 ◽  
Vol 63 (4) ◽  
pp. 651-662 ◽  
Author(s):  
P. Calabresi ◽  
N. B. Mercuri ◽  
A. Stefani ◽  
G. Bernardi
Keyword(s):  
Substantia Nigra ◽  
Firing Rate ◽  
Action Potentials ◽  
Input Resistance ◽  
Membrane Properties ◽  
Strong Increase ◽  
Synaptic Potential ◽  
Membrane Excitability ◽  
Stimulation Of

1. The relationship between membrane properties of neostriatal neurons and spontaneous and evoked synaptic potentials was studied with the use of intracellular recordings from anesthetized rats. Most of these neurons showed regular or irregular spontaneous depolarizing potentials that only in a few cases triggered action potentials at resting level. 2. The stimulation of the ipsilateral substantia nigra or of the sensorimotor cortex produced a relatively fast depolarizing post-synaptic potential (EPSP). In some cells this potential was followed by an inhibitory period that appeared as an hyperpolarization when the cell was depolarized from the resting level (inhibitory postsynaptic potential, IPSP). A late and long-lasting depolarization (LD) followed the EPSP or the EPSP-IPSP sequence. 3. Repetitive discharge with little adaptation was observed during direct depolarization. Most of the neurons tested for current-voltage (I-V) relationship showed nonlinearity of the input resistance in the hyperpolarizing direction. Spontaneous and evoked EPSPs were decreased in their amplitude and duration when the membrane potential was held at levels more hyperpolarized than -85 mV because of the strong rectification at these levels of hyperpolarization. 4. Local microiontophoretic application of bicuculline (BIC) or systemic administration of BIC and pentylenetetrazole (PTZ) produced a reduction of the IPSPs. The reduction of the inhibitory transmission caused a strong increase of the LD. The current-evoked firing pattern was not greatly altered. 5. The intracellular application of cesium increased the amplitude and the duration of the spontaneous depolarizations that triggered bursts of action potentials under this condition. Spikes were broadened and the rectification in the hyperpolarization direction was reduced. 6. Iontophoretically applied cadmium strongly depressed the amplitude of the spontaneous and evoked postsynaptic potentials. During cadmium application, nigral stimulation produced constant latency, all-or-none spikes in the absence of any synaptic potential. 7. Repetitive stimulation of the ipsilateral substantia nigra by electrical shocks (5 Hz, 25 s) produced a progressive and reversible decrease of the spontaneous depolarizing potentials (SDPs) and a decrease of the firing rate. In the same cells, when the train of stimulation was delivered in the ipsilateral cortex, a membrane depolarization coupled with an increase of the firing rate was observed. 8. We conclude that although synaptic circuits mediate a phasic inhibition in neostriatum, the low level of spontaneous firing of most neostriatal neurons is mainly because of the effects that membrane properties exert on the spontaneous and the evoked synaptic depolarizations in the striatum.(ABSTRACT TRUNCATED AT 400 WORDS)

A simulation of action potentials in synaptic boutons during presynaptic inhibition

1994 ◽  
Vol 71 (2) ◽  
pp. 538-549 ◽  
Author(s):  
B. Graham ◽  
S. Redman
Keyword(s):  
Action Potential ◽  
Transmitter Release ◽  
Action Potentials ◽  
Presynaptic Inhibition ◽  
Chloride Conductance ◽  
Membrane Properties ◽  
Published Data ◽  
Myelinated Nerve ◽  
Synaptic Boutons ◽  
The Relationship

1. During presynaptic inhibition, an increased conductance in the membrane of the presynaptic bouton is presumed to reduce the action potential, thereby reducing transmitter release. The object of the simulation has been to determine the magnitude of a chloride conductance required to reduce transmitter release, for various diameters of synaptic boutons, connected to axons with diameters in the range 0.1-1.0 microns. 2. A propagating action potential was simulated in axons connected to either side of a hemispherical bouton. The axons could be myelinated or unmyelinated, while the bouton membrane could be passive, a node of the myelinated nerve, or have the same active properties as the attached unmyelinated nerve. Membrane properties of the axons were derived from mammalian data and scaled to 37 degrees C. 3. A steady-state chloride conductance was included in the bouton membrane, with ECl = -40 mV. The amplitude of the action potential in the bouton was calculated for different diameters of axon and bouton and for different magnitudes of chloride conductance. 4. Using published data on the relationship between the amplitude of a presynaptic action potential and the resulting postsynaptic potential, the relationship between the chloride conductance and the postsynaptic response was calculated for different geometries. Transmitter release was reduced when an action potential was 90 mV or smaller, with no transmission for action potentials smaller than 50 mV. 5. Conductance increases in the range 3 to 10 nS were required to reduce the action potential to 90 mV, depending on the diameter of the axon (0.5-1.0 microns), diameter of the bouton (3-6 microns), whether the bouton had passive or active membrane, and whether the axon was myelinated or unmyelinated. A 3 microns passive bouton connected to a 0.5 micron myelinated axon was most sensitive to the effects of a chloride conductance, while a 6 microns active bouton connected to a 1 micron myelinated nerve was least sensitive to the effects of a chloride conductance. 6. The reduction in the action potential was compared when ECl = -40 mV and when ECl = E(rest) = -80 mV. Inactivation of the sodium conductance by terminal depolarization was the dominant influence on the amplitude of the action potential. 7. Conductances that were sufficient to completely block synaptic transmission at a bouton were insufficient to prevent the spread of the action potential away from that bouton.(ABSTRACT TRUNCATED AT 400 WORDS)

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