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PubMed1997

Stochastic threshold characterization of the intensity of active channel dynamical action potential generation.

Stochastic threshold characterization of the intensity of active channel dynamical action potential generation. J. Neurophysiol. 78: 2616-2630, 1997. This paper develops a stochastic intensity description for action potential generation formulated in terms of stochastic processes, which are direct analogues of the physiological processes of the pre- and postsynaptic complex of the cochlear nerve: 1) neurotransmitter release is modeled as an inhomogeneous Poisson counting process with release intensity mu t, 2) the excitatory postsynaptic conductance (EPSC) process is modeled as a marked, linearly filtered Poisson process resulting from the linear superposition of standard shaped postsynaptic conductances of size G, and 3) action potential generation is modeled as resulting from the EPSC exceeding a random threshold determined by active channel dynamics of the Hodgkin-Huxley type. The random threshold is defined to be the least upper bound in the size of a standard-shaped neurotransmitter release injected at time t given the previous action potential time and the number of releases occurring in a short preconditioning time increment. The action potential process is modeled as a self-exciting point process with stochastic intensity resulting from the probability that the random threshold process crosses the threshold in some small time increment that is a function of time since previous action potential, release intensity, and the probability that a single synaptic event exceeds the stochastic threshold. The stochastic intensity model is consistent with a direct simulation of the nonlinear Hodgkin-Huxley differential equations over a variety of parameters for the vesicle release intensity, vesicle size, vesicle duration, and temperatures. Results are presented showing that the regularity properties seen in the vestibular primary afferent in the lizard, Calotes versicolor, associated with a slow-to-activate potassium channel resulting in a long afterhyperpolarization can be accommodated directly by the stochastic intensity description. The stimulus dependence of the model is attributed to synaptic transmission and the probabilistic nature to the threshold conductance process, which is dependent upon the EPSC process. The stochastic intensity is seen to have a form consistent with the phenomenologically based Siebert-Gaumond model, a stimulus-related function of time multiplied by a refractory-related function of time since previous action potential.

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PubMed1998

Potassium channel blockers have minimal effect on repolarization of spontaneous action potentials in rat pituitary lactotropes.

Patch-clamp techniques were used in primary cultures of rat lactotropes and the rat pituitary clonal cell line GH3 to determine the population characteristics of spontaneous action potentials and the nature of the currents responsible for repolarization of spontaneous action potentials. Spontaneous action potentials were observed in 75% of lactotropes (74/99) and 80% of GH3 cells (42/51). Lactotropes exhibited broad and shallow action potentials (average duration 460 ms, peak -17 mV, slope of upstroke 0.5 mV/ms) compared to the GH3 cells which displayed narrow and tall action potentials (average duration 177 ms, peak -10 mV, slope of upstroke 1.6 mV/ms). Blockers of potassium currents were used to determine the role of specific potassium currents in the repolarization process. Spontaneous action potentials in lactotropes were largely unaffected by 4-aminopyridine (4AP), charybdotoxin, and apamin. Tetraethylammonium (TEA) caused only an small increase in peak amplitude and, in a subset of cells, a small increase in duration. In contrast, in GH3 cells, TEA, 4AP, charybdotoxin, and apamin all caused a significant increase in duration, while TEA and charybdotoxin also caused an increase in peak amplitude. Further, apamin caused a positive shift in the afterhyperpolarization voltage. In lactotropes, strong buffering of intracellular calcium with calcium chelators (EGTA or BAPTA) caused a profound increase in action potential duration. Thus, repolarization of action potentials in lactotropes is a calcium-dependent process, but unlike GH3 cells, is not mediated by calcium-dependent potassium currents, nor is it strongly influenced by voltage-dependent potassium currents.

4-Aminopyridine↗

PubMed1977

Prolongation of ventricular action potential due to sympathetic stimulation.

The changes of monophasic action potential durations due to stellate stimulation for the period of 3 sec were studied in dogs with suction electrodes from the anterior surface of the right ventricle and the posterior surface of the left ventricle. Prolongation of monophasic action potential duration was observed from the period of 2 to 3 sec during stimulation to that of 10 to 20 sec after the termination of stimulation. Prolongation of monophasic action potential duration due to right stellate stimulation was predominant in the right ventricle and that due to left stellate stimulation was predominant in the left ventricle. The transient T wave change in the surface electrocardiogram occurring immediately after the beginning of stellate stimulation could be explained by this local difference in prolongation of ventricle repolarization. Since the onset of prolongation of monophasic action potential duration preceded increase in blood pressure following stellate stimulation, this prolongation of monophasic action potential duration did not result from the hemodynamic changes and could be a primary effect of the sympathetic nerve stimulation.

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PubMed1986

Depressant action of Ca-antagonists on slow action potentials in guinea pig ventricular muscles.

The depressant action of four Ca antagonists, including a novel drug, tiapamil, on Ca channels was investigated using a conventional microelectrode technique. "All or none" slow action potentials were recorded in K+-depolarized guinea-pig papillary muscles. Verapamil and diltiazem decreased the amplitude and maximum rate of rise (Vmax) of the slow action potentials at concentrations up to 2 microM. The depressant effect of a novel Ca-antagonist, tiapamil, on the slow action potentials was as marked as that of verapamil and diltiazem. However, prenylamine was less potent than the other 3 drugs. In addition, the action of all drugs on the slow action potentials was enhanced as the frequency of stimulation was increased between 0.0083 and 1 Hz. It was concluded that tiapamil, as verapamil and diltiazem, produced a frequency-dependent blockade of the slow Ca channel.

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PubMed2000

Action potentials reliably invade axonal arbors of rat neocortical neurons.

Neocortical pyramidal neurons have extensive axonal arborizations that make thousands of synapses. Action potentials can invade these arbors and cause calcium influx that is required for neurotransmitter release and excitation of postsynaptic targets. Thus, the regulation of action potential invasion in axonal branches might shape the spread of excitation in cortical neural networks. To measure the reliability and extent of action potential invasion into axonal arbors, we have used two-photon excitation laser scanning microscopy to directly image action-potential-mediated calcium influx in single varicosities of layer 2/3 pyramidal neurons in acute brain slices. Our data show that single action potentials or bursts of action potentials reliably invade axonal arbors over a range of developmental ages (postnatal 10-24 days) and temperatures (24 degrees C-30 degrees C). Hyperpolarizing current steps preceding action potential initiation, protocols that had previously been observed to produce failures of action potential propagation in cultured preparations, were ineffective in modulating the spread of action potentials in acute slices. Our data show that action potentials reliably invade the axonal arbors of neocortical pyramidal neurons. Failures in synaptic transmission must therefore originate downstream of action potential invasion. We also explored the function of modulators that inhibit presynaptic calcium influx. Consistent with previous studies, we find that adenosine reduces action-potential-mediated calcium influx in presynaptic terminals. This reduction was observed in all terminals tested, suggesting that some modulatory systems are expressed homogeneously in most terminals of the same neuron.

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PubMed1980

Calcium action potentials in single freshly isolated smooth muscle cells.

The ionic basis of the action potential was investigated using intracellular microelectrodes in single smooth muscle cells freshly isolated from the stomach of the toad Bufo marinus. When [Ca2+]0 was elevated (> 8mM), action potentials were readily elicited, which had similar characteristics to those found in many tissue preparations of visceral smooth muscle. There was a decrease in membrane resistance at the peak of the action potential and during the undershoot. The following evidence indicated that the inward current is carried by Ca2+: 1) Raising [Ca2+]0 from 15 to 49.6 mM in the presence of 18.2 mM tetraethylammonium chloride (TEA) increased the maximum rate of rise and the overshoot amplitude, the latter by 15 mV, i.e., 29.5 mV/10-fold change in [Ca2+]0. Changing [Na2+]0 from 11.8 to 81.8 mM had no significant effect on the maximum rate of rise or the overshoot. 2) The action potentials were blocked by 8 mM Mn2+ ([Ca2+]0 = 14.6 mM) but not by 14.3 microM tetrodotoxin (TTX) ([Na2+]0 = 100 mM). 3) Action potentials could be elicited when [Ba2+]0 or [Sr2+]0 were present in high concentrations ([Ca2+]0 less than or equal to 31 microM,[Na2+]0 = 11.8 mM). Both the maximum rate of rise and overshoot amplitude of the action potential increased as the membrane potential became more negative, suggesting increased activation of the inward current. Both TEA and Ba2+ prolonged the action potential, suggesting that a K+ current is responsible for repolarization. Action potentials could also be elicited on anode break at elevated [K+]0 (91 mM).

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PubMed1992

A reconstruction of charge movement during the action potential in frog skeletal muscle.

The transfer of intramembrane charge during an action potential at 4 degrees C was reconstructed for a model representing the electrical properties of frog skeletal muscle by a cylindrical surface membrane and 16 concentric annuli ("shells") of transverse tubular membrane of equal radial thickness. The lumina of the transverse tubules were separated from extracellular fluid by a fixed series resistance. The quantity, geometrical distribution and steady-state and kinetic properties of charge movement components were described by equations incorporating earlier experimental results. Introducing such nonlinear charge into the distributed model for muscle membrane diminished the maximum amplitude of the action potential within the transverse tubules by 2 mV but increased the maximum size of the after-depolarization by 3-5 mV and also its duration. However, these changes were small in comparison to the 135-mV deflection represented by the action potential. They therefore did not justify altering the values of the electrical parameters adopted by Adrian R.H., and L.D. Peachey (1973. J. Physiol. [Lond.]. 235:103-131.) and used in the present calculations. Cable properties significantly affected the time course and extent of charge movement in each shell during action potential propagation into the tubular system. Q beta charge moved relatively rapidly in all annuli, and did so without significant latency (approximately 0.3 ms) after the surface action potential upstroke. Its peak displacement varied between 53 and 58% (the range representing the difference fiber edge/fiber axis) of the total Q beta charge. This was attained at 5.4-7.3 ms after the stimulus, depending on depth within the tubules. In contrast, q gamma moved after a 1.7-2.9 ms latency and achieved a peak displacement of up to 22-34% of available charge. Both charge movement species could be driven by repetitive (47.7 Hz) action potentials without buildup of charge transfer. Such stimulus frequencies would normally cause tetanus. Latencies in q gamma charge movement in response to an action potential were resolved into (a) propagation of tubular depolarization required to gain the "threshold" of q gamma charge (0.8-1.5 ms) and (b) dielectric loss processes. The latter took consistently around 1.5 ms throughout the tubular system. Taken with (c) the earlier reports of a minimal latency in delta [Ca2+] signals attributed to tubulo-cisternal coupling following voltage sensing (approximately 2 ms: Zhu, P.H., I. Parker, and R. Miledi., 1986. Proc. R. Soc. Lond. B. Biol. Sci. 229:39-46.). these times can be reconciled to the latency (~ 4-5 ms) reported between the onset of the surface action potential and that of delta [Ca2+] signals (Vergara, J., and M. Delay. 1986. Proc. R. Soc. Lond. B. Biol. Sci. 229:97-110.). This is consistent with a relationship between the q gamma system and excitation-contraction coupling whether as an independent event (e.g.,Adrian, R.H., and C.L.-H. Huang. 1984. J. Physiol. (Lond.). 353:419-434.) or as an end reaction following earlier (q beta) transfers of charge (e.g., Horowicz, P., and M.F. Schneider. 1981. J. Physiol. (Lond.). 314:565-593.; Melzer, W., M.F. Schneider, B.J. Simon,and G. Szucs. 1986. J. Physiol. (Lond.). 373:481-512.)

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PubMed2000

Electrochemical signaling in green plants: effects of 2,4-dinitrophenol on variation and action potentials in soybean.

Nerve cells in animals and phloem cells in plants share one fundamental property: they possess excitable membranes by which electrical excitations in the form of action potentials can propagate. Action potentials in green plants can be as fast as the action potentials in axons of nervous cells. The presence of the pesticide 2,4-dinitrophenol (DNP) in soil is a most serious environmental problem and has an impact on agriculture and human health. In the present work we show that DNP induces fast action potentials and decreases the variation potential in a soybean. The speed of the propagation of action potentials is up to 2 m/s, and the duration time of single action potentials is typically 20 ms. The automatic measurement of the electrical potential difference can be effectively used in environmental plant physiology, as well as for studying molecular mechanisms of transport processes and the influence of external stimuli on plants.

2,4-Dinitrophenol↗

PubMed2005

Schwann cell engraftment into injured peripheral nerve prevents changes in action potential properties.

Peripheral nerve injury results in changes in action potential waveform, ion channel organization, and firing properties of primary afferent neurons. It has been suggested that these changes are the result of reduction in basal trophic support from skin targets. Subcutaneous injections of Fluro-Gold (FG) in the hind limb of the rat were used to identify cutaneous primary afferent neurons. Five days after FG injection, sciatic nerves were ligated and encapsulated in a silicon tube allowing neuroma formation. Green fluorescent protein (GFP)-expressing Schwann cells (SCs) were injected proximal to the cut end of the nerve. Thirteen to 22 days after injury and SC injection, the L4 and L5 dorsal root ganglia (DRG) were prepared for acute culture. Whole cell patch-clamp recordings in current clamp mode were obtained and action potential properties of medium-sized (34-45 microm) FG+ DRG neurons were characterized. In the neuroma group without cell transplantation, action potential duration and spike inflections were reduced as were the amplitude and duration of spike afterhyperpolarizations. These changes were not observed after transection by nerve crush where axons were allowed to regenerate to distal peripheral targets. In the transplantation group, GFP(+)-SCs were extensively distributed throughout the neuroma, and oriented longitudinally along axons proximal to the neuroma. Changes in action potential properties were attenuated in the GFP(+)-SC group. Thus the engrafted SC procedure ameliorated the changes in action potential waveform of cutaneous primary afferents associated with target disconnection and neuroma formation.

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PubMed1983

Ionic dependence and transmission of epidermal action potentials in a newt embryo.

The ionic dependency and transmission of epidermal action potentials have been examined from tailbud to hatching stages of newt embryos. Previously we have reported that the epidermal action potential is composed of a fast- and slow-action component; only the slow-action component, however, is transmitted to other cells. We address in this report the mechanism by which these responses are mediated. The slow-action potential is not produced in Na+-free saline, tricaine saline, or following the application of TTX, and thus appears to be Na+ dependent. The fast-action potential on the other hand is blocked by application of Co2+ and verapamil saline and thus appears to be Ca2+ dependent. The slow-action potentials appear to be chemically transmitted since they are transmitted even to those cells which are electrically uncoupled at low intracellular pH (NaHCO3 + HCl, pH 6.2). Furthermore 1 microM curare and atropine are inhibitory to transmission of the slow potential. Epidermal cells of the newt embryo are sensitive to acetylcholine (ACh) applied by hydrostatic ejection through a micropipet. The latter observation further suggests that propagation of the slow-action potential is, in part, a chemical event.

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PubMed1999

Calcium-dependent modulation of the plateau phase of action potential in isolated ventricular cells of rabbit heart.

[Ca2+]i-dependent modulation of the action potential has been studied in Fura-2 dialysed ventricular myocytes of the rabbit using the whole-cell current-clamp method. Fifteen consecutive action potentials (AP1-AP15) and [Ca2+]i transients were elicited at a frequency of 0.2 Hz. A single, brief application of caffeine (during AP9) first enhanced and thereafter attenuated the [Ca2+]i transients accompanying AP9 and AP10-AP12, respectively. This approach provided direct comparison between time courses of action potentials: during the initial steady state (e.g. AP8) and when Ca2+ release from the sarcoplasmic reticulum was increased by caffeine (AP9) or decreased by depletion (AP10). The increase in [Ca2+]i facilitated repolarization and decreased action potential duration. However, action potentials at reduced Ca2+ release (AP10) had longer duration than during steady state. The caffeine-induced changes in L-type Ca2+ current (ICa,L), during voltage-clamp conditions partially explained the effects of caffeine on action potentials. When ICa,L was blocked by 500 micromol L-1 Cd2+, enhanced [Ca2+]i transients revealed an extra current component which was outward at +10 mV and inward at the resting membrane potential (most probably the transient inward current). In the presence of Cd2+, however, AP8 and AP10 had identical time courses, suggesting that ICa,L alone was responsible for the lengthening of AP10. Alterations in the transmembrane Na+ gradient resulted in changes of the steady state action potential durations (AP8) consistently with the expected modulation of the Na+-Ca2+ exchange current. However, the contribution of this current to the [Ca2+]i-dependent behaviour of action potential plateau could not be demonstrated.

Action Potentials↗

PubMed1977

[Simple on-line digital determination of the cardiac action potential and its application].

A system of digital measuring of the cardiac action potential was constructed in order to measure quickly and accurately the resting potential or maximum diastolic potential, overshoot potential, amplitude, time for 50% repolarization and time for 90% repolarization. This system consists of a dual-beam oscilloscope, a digital voltage meter, a digital interval meter and a simple circuit constructed by operational amplifiers. The measurement of the action potential was achieved by tracing only the resting potential or the maximum diastolic potential and the crest of the action potential on the oscilloscope using another beam. The time for measurement is usually 10-15 sec and errors in measurement were considered to be negligible. This system is considered to be useful for digital measurement of the action potential of various cardiac tissues. This system was applied for observation of effects of bufetolol, an adrenergic beta-receptor blocking drug on the action potential of the dog Purkinje fibres. Bufetolol (10(-5) M) caused a slight depolarization of the maximum diastolic potential, decreased overshoot potential, amplitude and maximum rate of rise, and shortened the time for 50% repolarization of the action potential. Bufetolol (10(-4) M) additionally prolonged the time for 90% repolarization.

Action Potentials↗

PubMed1984

Multiple effects of alpha-adrenoceptor stimulation on the action potential of the rabbit atrium.

Effects of alpha-adrenoceptor stimulation by phenylephrine (10(-7)-10(-4) mol/l) in the presence of pindolol (10(-7) mol/l) on the action potential and force of contraction were observed in the rabbit left atrium. Phenylephrine reduced resting potential, prolonged action potential duration (APD), decreased maximum rate of rise of action potential (Vmax) and increased force of contraction in a concentration-dependent manner. Effects of phenylephrine (10(-5) mol/l) were antagonized by prazosin (10(-7) mol/l) or phentolamine (10(-6) mol/l). APD which had been prolonged by phenylephrine (10(-5) mol/l) was slightly shortened by Ni2+ (0.3 mmol/l) at the level of 50% repolarization but almost unaffected at the level of 90% repolarization. TTX (10(-6) mol/l) had no effect on ADP which had been prolonged by phenylephrine (10(-5) mol/l). Cs+ (10 mmol/l), which inhibits outward current ik1, depolarized resting potential, but in contrast with phenylephrine Cs+ did not affect APD at 90% repolarization. Phenylephrine (10(-5) or 3 X 10(-5) mol/l) restored Ca2+-dependent action potential and force of contraction in 20 mmol/K+-Tyrode solution. These responses were suppressed by prazosin (10(-7) mol/l) or Ni2+ (0.3 mmol/l). Phenylephrine (10(-5) or 10(-4) mol/l) had no effect on steady-state membrane potential--Vmax relationship. It is concluded that in the rabbit left atrium phenylephrine, via alpha-adrenoceptors may suppress outward currents perhaps ik1 and ix, and might increase slow inward current.

Action Potentials↗

PubMedDate not supplied

A microcomputer system for real-time analysis of cardiac action potentials.

A system for performing real-time analysis of cardiac action potentials has been developed using a microcomputer based on the Motorola 6800 central processor. Transmembrane potentials obtained using standard microelectrodes were digitized to 8 bits at 80 ms intervals, stored in cyclic memory buffer from which they could be selected for analysis, converted back to analogue form and displayed on an oscilloscope in real time. For each action potential, amplitude, the maximum rate of change of potential and the action potential duration at 50% repolarization and 100% repolarization were measured. In addition, conduction time (taken as the interval between the stimulus artefact and the action potential) was measured. All data were stored in memory and later printed, together with the time at which the recording was made. The system was designed for analysis of action potentials recorded using floating microelectrodes. The computer was controlled by three remote switches and a potentiometer, positioned close to the muscle bath. The program was written in Motorola 6800 assembly language and stored in erasable programmable read-only memory.

Animals↗

PubMed1997

Calcium action potentials restricted to distal apical dendrites of rat neocortical pyramidal neurons.

1. Simultaneous whole-cell voltage and Ca2+ fluorescence measurements were made from the distal apical dendrites and the soma of thick tufted pyramidal neurons in layer 5 of 4-week-old (P28-32) rat neocortex slices to investigate whether activation of distal synaptic inputs can initiate regenerative responses in dendrites. 2. Dual whole-cell voltage recordings from the distal apical trunk and primary tuft branches (540-940 microns distal to the soma) showed that distal synaptic stimulation (upper layer 2) evoking a subthreshold depolarization at the soma could initiate regenerative potentials in distal branches of the apical tuft which were either graded or all-or-none. These regenerative potentials did not propagate actively to the soma and axon. 3. Calcium fluorescence measurements along the apical dendrites indicated that the regenerative potentials were associated with a transient increase in the concentration of intracellular free calcium ([Ca2+]i) restricted to distal dendrites. 4. Cadmium added to the bath solution blocked both the all-or-more dendritic regenerative potentials and local dendritic [Ca2+]i transients evoked by distal dendritic current injection. Thus, the regenerative potentials in distal dendrites represent local Ca2+ action potentials. 5. Initiation of distal Ca2+ action potentials by a synaptic stimulus required coactivation of AMPA- and NMDA-type glutamate receptor channels. 6. It is concluded that in neocortical layer 5 pyramidal neurons of P28-32 animals glutamatergic synaptic inputs to the distal apical dendrites can be amplified via local Ca2+ action potentials which do not reach threshold for axonal AP initiation. As amplification of distal excitatory synaptic input is associated with a localized increase in [Ca2+]i these Ca2+ action potentials could control the synaptic efficacy of the distal cortico-cortical inputs to layer 5 pyramidal neurons.

Action Potentials↗

PubMed1985

Prolonged modification of action potential shape by synaptic inputs in molluscan neurones.

1. Somatic action potentials of Lymnaea neurons are modified by excitatory or inhibitory synaptic inputs and have been studied using phase-plane techniques and an action potential duration monitor. 2. Excitatory synaptic inputs increase the rate of neuronal discharge, cause action potential broadening, a decrease in the maximum rate of depolarization (Vd) and a decrease in the maximum rate of repolarization (Vr). 3. Inhibitory synaptic inputs decrease the discharge rate and cause narrowing of action potentials, an increase in Vd and an increase in Vr. 4. The effects reported above outlast the original synaptic inputs by many seconds and, if the somatic action potentials are similar to those in the axon terminals, they may have far-reaching effects on transmitter release.

Action Potentials↗

PubMed1976

Manganese-dependent propagated action potentials and their depression by electrical stimulation in guinea-pig myocardium perfused by sodium-free media.

1. Propagated action potentials were recorded in right ventricular papillary muscles from guinea-pig heart while exposed to Na-free, Ca-free and Mg-free solutions containing Mn. 2. When Na was totally replaced by 95 mM-Mn the overshoot was about 45 mV while the resting potential was about -90mV. 3. The overshoot of action potentials was increased by about 20-30 mV per tenfold increase of Mn concentration over the range of 2-50 mM. 4. Similar increases of overshoots with increasing of Mn concentration also occurred in the presence of 0-6 mM-Ca. Increasing of Ca from 5 to 20 mM had little influence on the overshoot but shortened the duration of the Mn-dependent action potential in the presence of 5 mM-MN. 5 Mn-dependent action potentials were not depressed by 3 X 10(5) M tetrodotoxin but by La. 6. These results suggest that Mn passes through the slow inward current channel to generate the action potential seen under the Na-free condition. 7. The overshoot and duration of the Mn-dependent action potential decreased with stimulation. At stimulus frequencies (Hz) of 0-5, 0-2, 0-1, 0-017 and 0-0033 the overshoot of action potential in 5 mM-Mn Tyrode decreased by 0-5-1 mV per an action potential. This depression of the action potential is explained by assuming intracellular accumulation of Mn.

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PubMed1998

Modeling action potential initiation and back-propagation in dendrites of cultured rat motoneurons.

Regardless of the site of current injection, action potentials usually originate at or near the soma and propagate decrementally back into the dendrites. This phenomenon has been observed in neocortical pyramidal cells as well as in cultured motoneurons. Here we show that action potentials in motoneurons can be initiated in the dendrite as well, resulting in a biphasic dendritic action potential. We present a model of spinal motoneurons that is consistent with observed physiological properties of spike initiation in the initial segment/axon hillock region and action potential back-propagation into the dendritic tree. It accurately reproduces the results presented by Larkum et al. on motoneurons in organotypic rat spinal cord slice cultures. A high Na+-channel density of Na = 700 mS/cm2 at the axon hillock/initial segment region was required to secure antidromic invasion of the somato-dendritic membrane, whereas for the orthodromic direction, a Na+-channel density of Na = 1,200 mS/cm2 was required. A "weakly" excitable (Na = 3 mS/cm2) dendritic membrane most accurately describes the experimentally observed attenuation of the back-propagated action potential. Careful analysis of the threshold conditions for action potential initiation at the initial segment or the dendrites revealed that, despite the lower voltage threshold for spike initiation in the initial segment, an action potential can be initiated in the dendrite before the initial segment fires a spike. Spike initiation in the dendrite depends on the passive cable properties of the dendritic membrane, its Na+-channel density, and local structural properties, mainly the diameter of the dendrites. Action potentials are initiated more easily in distal than in proximal dendrites. Whether or not such a dendritic action potential invades the soma with a subsequent initiation of a second action potential in the initial segment depends on the actual current source-load relation between the action potential approaching the soma and the electrical load of the soma together with the attached dendrites.

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