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At least 109 records · Page 6Linked to original sources

PubMed1975

Polyphasic synaptic potentials in the ganglion of the mollusc, Navanax.

1. Included in the ensemble of synaptic input received by identified neurones in the ganglion of the marine mollusc Navanax are biphasic synaptic potentials, consisting of a depolarization followed by a hyperpolarization. 2. Both phases are chemically mediated as judged by their susceptibility to a high magnesium medium and neither exhibits depression with repetition. 3. The hyperpolarizing phase has a reversal potential of about -50mV, which varies only with changes in the external chloride concentration. This phase is unaffected by cholinolytics. 4. The depolarizing phase reverses at a more positive potential, is probably the result of a change in sodium conductance and is blocked by hexamethonium and high concentrations of eserine. 5. The biphasic synaptic potentials are therefore similar in many respects to the biphasic response evoked by iontophoretic application of acetylcholine on to these cells, suggesting that the two types of cholinergic receptors previously characterized on these neurones are both functional.

Animals↗

PubMed1993

Bayesian analysis of mixtures applied to post-synaptic potential fluctuations.

Bayesian inference techniques have been applied to the analysis of fluctuation of post-synaptic potentials in the hippocampus. The underlying statistical model assumes that the varying synaptic signals are characterized by mixtures of (unknown) numbers of individual gaussian, or normal, component distributions. Each solution consists of a group of individual components with unique mean values and relative probabilities of occurrence and a predictive probability density. The advantages of bayesian inference techniques over the alternative method of maximum likelihood estimation (MLE) of the parameters of an unknown mixture distribution include the following: (1) prior information may be incorporated in the estimation of model parameters; (2) conditional probability estimates of the number of individual components in the mixture are calculated; (3) flexibility exists in the extent to which the estimated noise standard deviation indicates the width of each component; (4) posterior distributions for component means are calculated, including measures of uncertainty about the means; and (5) probability density functions of the component distributions and the overall mixture distribution are estimated in relation to the raw grouped data, together with measures of uncertainty about these estimates. This expository report describes this novel approach to the unconstrained identification of components within a mixture, and provides demonstration of the usefulness of the technique in the context of both simulations and the analysis of distributions of synaptic potential signals.

Action Potentials↗

PubMed2006

Nuclear calcium signals during L-LTP induction do not predict the degree of synaptic potentiation.

The magnitude and/or duration of nuclear Ca(2+)-transients has been shown to dose-dependently modulate gene transcription upon neuronal activation. This is an attractive model for synapse-to-nucleus communication. In order to encode synaptic information, these nuclear Ca(2+)-transients have to be correlated with changes in synaptic strength rather than changes in gene expression patterns. In this study, we analysed nuclear Ca(2+) signals during L-LTP induction. Using a combined approach of fEPSP recordings and two-photon imaging, these Ca(2+) signals were correlated with different degrees of synaptic potentiation in CA1 hippocampal slices. To refine our analysis on the single-cell level, we developed a new approach called single-cell-excitability-probing (SCEP) to assay the plasticity outcome of individual cells by optical means. The degrees of synaptic potentiation we observed could be categorized into transcription independent, transcription-dependent and reduced transcription-dependent. There is no consistent dose-dependent relationship between these different degrees of synaptic potentiation and the magnitude, the decay time and the area under the curve of nuclear Ca(2+)-transients during L-LTP induction. This indicates that nuclear Ca(2+)-transients during induction are unsuited to grade the degree of plasticity in an analogue manner. We propose a role for nuclear Ca(2+) as a digital on/off switch for activating transcription.

Animals↗

PubMed1983

Relation between shapes of post-synaptic potentials and changes in firing probability of cat motoneurones.

1. The shapes of post-synaptic potentials (p.s.p.s) in cat motoneurones were compared with the time course of changes in firing probability during repetitive firing. Excitatory and inhibitory post-synaptic potentials (e.p.s.p.s and i.p.s.p.s) were evoked by electrical stimulation of peripheral nerve filaments. With the motoneurone quiescent, the shape of each p.s.p. was obtained by compiling post-stimulus averages of the membrane potential. Depolarizing current was then injected to evoke repetitive firing, and the post-stimulus time histogram of motoneurone spikes was obtained; this histogram reveals the primary features (peak and/or trough) of the cross-correlogram between stimulus and spike trains. The time course of the correlogram features produced by each p.s.p. was compared with the p.s.p. shape and its temporal derivative.2. E.p.s.p.s of different sizes (0.15-3.1 mV, mean 0.75 mV) and shapes were investigated. The primary correlogram peak began, on the average, 0.48 msec after onset of the e.p.s.p., and reached a maximum 0.29 msec before the summit of the e.p.s.p; in many cases the correlogram peak was followed by a trough, in which firing rate fell below base-line rate. The height of the correlogram peak with respect to base-line firing rate increased in proportion to both the amplitude of the e.p.s.p.s and the magnitude of their rising slope (in these data, amplitude and rising slope also covaried).3. The mean half-width of the correlogram peaks (0.65+/-0.28 msec (S.D.)) agreed better with the average half-width of the e.p.s.p. derivatives (0.55+/-0.33 msec) than with the half-width of the e.p.s.p.s (4.31+/-1.50 msec). The shape of the primary correlogram peak produced by simple e.p.s.p.s often resembled the temporal derivative of the e.p.s.p. rise. For larger e.p.s.p.s, the shape of the correlogram peak closely matched the e.p.s.p. derivative, while smaller e.p.s.p.s in appreciable synaptic noise often generated correlogram peaks somewhat wider than their derivatives. On the other hand, the match between the correlogram trough that followed the peak and the negative slope of the e.p.s.p. was better for the small e.p.s.p.s than for the large e.p.s.p.s; for large e.p.s.p.s the drop in firing rate during the trough was typically limited at zero. These relations were tested further by comparing the integral of the correlogram with the time course of the e.p.s.p. For large e.p.s.p.s, the correlogram integral matched the rising phase of the e.p.s.p. quite well, although it underestimated the rate of decline of the e.p.s.p.4. Complex e.p.s.p.s with distinct components during their rising phase often produced correlogram peaks that did not accurately reflect the features in their temporal derivative. Temporal summation of large e.p.s.p.s and summation of their derivatives was linear, but the resulting correlogram peaks did not add linearly; the second correlogram peak was often smaller than the first. However, when small e.p.s.p.s were summed, the correlogram peaks more closely matched the e.p.s.p. derivatives.5. Compound i.p.s.p.s produced primary correlogram troughs followed by a shallow compensatory peak. The width of the trough extended through the peak of the i.p.s.p., well into the falling phase of the i.p.s.p. During the trough the firing rate usually dropped to zero. Thus, the primary correlogram features produced by large i.p.s.p.s did not resemble any linear combination of the shape of the i.p.s.p. and/or its temporal derivative. Moreover, the integral of the correlogram did not resemble the i.p.s.p.6. The major observations are consistent with a motoneurone model in which a membrane potential ramp approaches a voltage threshold for spike initiation. Near threshold, e.p.s.p.s superimposed on the ramp advance the occurrence of spikes to their rising phase, producing a correlogram peak resembling their temporal derivative. Synaptic noise would increase the probability of sampling the peak of the e.p.s.p., leading to wider correlogram peaks. I.p.s.p.s would delay the occurrence of spikes to their falling phase.

Action Potentials↗

PubMed1995

Differential effects of zinc on hyperpolarizing and depolarizing GABAA synaptic potentials in hippocampal slice cultures.

We have examined the changes in GABAA-mediated synaptic potentials recorded from CA3 pyramidal neurons in hippocampal slice cultures following application of zinc (Zn2+). Unlike 4-AP, Zn2+ did not enhance fast hyperpolarizing potentials but primarily enhanced depolarizing GABAA potentials. Zn2+ did not alter the postsynaptic response of pyramidal neurons to pressure applied GABA, consistent with previous reports that Zn2+ enhances the release of GABA from presynaptic terminals. To examine the role of local circuitry in the production of Zn2+ responses, we recorded from cultures maintained for 7-10 days following removal of the dentate and hilus to allow complete degeneration of the mossy fibers (DGX cultures). Zn2+ produced giant depolarizing potentials (GDPs) in DGX cultures that were identical to those in intact cultures. In contrast, the 4-AP response was dramatically altered in DGX cultures. In DGX cultures, Zn2+ co-applied with 4-AP appeared to inhibit the production of fast hyperpolarizing GABAA synaptic potentials produced by 4-AP alone. This inhibition of fast hyperpolarizing potentials suggests that Zn2+ may reduce the release of GABA onto pyramidal cell somata. These observations suggest that Zn2+ enhances GABA release from local circuit neurons that synapse onto pyramidal cell dendrites, and inhibits GABA release onto pyramidal cell somata.

4-Aminopyridine↗

PubMed1989

5-HT-mediated synaptic potentials in the dorsal raphe nucleus: interactions with excitatory amino acid and GABA neurotransmission.

1. Intracellular recordings from neurons within dorsal raphe nucleus in slices from rat brain were used to study an inhibitory postsynaptic potential (IPSP) evoked by electrical stimulation. 2. The IPSP was observed in approximately 70% of neurons, had a latency to onset of 40-65 ms, reached a peak in 350-400 ms, had a total duration of 1-2 s, and reversed polarity at the potassium equilibrium potential. 3. This IPSP was blocked by spiperone (1 microM) and prolonged by fluoxetine (300 nM-30 microM) suggesting that it was mediated by 5-hydroxytryptamine (5-HT). 4. Superfusion with gamma-aminobutyric acid (GABA) and excitatory amino acid receptor antagonists were used to block "fast" synaptic potentials that preceded the IPSP such that it could be studied in isolation. Blockade of the GABA-mediated synaptic potentials increased the amplitude of the IPSP by 1.3-fold. The amplitude of the IPSP was reduced by 30% after blockade of the excitatory amino acid-mediated synaptic potential. 5. The results indicate that the IPSP recorded in dorsal raphe neurons was caused by 5-HT released at least in part from indirect (synaptically induced) excitation of 5-HT-containing cells within the slice.

Animals↗

PubMed1993

Allosteric potentiation by diazoxide of AMPA receptor currents and synaptic potentials.

Diazoxide (100-560 microM) reversibly increased the amplitude and duration of excitatory post-synaptic field potentials recorded in the dentate gyrus of hippocampal slices following stimulation of the perforant pathway. In rat cortex mRNA-injected Xenopus oocytes diazoxide (1-1000 microM) alone had little effect on membrane current, but rapidly and reversibly increased (up to 5-fold) current responses to (R,S)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA, 30 microM), L-glutamate (100 microM), quisqualate (3 microM), kainate (100 microM) and domoate (3 microM), an effect that was neither mimicked by other activators of ATP-sensitive potassium channels nor blocked by glibenclamide. Diazoxide increased current amplitudes for all concentrations of the 'inactivating' ligands, AMPA, L-glutamate and quisqualate but had little effect on their EC50 values. In contrast, diazoxide increased the apparent potency of the 'non-inactivating' ligands, kainate and domoate, but increased the efficacy of saturating concentrations by only 10-20%. Diazoxide did not modify the competitive inhibition of AMPA and kainate currents by 6-nitro-7-sulfamoylbenzo[f]quinoxaline-2,3-dione (NBQX) and thus does not compete for the agonist site as do AMPA and kainate. Similarly, diazoxide neither inhibited the binding of [3H]AMPA or [3H]kainate to rat cortical membranes in competition experiments nor consistently modified the apparent [3H]AMPA affinity (Kd) or receptor density (Bmax) in saturation experiments. These data suggest that diazoxide acts at an allosteric site on the AMPA receptor/channel to potentiate activation in a manner dependent upon the properties of the excitatory agonist.

Allosteric Regulation↗

PubMed2003

Simulation framework for electrophysiological networks: effect of syncytial properties on smooth-muscle synaptic potentials.

A building block-based software framework was developed to simulate electrophysiological networks. The synaptic potentials generated during neurotransmission were simulated in an existing discrete bidomain model of smooth muscle, using cubic, three-dimensional grids of varying sizes. The model is automatically derived and numerically solved, and the results of the simulation agree with previous results obtained analytically. An enhanced model was also proposed, incorporating an additional (junctional) capacitance in the network. The correctness of the model was verified, and the effect of the extra capacitance on the synaptic potentials was explored. It was found that, with a junctional capacitance C(i) of 1.4 x 10(-10) F incorporated, the peak amplitude of the spontaneous excitatory junction potential V(peak) declined by approximately 13% at node 0 and by approximately 37% at node 3x for a system size of 9(3). Similar results were obtained for different system sizes. V(peak) also declined as the junctional capacitance Ci was increased. In a system of size 11(30, a 200-fold increase in C(i) induced a 55% reduction at node 0. It is suggested that the type of modular simulation framework developed here may find general applicability for simulations of other physiological systems.

Electrophysiology↗

PubMed1984

Unitary inhibitory synaptic potentials in the guinea-pig hippocampus in vitro.

Mechanisms involved in the generation of synaptic inhibition have been investigated by making simultaneous intracellular recordings from pairs of neurones in the CA3 pyramidal cell field of guinea-pig hippocampal slices. Inhibitory post-synaptic potentials dependent on single presynaptic action potentials (i.p.s.p.s) and mediated through monosynaptic and disynaptic connexions have been identified. The recurrent nature of some hippocampal inhibition has been demonstrated by showing that activity in a single cell may initiate feed-back i.p.s.p.s onto itself. The observation of synchronous i.p.s.p.s in recordings from two cells illustrates the divergence of synaptic contacts made by inhibitory neurones. The peak conductance change associated with an i.p.s.p. was in the range 5-9 nS and it reversed uniformly throughout its time course at membrane potentials between -73 and -80 mV. The shortest time-to-peak of synaptic potentials was approximately 3 ms and in this case the i.p.s.p. decayed with a time constant comparable to the passive membrane time constant of the post-synaptic neurone. The peak amplitude of i.p.s.p.s fluctuated in a way consistent with the quantal release of inhibitory neurotransmitter. Inhibitory neurones could fire bursts of action potentials not unlike those generated by pyramidal cells in this area. A comparison of the conductance change associated with identified i.p.s.p.s with that associated with the maximal inhibitory post-synaptic potential resulting from electrical stimulation of fibre pathways suggested that, in the slice, a pyramidal cell is innervated by up to fifteen inhibitory neurones.

Action Potentials↗

PubMed1984

A bicuculline-resistant inhibitory post-synaptic potential in rat hippocampal pyramidal cells in vitro.

Experiments were performed on rat hippocampal CA1 pyramidal cells in vitro in order to elucidate the origin of the late hyperpolarizing potential, which follows the gamma-aminobutyric acid (GABA)-mediated inhibitory post-synaptic potential (GABA-i.p.s.p.). The late hyperpolarizing potential could be evoked by orthodromic stimulation via stratum radiatum or stratum oriens but not by selective antidromic stimulation. The membrane soluble analogue of cyclic AMP, 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br cyclic AMP), which blocks calcium-activated potassium hyperpolarizations (GK(Ca], did not reduce the late hyperpolarizing potential. The enkephalin analogue, (D-ala2-met5)-enkephalinamide (DALA) reversibly reduced both the GABA-i.p.s.p. and the late hyperpolarizing potential. The late hyperpolarizing potential and GABA-i.p.s.p. were more sensitive to low doses of the calcium antagonist, cadmium, than the excitatory post-synaptic potential (e.p.s.p.). The local application of cadmium to the pyramidal cell layer blocked the antidromic i.p.s.p. but the orthodromically evoked late hyperpolarizing potential was less affected. In contrast to the GABA-i.p.s.p., the late hyperpolarizing potential was not reversed by chloride injection and was enhanced, rather than depressed, by bicuculline. We conclude that the late hyperpolarizing potential is a bicuculline-resistant i.p.s.p. The unidentified transmitter for this i.p.s.p. is released from feed-forward interneurones primarily onto the dendrites of the pyramidal cell and may act by increasing the potassium permeability of the membrane. The epileptiform burst after-hyperpolarization evoked in the presence of GABA antagonists is composed of at least two components, a long-duration hyperpolarization mediated GK(Ca) and an earlier and shorter late hyperpolarizing potential. Blockade of the GK(Ca) by 8-Br cyclic AMP did not alter the duration of epileptiform bursts but did markedly increase the frequency of their occurrence. This suggests that GK(Ca) is involved in controlling the interval between bursts.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1991

Subpopulations of GABA-mediated synaptic potentials in slices of rat dorsal striatum are differentially modulated by presynaptic GABAB receptors.

gamma-Aminobutyric acid (GABA)-mediated synaptic potentials in rat dorsal striatum in vitro were reduced in amplitude by the GABAB receptor agonists baclofen and 3-aminopropyl-(methyl)-phosphinic acid (SK&F 97541), without any detectable postsynaptic effect. Synaptic potentials in 40% of neurones were distinctly multiphasic, the components of which exhibited a differential sensitivity to GABAB agonists. One population of GABA-releasing neurones within the striatum had presynaptic GABAB autoreceptors, whereas others were not directly affected by GABAB agonists.

Animals↗

PubMed1988

Effect of subthreshold voltage-dependent conductances on the transfer function of branched excitable cells and the conduction of synaptic potentials.

1. Impulse response functions were determined from complex point impedance and transfer functions from cultured NG-108 cells to simulate the propagation of a synaptic potential in response to the release of transmitter. In general, the flow of synaptic current has a much shorter duration than the normal membrane time constant, thereby making the use of impulse response functions useful approximations to synaptic events. 2. The resonance observed during the activation of the potassium conductance was reflected in the impulse response function as a pronounced damped oscillation. A comparison of the impulse response functions calculated from point impedance and transfer functions showed similar results for current injections in the growth cone. 3. In addition to the resonance effects of the voltage-dependent conductances on transfer and impulse response functions due principally to the activation of conductances for outward currents, transfer functions were measured during the activation of a steady-state negative conductance. Under these conditions the phase function approaches 180 degrees, indicating that the voltage response is out of phase with the current. 4. In the steady state, the effect of a negative conductance is to algebraically add to the positive conductances and generally decrease the absolute conductance unless there is a net negative current. The decreased conductance enhances the impulse response and the DC space constant, thus leading to a better propagation of slow potentials. This effect can be seen as a decrease in the electrotonic length, L, with intermediate depolarizations. At large depolarizations the steady-state activation of the K conductance generally dominates and leads to a greatly increased electrotonic length. 5. Both the net conductances and the associated kinetics play a role in shaping the potential changes during a synaptic current. This is especially critical if there is a net negative steady-state conductance. Under these conditions there is a surprising reduction in the impulse response function. 6. Thus, during a subthreshold activation of the voltage-dependent negative conductances, the observable synaptic potentials would be either large potential responses due to an apparent increase in the impedance (algebraic summation of positive and negative conductances with a net positive conductance) or a minimal response because of the phasic cancellation due to a net negative conductance. The latter condition could exist near the synaptic reversal potential due to a large synaptic drive and would appear experimentally as a form of inhibition.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1994

A new approach to the estimation of post-synaptic potentials in human motoneurones.

A new method is described for estimating the shape of the compound post-synaptic potentials evoked by stimuli in human motoneurones. The method is based on changes in the duration of the interspike intervals in motor-unit spike trains that are time-locked to the stimulus. This is particularly helpful in estimating the profile of long-latency slow rise-time post-synaptic potentials that are difficult to estimate with other methods. The method is simple to apply and the analysis is readily implemented on a personal computer.

Electric Stimulation↗

PubMed1984

Excitatory synaptic potentials due to activation of neurons with short projections in the myenteric plexus.

Intracellular microelectrodes have been used to examine the effects, on excitatory inputs to myenteric nerve cells, of lesions of intrinsic pathways in the myenteric plexus of the guinea-pig small intestine. The lesions consisted of circumferential cuts (myotomies) which severed the external musculature to the depth of the submucosa and thus interrupted pathways in the myenteric plexus. Sufficient time was allowed between creating the lesions and recording from the neurons for the endings of severed neurites to degenerate and this was confirmed histochemically by examining the distribution of varicose fibres with 5-hydroxytryptamine immunoreactivity in myenteric ganglia from which recordings were made. Two types of excitatory input, eliciting fast and slow excitatory post-synaptic potentials, respectively, were demonstrable in response to focal stimulation of nerves in the ganglia from which recordings were made. There were no differences in the proportions of neurons in which fast or slow excitatory synaptic potentials were evoked in unoperated preparations (controls), in islands 1.5-4 mm wide between myotomies, or within 1 mm on the oral or anal sides of myotomies. Possible differences in the amplitudes, durations at half amplitude, and threshold numbers of stimuli for initiation of slow excitatory synaptic potentials were analyzed. The only significant differences were found when data from control and oral areas were pooled and compared with combined data from island and anal areas (this assessed differences that could arise from severing nerve fibres running from oral to anal).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Synaptic potentials in locus coeruleus neurons in brain slices.

Neurons of the locus coeruleus (LC) fire action potentials spontaneously in vitro in the absence of any stimulation. This spontaneous activity is thought to arise from intrinsic membrane properties that include a balance between at least two ion conductances. One is a persistent inward sodium current that is active near the threshold for action potential generation. The second is a calcium-dependent potassium current that is activated following the entry of calcium during the action potential, is responsible for the after-hyperpolarization following the action potential, and decays over a period of 1-2 sec following the action potential. The spontaneous activity of LC neurons can be altered by both excitatory and inhibitory synaptic inputs. One excitatory input has been described that is mediated by glutamate receptors of both the non-NMDA and NMDA subtypes. Inhibitory synaptic potentials include those mediated by GABA (acting on GABAA-receptors), glycine (acting on a strychnine-sensitive receptor) and noradrenaline (acting on alpha 2-adrenoceptors). The presence of synaptic potentials mediated by these transmitters, studied in vitro, correlate with studies made in vivo and with histochemical identification of synaptic inputs to the locus coeruleus.

Action Potentials↗

PubMed1996

Interactions between associative synaptic potentials in the piriform cortex of the in vitro isolated guinea pig brain.

The interaction between synaptic potentials generated by the activation of separate sets of associative fibres was investigated in the piriform cortex of an in vitro isolated guinea pig brain preparation. Restricted regions of the piriform cortex served by separate contingents of afferent fibres of the lateral olfactory tract were isolated surgically. The activity generated by these patches of cortex in response to afferent stimulation propagates to remote cortical regions along cortico-cortical associative fibres. Current source density (CSD) analysis of field potential laminar profiles evoked by lateral olfactory tract stimulation confirmed that the synaptic sinks induced by distinct associative fibre contingents converge on the apical dendrites of piriform cortex neurons in the superficial lb layer. Pairing between potentials evoked by activation of two separate sets of associative fibres resulted in an almost linear summation when the two responses coincided. For interstimulus intervals of <100 ms, heterosynaptic pairing of independent associative inputs induced a facilitation of the conditioned associative potential, which correlated with an increase in the associative sink located in layer lb, as demonstrated by CSD analysis. The evaluation of the pairing intervals suggests that the heterosynaptic facilitation of the conditioned associative potentials may be due to the summation of local and remote associative synaptic events. It is concluded that separate associative inputs converge on the apical dendrites of piriform cortex pyramidal neurons to generate synaptic potentials through the activation of spatially close but independent synapses. The role of associative synaptic integration in the functional organization of the olfactory cortex is discussed.

Afferent Pathways↗

PubMed2004

Eye opening rapidly induces synaptic potentiation and refinement.

NMDA receptor (NMDAR)-mediated increases in AMPA receptor (AMPAR) currents are associated with long-term synaptic potentiation (LTP). Here, we provide evidence that similar changes occur in response to normal increases in sensory stimulation during development. Experiments discriminated between eye opening-induced and age-dependent changes in synaptic currents. At 6 hr after eye opening (AEO), a transient population of currents mediated by NR2B-rich NMDARs increase significantly, and silent synapses peak. Sustained increases in evoked and miniature AMPAR currents occur at 12 hr AEO. Significant changes in AMPAR:NMDAR evoked current ratios, contacts per axon, and inputs per cell are present at 24 hr AEO. The AMPAR current changes are those seen in vitro during NMDAR-dependent LTP. Here, they are a consequence of eye opening and are associated with a new wave of synaptic refinement. These data also suggest that new NR2B-rich NMDAR currents precede and may initiate this developmental synaptic potentiation and functional tuning.

Animals↗

PubMed1969

Field potentials generated by dendritic spikes and synaptic potentials.

Predictions from the cable model and equations for field potentials generated by single neurons are computed and compared with extra cellular recordings from synaptically activated cerebellar Purkinje cell dendrites. Neither theory predicts the results, nor does the expermental situation satisfy the assumptions of either theory. Theoretical calculations from a recent formulation developed by Rall compare favorably with potentials recorded by others authors. A pplications of these formulations are discussed.

Action Potentials↗