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S J Redman

Publications and source records attributed to S J Redman.

At least 37 records · Page 2Linked to original sources
PubMed1989

Reduction by general anaesthetics of group Ia excitatory postsynaptic potentials and currents in the cat spinal cord.

1. The effects of thiopentone and halothane on excitatory synaptic transmission at group Ia afferent synapses on lumbosacral motoneurones were studied in the anaesthetized or decerebrate cat. 2. Thiopentone (10 mg kg-1) infused on a background of light pentobarbitone anaesthesia caused a decrease in single-fibre monosynaptic group Ia excitatory postsynaptic potentials (EPSPs) of between 0 and 24%. A step increase in inspired halothane concentration in the range 0.7-0.9% produced a decrease in EPSP amplitude of between 0 and 31%. These effects were reversible when the anaesthetic level was reduced. 3. Fluctuation analysis of selected single-fibre group Ia EPSPs revealed that these effects could be accounted for by a decrease in the probability of occurrence of EPSPs of larger amplitude, and an increase in the probability of occurrence of EPSPs of smaller amplitude. The mean separation between discrete amplitudes was not altered by either anaesthetic agent. 4. EPSPs whose time course indicated a somatic site of origin were voltage clamped to study the effect of the anaesthetics on the time course of the synaptic currents. Neither thiopentone nor halothane produced a consistent effect on the time constant of decay of the current, although they both depressed its peak amplitude. 5. The results are interpreted as indicating a presynaptic site of action of both anaesthetics at the concentrations studied: the probability of release of neurotransmitter is reduced, without any detectable change in the mean duration of the postsynaptic conductance increase. These findings are discussed in relation to the mechanisms of action of anaesthetics on exocytosis and presynaptic inhibition.

Animals↗
PubMed1989

Amplitude fluctuations in small EPSPs recorded from CA1 pyramidal cells in the guinea pig hippocampal slice.

EPSPs have been evoked in CA1 pyramidal cells by (1) activation of single CA3 neurons (unitary EPSPs), and (2) low-intensity stimuli to the CA1 stratum radiatum. Five unitary EPSPs were obtained; their mean peak amplitudes ranged from 85 to 275 microV and 3 of the 5 showed fluctuations in amplitude that were too great to be attributed to baseline noise. After subtraction of the variance due to the noise, these EPSPs had coefficients of variation much higher than those reported for variability in the quantal EPSP in other preparations. These results suggest that intermittent transmitter release is a major cause of EPSP amplitude fluctuation at this synapse. A noise deconvolution technique based on a nonrestrictive model of transmitter release was applied to the EPSPs obtained in this study. For 2 of the EPSPs evoked by stratum radiatum stimulation, the amplitudes fluctuated between discrete values that were sufficiently separated with respect to the noise to be resolved by the deconvolution procedure. Quantal increments of 224 and 193 microV were determined for the 2 EPSPs.

Animals↗
PubMed1988

The dependence of motoneurone membrane potential on extracellular ion concentrations studied in isolated rat spinal cord.

1. Intracellular recordings from ninety-nine motoneurones have been made in an in vitro hemisected spinal cord preparation. Their mean resting membrane potential in normal artificial cerebrospinal fluid (CSF) was -71 +/- 0.5 mV (+/- S.E.M.). The mean amplitude of the action potential was 84.0 +/- 1.4 mV (n = 50), and the mean input conductance was 101 +/- 7 nS (n = 49). 2. Both membrane potential and input conductance were sensitive to changes in [K+]o, [Na+]o, [Cl-]o and [Ca2+]o. 3. Replacement of extracellular Ca2+ by Mn2+ resulted in less than 1 mV hyperpolarization and a decrease in input conductance from 102 +/- 7 to 93 +/- 6 nS (n = 15). 4. At high [K+]o (greater than 10 mM) the membrane potential followed the potential predicted by the Nernst equation for K+ ions with a slope of 58 mV per 10-fold change in [K+]o. At low [K+]o (less than 10 mM) there was significant deviation from K+ equilibrium potential (EK). 5. [K+]i was found to be 106 mM when estimated from the reversal potential of the after-hyperpolarization of the antidromic action potential. 6. The reversal potential of the recurrent inhibitory postsynaptic potential (IPSP) in normal CSF was used to calculate [Cl-]i. This was 6.6 mM, which is less than would be expected if Cl- was passively distributed, indicating the presence of an outwardly directed Cl- pump. 7. Decreasing [Cl-]o from control (134 mM) to 4 mM resulted in a depolarization of 6.9 +/- 0.9 mV and a decrease in input conductance from 102 +/- 5 to 90 +/- 5 nS (n = 14) in 3 mM [K+]o. 8. Decreasing [Na+]o from 156 to 26 mM by substitution with choline resulted in a 6.2 +/- 0.5 mV hyperpolarization and a decrease in input conductance from from 102 +/- 4 to 76 +/- 4 nS (n = 5) in 3 mM [K+]o. 9. The input conductances for Na+, Cl- and K+ at the resting potential were calculated. After allowing for a microelectrode leak conductance, the relative input conductances were gNa/gK = 0.13 and gCl/gK = 0.25.

Action Potentials↗
PubMed1987

Presynaptic inhibition of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia axons.

1. Single-fibre group Ia excitatory post-synaptic potentials (e.p.s.p.s) were evoked in triceps surae motoneurones. These e.p.s.p.s were reduced by conditioning stimulation of group I axons in posterior biceps-semitendinosus nerves. 2. The investigation concentrated on e.p.s.p.s of somatic origin, because the amplitude of these e.p.s.p.s is not reduced by post-synaptic conductance increases. Any reduction in these e.p.s.p.s could therefore be attributed to presynaptic inhibition. 3. The reduction in somatic e.p.s.p. amplitude was greatest when the conditioning stimulus preceded the e.p.s.p. by 30 ms, and was negligible when the conditioning interval was extended to 200-300 ms. 4. The percentage reduction of somatic e.p.s.p.s was independent of their unconditioned peak amplitude. 5. E.p.s.p.s of somatic origin were reduced by the same amount, on average, as e.p.s.p.s of dendritic origin. 6. E.p.s.p.s evoked in the same motoneurone by impulses in different Ia axons were reduced by different amounts and e.p.s.p.s evoked in different motoneurones by impulses in the same Ia axon were also reduced by different amounts. 7. Analysis of fluctuations in e.p.s.p.s before and after conditioning indicated that after conditioning, larger discrete amplitudes became less probable, while smaller discrete amplitudes became more probable. The average increment between discrete amplitudes did not alter; nor were the discrete amplitudes reduced. 8. The probabilities of transmitter release at synaptic boutons were calculated before and during presynaptic inhibition. The maximum decrease in release probability was 0.64, suggesting a reduction in calcium influx of 10-15%.

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PubMed1987

Nonuniform passive membrane properties of rat lumbar sympathetic ganglion cells.

We have studied the passive membrane properties of sympathetic neurons in isolated lumbar paravertebral ganglia of young rats by recording the voltage response to small steps of current passed through an intracellular microelectrode. Substitution of Ba2+ (2.5 mM) for Ca2+ (2.5 mM) in the bathing solution increased the input resistance and the time constant of the voltage response, but the increase in time constant was disproportionately large relative to the increase in input resistance. After consideration of the passive electrical properties and the geometry of the soma and dendrites, it was concluded that the disproportionate change in input resistance and time constant could be explained if barium inactivated a resting potassium conductance that was concentrated in the distal dendrites. In the APPENDIX, the effect of nonuniform membrane conductance on the relationship between input resistance and time constant in models of these neurons is analyzed.

Animals↗
PubMed1986

Intracellular tetraethylammonium ions enhance group Ia excitatory post-synaptic potentials evoked in cat motoneurones.

Single fibre group Ia excitatory post-synaptic potentials (e.p.s.p.s) were recorded in cat spinal motoneurones after the neurones were injected with tetraethylammonium (TEA) ions. TEA injection increased the peak amplitude of most e.p.s.p.s. The time course of e.p.s.p.s generated at the soma was unaffected, but the time course of e.p.s.p.s generated in the dendrites was prolonged. The membrane time constant did not change after TEA injection. Somatic e.p.s.p.s were voltage clamped after TEA was injected. The reversal potential for these e.p.s.p.s was more positive than for e.p.s.p.s unaffected by TEA. Composite e.p.s.p.s added linearly, or greater than linearly, whereas in motoneurones without TEA they added linearly or less than linearly. The enhanced amplitude and prolonged time course observed in dendritic e.p.s.p.s after TEA injection was reduced by small hyperpolarizing currents. Greater than linear summation of composite e.p.s.p.s was converted to linear summation by small hyperpolarizing currents. The increase in somatic e.p.s.p.s was attributed to a more positive reversal potential for the e.p.s.p.s. We suggest that TEA decreases the relative permeability of K+ in the subsynaptic channels. We propose that in the presence of TEA, dendritic depolarization activates an inward current which amplifies and prolongs synaptic potentials spreading towards the soma.

Action Potentials↗
PubMed1985

Corticomotoneuronal synapses in the monkey: light microscopic localization upon motoneurons of intrinsic muscles of the hand.

Some corticospinal neurons give rise to axons which terminate directly upon motoneurons, thereby establishing corticomotoneuronal connections. The location of corticomotoneuronal synapses upon motoneurons innervating intrinsic muscles of the hand in the monkey was demonstrated by the use of intra-axonal and intracellular horseradish peroxidase (HRP). After a number of corticospinal axons originating from the "hand" area of the precentral gyrus had been injected with HRP in the lateral funiculus at C7-C8, a number of nearby identified intrinsic hand muscle motoneurons were also injected. Connections between corticomotoneuronal fibres and motoneurons were reconstructed from longitudinal parasagittal sections treated by the cobalt-enhanced diaminobenzidine method. Corticospinal axons in the lateral funiculus gave rise to main collaterals which provided an extensive arborization in lamina IX, where it was predominantly longitudinal, and in the adjacent intermediate zone. En passant and single or clustered groups of terminal boutons arose from preterminal branches of these arbors. Seven light-microscopically identified corticomotoneuronal synapses were found. They were located upon the dendrites of recipient motoneurons at 40 micron to 750 micron from the soma and ranged in size from 0.6 X 3.0 micron to 2.4 X 3.6 micron. The results suggest that each main collateral of a corticomotoneuronal axon establishes very few synaptic contacts, and possibly only one, with the dendrites of recipient motoneurons. This small number of contracts per motoneuron is consistent with the small amplitudes of minimal and unitary corticomotoneuronal EPSPs recorded from forelimb and hand motoneurons.

Animals↗
PubMed1983

The synaptic current evoked in cat spinal motoneurones by impulses in single group 1a axons.

Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in motoneurones of anaesthetized cats by impulses in single group 1 a axons. E.p.s.p.s with a time course which indicated a somatic site of origin were voltage-clamped using a single micro-electrode clamp. Excitatory post-synaptic currents (e.p.s.c.s) were found to peak in less than 0.2 ms, and to decay with an exponential time course. The time constant of decay was usually in the range 0.3-0.4 ms (at 37 degrees C). At the resting membrane potential, an e.p.s.p. with a peak of 100 microV was generated by an average peak e.p.s.c. of 330 pA. This corresponded to an average peak conductance increase of 5 nS. The e.p.s.c. decreased with membrane depolarization, and reversed to become an outward current at a null potential of +4.6 +/- 2 mV (+/- S.E. of mean; n = 7). Membrane hyperpolarization caused the peak e.p.s.c. to increase and the time constant of decay of the e.p.s.c. to decrease. The total charge in the synaptic current did not increase with hyperpolarization. This observation can explain earlier observations which showed that the peak amplitude of the e.p.s.p. did not increase with hyperpolarization. The number of ion channels opened by transmitter release at a single somatic bouton was estimated to be in the range 40-240.

Animals↗
PubMed1981

The components of synaptic potentials evoked in cat spinal motoneurones by impulses in single group Ia afferents.

1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in cat spinal motoneurones by impulses in single group Ia afferent fibres. The probability density of the fluctuations in peak amplitude of each e.p.s.p. was calculated from the recorded peak amplitude and the probability density of the recording noise. 2. Most e.p.s.p.s fluctuated between different components (i.e. individual e.p.s.p.s of a particular discrete amplitude) with peak amplitudes which were integer multiples of the increment between successive components. The average peak amplitude of this incremental e.p.s.p. was about 90 microV for e.p.s.p.s generated at or near the soma. 3. In general, the probability density of the peak amplitude could not be described using Poisson or binomial distributions. 4. For many e.p.s.p.s the complete time course of each component could be calculated. There was no variability in the amplitude of these components nor in their latency of onset. For some e.p.s.p.s there were differences in the latency and time course of the components. 5. The increments between successive components of e.p.s.p. generated proximally were no larger (at the soma) than the corresponding increments for e.p.s.p.s generated at more distal dendritic sites. 6. These results and those from subsequent papers (Jack, Redman & Wong, 1981; Hirst, Redman & Wong, 1981) reinforce earlier suggestions that each bouton behaves in an all-or-nothing manner with respect to post-synaptic effect, and the probability of failure varies at different boutons arising from the same afferent.

Animals↗
PubMed1981

Post-tetanic potentiation and facilitation of synaptic potentials evoked in cat spinal motoneurones.

1. Excitatory post-synaptic potentials (e.p.s.p.s) were evoked in spinal alpha-motoneurones of the cat by impulses in single group Ia nerve fibres. 2. The average peak amplitude of some of these e.p.s.p.s was increased by a conditioning tetanus. The maximum increase observed was 54% of the control amplitude. 3. The average peak amplitude of some e.p.s.p.s was increased by a single conditioning stimulus which preceded the test stimulus by 1 or 2 msec. The maximum increase observed was 28% of the control amplitude. 4. The ability of e.p.s.p.s to potentiate following a tetanus was correlated with their ability to be facilitated by a single conditioning stimulus. 5. If an e.p.s.p. could be facilitated prior to a tetanus, the amount of facilitation was reduced after the tetanus, with all facilitation being abolished when post-tetanic potentiation was maximal. 6. The fluctuations of an e.p.s.p. were analysed before and after a tetanus. The peak amplitudes that an e.p.s.p. fluctuated between while potentiated did not gradually diminish as the effect of the tetanus disappeared. Post-tetanic potentiation, when it occurred, was accompanied by a decrease in the probability of occurrence of components with smaller peak amplitudes and an increase in the probability of occurrence of components with larger peak amplitudes. 7. These results are consistent with the suggestion that the magnitude of the synaptic potential generated at a single bouton does not vary from trial to trial (Jack, Redman & Wong, 1981a). Nor does the amplitude of this potential vary following a single conditioning stimulus or a tetanus. Post-tetanic potentiation and facilitation result from a decrease in the probability of failure to release transmitter following the conditioning stimuli.

Animals↗
PubMed1981

Modifications to synaptic transmission at group Ia synapses on cat spinal motoneurones by 4-aminopyridine.

1. The average amplitude of e.p.s.p.s evoked in cat spinal motoneurones by impulses in single group Ia afferents usually increased following the intravenous injection of 4-aminopyridine (4-AP). Most of this increase occurred over the first 30 min following injection of 4-AP. 2. The increase in the average amplitude following 4-AP occurred by a reduction in the probability of occurrence of component e.p.s.p.s with smaller peak amplitudes, and an increase in the probability of occurrence of component e.p.s.p.s with larger peak amplitudes. There was no evidence that the discrete amplitudes of components after 4-AP were a result of graded increases of the discrete amplitudes before 4-AP. 3. The interpretation suggested for these results is that each component e.p.s.p. is generated by transmission at a different combination of boutons. At each of these boutons sufficient transmitter is released to saturate all available receptors. The effect of 4-AP is to decrease the probability of failure to release transmitter at each bouton, including some boutons which, before 4-AP, did not release transmitter.

4-Aminopyridine↗
PubMed1976

Statistical fluctuations in charge transfer at Ia synapses on spinal motoneurones.

1. Net inward charge is calculated for unitary Ia e.p.s.p.s. evoked in spinal motoneurones. Fluctuations in this charge are used to describe the fluctuations in transmission at the Ia synapse. 2. The statistical details of variation in transmission at Ia synapses are largely obscured by noise, arising from spontaneous activity and recording apparatus. 3. A computational procedure is described, which utilized the measured statistical properties of the recording noise, and the measured charge histogram of the evoked e.p.s.p. (with noise) to calculate the variations in charge due to the e.p.s.p. alone. 4. The fluctuation in charge transmission at Ia synapses are, in general, non-quantal. Nor are they described by binomial or Poisson statistics. 5. It is suggested that the basic mode of transmission at a single terminal is all-or-none. The fluctuations result from the combined effect of failures at several terminals arising from a single afferent fibre. This hypothesis is supported by further analysis of these results in a subsequent paper (Edwards, Redman & Walmysley, 1976a).

Animals↗
PubMed1976

Non-quantal fluctuations and transmission failures in charge transfer at Ia synapses on spinal motoneurones.

1. The origins of fluctuations in charge transfer during the generation of Ia e.p.s.p.s have been investigated. The discrete components which make up the fluctuating e.p.s.p. have been separated. 2. Some e.p.s.p.s fluctuate between two different amplitudes and time courses. These fluctuations have been analysed to show that charge transmission always occurs at one synaptic location, but not always at a second synaptic location. 3. The failures in transmission were study by stimulating the afferent fibre at different frequencies. Although different probabilities of failure were obtained at different frequencies, there was no systematic change in probability with increasing frequency. 4. Single afferents were tetanized and histograms of charge transfer computed during post-tetanic potentiation (p.t.p.). Only half of the units studied showed any p.t.p. In those that did, evidence was found for a decrease in the probability of failure during potentiation. 5. The results could not be used to distinguish between failure of the impulse to always propagate into the terminals, and failure of the terminals to release transmitter following adequate depolarization. 6. The fluctuations in transmission at a single synapse can be described by a binomial process with n = 1 and p less than or equal to 1. Junctional mechanisms consistent with this description are discussed. Alternative mechanisms which associate failures with failure of impulse transmission at afferent fibre branch points are also suggested.

Action Potentials↗
PubMed1976

The effect of polarizing currents on unitary Ia excitatory post-synaptic potentials evoked in spinal motoneurones.

1. Depolarizing and hyperpolarizing currents were applied to motoneurones in which unitary Ia e.p.s.p.s were evoked. The results concentrate on those e.p.s.p.s which had time courses which were compatible with somatically located synapses. 2. No reversal of these e.p.s.p.s was observed. Depolarizing currents up to 150 nA simply reduced the peak amplitude. 3. Hyperpolarizing currents caused little, if any, increase in the peak amplitude of the e.p.s.p. The time course of decay became briefer as the membrane was hyperpolarized. 4. Changes in decay time course of the e.p.s.p. which accompanied depolarization and hyperpolarization could be attributed to changes in membrane conductances, rather than to changes in synaptic current time course. 5. The failure of the e.p.s.p. to increase with hyperpolarization was shown to be due to the failure of the synaptic current to increase, rather than to the shunting of anomalous rectification. 6. Chemical and electrical transmission are evaluated against these results and those of the preceding papers.

Action Potentials↗
PubMed1973

An analysis of the cable properties of spinal motoneurones using a brief intracellular current pulse.

1. A brief intracellular current pulse, with duration less than 500 musec, has been applied to lumbosacral motoneurones in anaesthetized cats. The resulting voltage transients have been analysed by the procedure suggested in Jack & Redman (1971b) to obtain the cable parameters for each motoneurone.2. Forty-three motoneurone responses were analysed. In all cases the voltage response indicated that the dendrites could be represented as uniform, finite length cables, with either a sealed distal end, or at least a high resistance distal termination. The electrical length of the equivalent uniform dendritic cable ranged from 1.0 to 2.1 space constants, with a mean value of 1.5.3. The initial decay of the membrane potential following the removal of the current pulse was more rapid than was predicted by the Rall model for the motoneurone, in approximately two thirds of the responses. Consequently a value of dendritic to soma conductance ratio could not be obtained for these motoneurones.4. The explanation given for the departure from the theoretical response to a brief current pulse is that the specific resistivity of the soma membrane is lower than the specific resistivity of the dendritic membrane. This explanation is complicated by the possibility of the electrode tip not lodging in the isopotential soma region. The contribution that each of these effects has on the early decay phase of the current pulse response has been assessed.5. It is concluded that the specific resistivity of the soma membrane could be as low as one third of the dendritic membrane resistivity. Tonic inhibitory activity restricted to the soma is suggested as an explanation.

Animals↗
PubMed1973

The attenuation of passively propagating dendritic potentials in a motoneurone cable model.

1. The Rall model of the motoneurone, which consists of a lumped resistance and capacitance, representing the soma, in parallel with a number of distributed resistance-capacitance networks of finite and equal electrical length, representing equivalent dendritic cables, has been used to study the effects of varying electrical and geometrical parameters on the time course and amplitude of transients generated at different locations on the dendritic cables.2. An analytical solution has been obtained for the time course of the voltage transient generated at the point of current injection on the parallel combination of all dendritic cables, in terms of the distance from the soma to the current injection point, the electrotonic length of the equivalent dendritic cable, the dendritic to soma conductance ratio and the membrane time constant. The current applied is a current impulse, and the response to any synaptic current time course may be obtained from the analytical expression for the current impulse response. A smooth current time course of the form Te(-alphaT) has been used in computations.3. An analytical expression has been obtained for the early part of the voltage response at the point of current injection, when the current is applied to a fraction of the total dendritic cable. This response is in terms of all the cable parameters, and the assumed fraction of the dendritic cable which receives the synaptic current. Computations of this response have been carried out assuming a smooth time course of synaptic current.4. The computations of the peak amplitude of the voltage transient obtained from these expressions, together with similar computations for the peak amplitude of the voltage transient after propagation to the soma (Jack & Redman, 1971b), have been used to derive a set of attenuation curves for dendritic propagation. These curves give the ratio of the peak amplitude of the voltage transient at the synaptic location on the dendritic cable, and the peak amplitude after propagation to the soma, in terms of the electrotonic distance to the synaptic location, the time course of current injection, and the cable parameters for the motoneurone model.

Action Potentials↗
PubMed1973

The amplitude, time course and charge of unitary excitatory post-synaptic potentials evoked in spinal motoneurone dendrites.

1. Group Ia e.p.s.p.s were recorded from lumbosacral motoneurones in anaesthetized cats after almost complete section of the appropriate dorsal roots. The cable parameters of these same motoneurones were obtained from the voltage response to a brief intracellular current pulse, as described in Iansek & Redman (1973).2. A total of thirty-three e.p.s.p.s, recorded in thirty different motoneurones, were analysed. E.p.s.p.s which were recorded in motoneurones which were not studied using an intracellular current pulse, or in which the resting membrane potential fell below 50 mV, were not considered. Also, e.p.s.p.s whose time course indicated more than one synaptic site of origin were not analysed. The selected e.p.s.p.s were plotted on a semilogarithmic amplitude scale, and their 10-90% rise time, half-width and peak amplitudes were measured.3. Using the previously determined values of the cable parameters L, rho(infinity) and tau(m), the rise time and half-width of each e.p.s.p. were used to determine the synaptic location (X), and the synaptic current time course (alpha). Twenty-seven e.p.s.p.s had time courses which allowed a value of X and alpha to be determined within the constraints of the measured cable parameters. The remaining six e.p.s.p.s either required an extension of the dendritic cable to be localized, or their time course was not compatible with a brief synaptic current.4. The synaptic locations lie in the range 0 (soma) to 1.25 space constants. When expressed as a fraction of the length of the dendritic cable, all but four of the twenty-seven e.p.s.p.s were located on the proximal half of the dendrites.5. The time to peak of synaptic current for each e.p.s.p. ranged from 30 to 390 musec, although a majority (70%) lay in the range 50 to 200 musec. There was no significant correlation between time to peak of synaptic current and synaptic location.6. The peak amplitude of e.p.s.p.s at the soma showed no significant correlation with synaptic location.7. The peak amplitude, and the cable parameters for each e.p.s.p. were used to compute the time course and amplitude of each e.p.s.p. at its point of generation on various fractions of the total dendritic cable, using the results derived in Redman (1973). These calculations showed the greatly increased rate of decay of e.p.s.p.s at their point of generation. Assuming that the synaptic input was restricted to one tenth of the total dendritic tree, the range of peak amplitudes at the synaptic site was from less than 100 muV (soma) to 20 mV.8. The net inward positive charge crossing the synaptic junction was calculated from the voltage-time integral of the e.p.s.p., as was the net outward positive charge crossing the soma membrane. These calculations showed that dendritic synapses caused up to ten times more net charge to be displaced across the synaptic junction than did synapses on or near to the soma, for similar durations of synaptic current. Similarly, dendritic synapses were generally more effective than somatic synapses in displacing charge across the soma membrane. It was concluded that the average quantal content in the conductance change at dendritic synapses is significantly greater than for somatic synapses.9. Some implications of the results for general integrative mechanisms in dendrites are discussed.

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