Electrical advantages of dendritic spines

Many neurons receive excitatory glutamatergic input almost exclusively onto dendritic spines. In the absence of spines, the amplitudes and kinetics of excitatory postsynaptic potentials (EPSPs) at the site of synaptic input are highly variable and depend on dendritic location. We hypothesized that dendritic spines standardize the local geometry at the site of synaptic input, thereby reducing location-dependent variability of local EPSP properties. We tested this hypothesis using computational models of simplified and morphologically realistic spiny neurons that allow direct comparison of EPSPs generated on spine heads with EPSPs generated on dendritic shafts at the same dendritic locations. In all morphologies tested, spines greatly reduced location-dependent variability of local EPSP amplitude and kinetics, while having minimal impact on EPSPs measured at the soma. Spine-dependent standardization of local EPSP properties persisted across a range of physiologically relevant spine neck resistances, and in models with variable neck resistances. By reducing the variability of local EPSPs, spines standardized synaptic activation of NMDA receptors and voltage-gated calcium channels. Furthermore, spines enhanced activation of NMDA receptors and facilitated the generation of NMDA spikes and axonal action potentials in response to synaptic input. Finally, we show that dynamic regulation of spine neck geometry can preserve local EPSP properties following plasticity-driven changes in synaptic strength, but is inefficient in modifying the amplitude of EPSPs in other cellular compartments. These observations suggest that one function of dendritic spines is to standardize local EPSP properties throughout the dendritic tree, thereby allowing neurons to use similar voltage-sensitive postsynaptic mechanisms at all dendritic locations.     

Generalized Stein's model for anatomically complex neurons

A neuron with a large dendritic structure is considered. The number of synapses located on the dendrites is substantially higher than on the soma. The synaptic input effect on the neuronal excitability decreases with distance between a synapse ending and the trigger zone. Two areas are distinguished in accordance with the effect of synaptic input--dendritic and somatic. The dendritic area, when compared to the soma, is characterized by much higher intensity of its activation but the amplitudes of synaptically evoked changes of the membrane potential at the trigger zone are in general small. This situation is suitable for a diffusion approximation. However, on the soma, especially in the proximity of the trigger zone, the membrane potential changes are a large fraction of the threshold depolarization. The membrane potential at the trigger zone is modelled by a one-dimensional stochastic process. The diffusion Ornstein-Uhlenbeck process serves as a basis of the model; however, at the moments of somatic synapses activation its voltage changes in jumps. Their sizes represent the amplitudes of the evoked postsynaptic potentials. The unimodal histograms of interspike intervals can be explained by the model. The values of the coefficient of variation greater than one are connected with substantial inhibition.     

Synaptic and Extrasynaptic Secretion of Serotonin

Serotonin is a major modulator of behavior in vertebrates and invertebrates and deficiencies in the serotonergic system account for several behavioral disorders in humans.The small numbers of serotonergic central neurons of vertebrates and invertebrates produce their effects by use of two modes of secretion: from synaptic terminals, acting locally in hard wired circuits, and from extrasynaptic axonal and somatodendritic release sites in the absence of postsynaptic targets, producing paracrine effects.In this paper, we review the evidence of synaptic and extrasynaptic release of serotonin and the mechanisms underlying each secretion mode by combining evidence from vertebrates and invertebrates. Particular emphasis is given to somatic secretion of serotonin by central neurons.Most of the mechanisms of serotonin release have been elucidated in cultured synapses made by Retzius neurons from the central nervous system of the leech. Serotonin release from synaptic terminals occurs from clear and dense core vesicles at active zones upon depolarization. In general, synaptic serotonin release is similar to release of acetylcholine in the neuromuscular junction.The soma of Retzius neurons releases serotonin from clusters of dense core vesicles in the absence of active zones. This type of secretion is dependent of the stimulation frequency, on L-type calcium channel activation and on calcium-induced calcium release.The characteristics of somatic secretion of serotonin in Retzius neurons are similar to those of somatic secretion of dopamine and peptides by other neuron types. In general, somatic secretion by neurons is different from transmitter release from clear vesicles at synapses and similar to secretion by excitable endocrine cells.     

Transmission Efficacy and Plasticity in Glutamatergic Synapses Formed by Excitatory Interneurons of the Substantia Gelatinosa in the Rat Spinal Cord

Background

Substantia gelatinosa (SG, lamina II) is a spinal cord region where most unmyelinated primary afferents terminate and the central nociceptive processing begins. The glutamatergic excitatory interneurons (EINs) form the majority of the SG neuron population, but little is known about the mechanisms of signal processing in their synapses.

Methodology

To describe the functional organization and properties of excitatory synapses formed by SG EINs, we did non-invasive recordings from 183 pairs of monosynaptically connected neurons. An intact presynaptic SG EIN was specifically stimulated through the cell-attached pipette while the evoked EPSCs/EPSPs were recorded through perforated-patch from a postsynaptic neuron (laminae I-III).

Principal Findings

We found that the axon of an SG EIN forms multiple functional synapses on the dendrites of a postsynaptic neuron. In many cases, EPSPs evoked by stimulating an SG EIN were sufficient to elicit spikes in a postsynaptic neuron. EPSCs were carried through both Ca²⁺-permeable (CP) and Ca²⁺-impermeable (CI) AMPA receptors (AMPARs) and showed diverse forms of functional plasticity. The synaptic efficacy could be enhanced through both activation of silent synapses and strengthening of already active synapses. We have also found that a high input resistance (R_IN, >0.5 GΩ) of the postsynaptic neuron is necessary for resolving distal dendritic EPSCs/EPSPs and correct estimation of their efficacy.

Conclusions/Significance

We conclude that the multiple synapses formed by an SG EIN on a postsynaptic neuron increase synaptic excitation and provide basis for diverse forms of plasticity. This functional organization can be important for sensory, i.e. nociceptive, processing in the spinal cord.     

Corticofugal influences on postsynaptic processes in rubrospinal neurons in the cat brain

Composite and unitary EPSPs of red nucleus neurons evoked by stimulation of the sensomotor and association parietal cortex and nucleus interpositus of the cerebellum were studied in acute experiments on cats anesthetized with pentobarbital. A monosynaptic connection was shown to exist between not only the sensomotor, but also the association cortex, and rubrospinal neurons, in which unitary EPSPs appeared during stimulation of the association cortex after a latent period of 1.5–2.7 msec, with a peak rise time of 1.1–3.1 msec and an amplitude of 0.22–0.65 mV. Analysis of the temporal characteristics of the unitary EPSP suggested that synapses formed by fibers from the association cortex occupy a position nearer the soma than synapses formed by axons of sensomotor cortical cells.L. A. Orbeli Institute of Physiology, Academy of Sciences of the Armenian SSR, Erevan. Translated from Neirofiziologiya, Vol. 16, No. 1, pp. 67–74, January–February, 1984.     

A mathematical model of the effects of spatio-temporal patterns of dendritic input potentials on neuronal somatic potentials

A mathematical model of a neuron was developed to investigate the effects of various spatio-temporal patterns of miniature dendritic input potentials on neuronal somatic potentials. The model treats spatio-temporal dendritic activation patterns as the input or forcing function in the non-homogeneous cable equation. The theoretical somatic potentials resulting from several different spatio-temporal input patterns were generated on an IBM 360/75 computer. The model allows the investigation of the theoretical effects of activations at several different synaptic sites, of repeated activations at one or more sites, and of changes in various parameters. The time-to-peak and amplitude of individual excitatory postsynaptic potentials, distance of synapses from the soma, and interactivation interval for repeated activations at the same synapse were among the parameters investigated. Not only the order of activations at different synaptic sites was important, but the time intervals between activations were shown to be important. For a given order of activations at different synapses, optimum time intervals between activations were demonstrated, with respect to the resulting peak somatic potentials. Possible consequences of some hypothetical learning and memory mechanisms upon neuronal excitability were discussed. It was also shown that a deterministic model can generate theoretical curves which appear to be almost of a random nature with respect to the observed numbers and amplitudes of peaks of individual EPSPs. The conditions for the appearance of extra peaks were discussed.This paper describes work done as a portion of G.M.B.'s Ph. D. thesis in biomathematics at N.C. State University, and was supported by Public Health Service Grant No. GM-678 from the National Institute of General Medical Sciences.     

Parameters of a model of transmitter depletion in synapses of identified snail neurons

Elementary EPSPs arising in two different identified neurons of the parietal ganglion ofHelix pomatia were recorded after stimulation of the identified triggering neuron. Repetitive stimulation (0.1–1.5 Hz) led to low-frequency depression of EPSPs. By the use of known and modified models of transmitter depletion parameters characterizing storage, mobilization, breakdown, and liberation of transmitter were determined. The fraction of available pool (F) released in two different synapses of the same trigger neuron did not differ significantly. The available pool of transmitter (C) and the demobilization constant ( ) in synapses on the RPa3 neuron were 2–3 times higher, and mobilization (M) was 10 times higher than on the LPa2 neuron. Predictions of the depletion model showed deviations from the experimental data. A method of calculating consistently whatever law of change of F was adopted was devised. Absence of correlation between parameters F and C of the depletion model and binomial parameters p and n, calculated on the basis of the quantal hypothesis of synaptic transmission shows that this hypothesis and the transmitter depletion model describe different synaptic mechanisms.Brain Institute, Academy of Medical Sciences of the USSR, Moscow. Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 13, No. 1, pp. 88–97, January–February, 1981.     

The granule-containing cell somata in the superior cervical ganglion of the rat,as studied by a serial sampling method for electron microscopy

Summary The surface of 4 granule-containing cells, in a cluster within the rat superior cervical ganglion, was studied by a serial sampling technique for electron microscopy. The result shows that all the 4 cells receive one, or three afferent synaptic boutons from the preganglionic fibers impinging upon their somata, and a somatic efferent synapse exists at two locations on each soma of the 2 of these cells. The postsynaptic element of the efferent synapse is observed to be represented by non-vesiculated and vesiculated segments of dendrites, soma and a possible axon collateral of the adrenergic principal neuron of the ganglion. There is a remarkably constant development of the attachment plaque between the granule-containing cells themselves, representing 1.7–2.3% of surface area for each cell. The surface area exposed to the extracellular space (covered only by a basal lamina) varies from 0.1 to 2.3% of the total perikaryal surface of the 4 cells. A tendency is noted that those cells without efferent synapses possess a more extensive area exposed to extracellular space than those forming somatic efferent synapse to the postganglionic elements.It is a pleasure to acknowledge the advice and encouragement of Professor A. Yamauchi throughout this work. I thank Mr. K. Kumagai and Miss K. Tsushida for their technical assistance.     

Biphasic Synaptic Ca Influx Arising from Compartmentalized Electrical Signals in Dendritic Spines

Excitatory synapses on mammalian principal neurons are typically formed onto dendritic spines, which consist of a bulbous head separated from the parent dendrite by a thin neck. Although activation of voltage-gated channels in the spine and stimulus-evoked constriction of the spine neck can influence synaptic signals, the contribution of electrical filtering by the spine neck to basal synaptic transmission is largely unknown. Here we use spine and dendrite calcium (Ca) imaging combined with 2-photon laser photolysis of caged glutamate to assess the impact of electrical filtering imposed by the spine morphology on synaptic Ca transients. We find that in apical spines of CA1 hippocampal neurons, the spine neck creates a barrier to the propagation of current, which causes a voltage drop and results in spatially inhomogeneous activation of voltage-gated Ca channels (VGCCs) on a micron length scale. Furthermore, AMPA and NMDA-type glutamate receptors (AMPARs and NMDARs, respectively) that are colocalized on individual spine heads interact to produce two kinetically and mechanistically distinct phases of synaptically evoked Ca influx. Rapid depolarization of the spine triggers a brief and large Ca current whose amplitude is regulated in a graded manner by the number of open AMPARs and whose duration is terminated by the opening of small conductance Ca-activated potassium (SK) channels. A slower phase of Ca influx is independent of AMPAR opening and is determined by the number of open NMDARs and the post-stimulus potential in the spine. Biphasic synaptic Ca influx only occurs when AMPARs and NMDARs are coactive within an individual spine. These results demonstrate that the morphology of dendritic spines endows associated synapses with specialized modes of signaling and permits the graded and independent control of multiple phases of synaptic Ca influx.     

Branch Input Resistance and Steady Attenuation for Input to One Branch of a Dendritic Neuron Model

Mathematical solutions and numerical illustrations are presented for the steady-state distribution of membrane potential in an extensively branched neuron model, when steady electric current is injected into only one dendritic branch. Explicit expressions are obtained for input resistance at the branch input site and for voltage attenuation from the input site to the soma; expressions for AC steady-state input impedance and attenuation are also presented. The theoretical model assumes passive membrane properties and the equivalent cylinder constraint on branch diameters. Numerical examples illustrate how branch input resistance and steady attenuation depend upon the following: the number of dendritic trees, the orders of dendritic branching, the electrotonic length of the dendritic trees, the location of the dendritic input site, and the input resistance at the soma. The application to cat spinal motoneurons, and to other neuron types, is discussed. The effect of a large dendritic input resistance upon the amount of local membrane depolarization at the synaptic site, and upon the amount of depolarization reaching the soma, is illustrated and discussed; simple proportionality with input resistance does not hold, in general. Also, branch input resistance is shown to exceed the input resistance at the soma by an amount that is always less than the sum of core resistances along the path from the input site to the soma.     

Virtual NEURON: a strategy for merged biochemical and electrophysiological modeling

Because of its highly branched dendrite, the Purkinje neuron requires significant computational resources if coupled electrical and biochemical activity are to be simulated. To address this challenge, we developed a scheme for reducing the geometric complexity; while preserving the essential features of activity in both the soma and a remote dendritic spine. We merged our previously published biochemical model of calcium dynamics and lipid signaling in the Purkinje neuron, developed in the Virtual Cell modeling and simulation environment, with an electrophysiological model based on a Purkinje neuron model available in NEURON. A novel reduction method was applied to the Purkinje neuron geometry to obtain a model with fewer compartments that is tractable in Virtual Cell. Most of the dendritic tree was subject to reduction, but we retained the neuron’s explicit electrical and geometric features along a specified path from spine to soma. Further, unlike previous simplification methods, the dendrites that branch off along the preserved explicit path are retained as reduced branches. We conserved axial resistivity and adjusted passive properties and active channel conductances for the reduction in surface area, and cytosolic calcium for the reduction in volume. Rallpacks are used to validate the reduction algorithm and show that it can be generalized to other complex neuronal geometries. For the Purkinje cell, we found that current injections at the soma were able to produce similar trains of action potentials and membrane potential propagation in the full and reduced models in NEURON; the reduced model produces identical spiking patterns in NEURON and Virtual Cell. Importantly, our reduced model can simulate communication between the soma and a distal spine; an alpha function applied at the spine to represent synaptic stimulation gave similar results in the full and reduced models for potential changes associated with both the spine and the soma. Finally, we combined phosphoinositol signaling and electrophysiology in the reduced model in Virtual Cell. Thus, a strategy has been developed to combine electrophysiology and biochemistry as a step toward merging neuronal and systems biology modeling.     

Relation between the excitatory synaptic currents and clamped somatic potential in the model of neuron with nonlinear dendrites

The influence of the clamped somatic potential on the excitatory synaptic current (EPSC) was studied in the model of the dendrite with N-shaped instantaneous stationary current--voltage curve. Proximal EPSC diminish and become narrower with decreasing hyperpolarization or modest depolarization, distal EPSC increase and become wider, intermediately distant EPSC change insignificantly. Under increasing depolarization all the EPSC become significantly wider and larger. EPSC facilitate stable depolarization of the dendrites. When the dendrite is stable depolarized EPSC becomes very small and narrow, but it becomes larger and wider as the soma is hyperpolarized. EPSC becomes especially large and wide when the soma is hyperpolarized just to terminate the stable depolarization of the dendrite branch where the active synapses are located. The model explains certain phenomena which are difficult to understand by the theory of ohmic dendrites. New phenomena are predicted.     

Method of evaluating the synaptic input to a single mesencephalic neuron]

The mathematical model of the spike activity of a neuron with synaptic input from many other neurons [1], describes adequately the firing of 5 from 7 neurons in the tegmentum of mesencephalic cat and changes of their activity evoked by glutamate iontophoresis. For these 5 neurons the estimates of the PSPs' average frequency of the threshold depolarization and of the constant decay of the EPSP were received. For different neurons the values of these parameters are 4--100 KHz, 100--800 average unitary EPSPs and 4--30 msec correspondingly. The stationary value of the average membrane potential (SVAMP) in all 5 neurons was removed significantly from the resting potential toward the threshold potential. SWAMP could be changed by the glutamate iontophoresis in such a degree to overlap the threshold potential.     

Axons Amplify Somatic Incomplete Spikes into Uniform Amplitudes in Mouse Cortical Pyramidal Neurons

Background

Action potentials are the essential unit of neuronal encoding. Somatic sequential spikes in the central nervous system appear various in amplitudes. To be effective neuronal codes, these spikes should be propagated to axonal terminals where they activate the synapses and drive postsynaptic neurons. It remains unclear whether these effective neuronal codes are based on spike timing orders and/or amplitudes.

Methodology/Principal Findings

We investigated this fundamental issue by simultaneously recording the axon versus soma of identical neurons and presynaptic vs. postsynaptic neurons in the cortical slices. The axons enable somatic spikes in low amplitude be enlarged, which activate synaptic transmission in consistent patterns. This facilitation in the propagation of sequential spikes through the axons is mechanistically founded by the short refractory periods, large currents and high opening probability of axonal voltage-gated sodium channels.

Conclusion/Significance

An amplification of somatic incomplete spikes into axonal complete ones makes sequential spikes to activate consistent synaptic transmission. Therefore, neuronal encoding is likely based on spike timing order, instead of graded analogues.     

A computer model of unitary responses from associational/commissural and perforant path synapses in hippocampal CA3 pyramidal cells

Despite the central position of CA3 pyramidal cells in the hippocampal circuit, the experimental investigation of their synaptic properties has been limited. Recent slice experiments from adult rats characterized AMPA and NMDA receptor unitary synaptic responses in CA3b pyramidal cells. Here, excitatory synaptic activation is modeled to infer biophysical parameters, aid analysis interpretation, explore mechanisms, and formulate predictions by contrasting simulated somatic recordings with experimental data. Reconstructed CA3b pyramidal cells from the public repository NeuroMorpho.Org were used to allow for cell-specific morphological variation. For each cell, synaptic responses were simulated for perforant pathway and associational/commissural synapses. Means and variability for peak amplitude, time-to-peak, and half-height width in these responses were compared with equivalent statistics from experimental recordings. Synaptic responses mediated by AMPA receptors are best fit with properties typical of previously characterized glutamatergic receptors where perforant path synapses have conductances twice that of associational/commissural synapses (0.9 vs. 0.5 nS) and more rapid peak times (1.0 vs. 3.3 ms). Reanalysis of passive-cell experimental traces using the model shows no evidence of a CA1-like increase of associational/commissural AMPA receptor conductance with increasing distance from the soma. Synaptic responses mediated by NMDA receptors are best fit with rapid kinetics, suggestive of NR2A subunits as expected in mature animals. Predictions were made for passive-cell current clamp recordings, combined AMPA and NMDA receptor responses, and local dendritic depolarization in response to unitary stimulations. Models of synaptic responses in active cells suggest altered axial resistivity and the presence of synaptically activated potassium channels in spines.     

Solutions for transients in arbitrarily branching cables: I. Voltage recording with a somatic shunt.

An analytical solution is derived for voltage transients in an arbitrarily branching passive cable neurone model with a soma and somatic shunt. The response to injected currents can be represented as an infinite series of exponentially decaying components with different time constants and amplitudes. The time constants of a given model, obtained from the roots of a recursive transcendental equation, are independent of the stimulating and recording positions. Each amplitude is the product of three factors dependent on the corresponding root: one constant over the cell, one varying with the input site, and one with the recording site. The amplitudes are not altered by interchanging these sites. The solution reveals explicitly some of the parameter dependencies of the responses. An efficient recursive root-finding algorithm is described. Certain regular geometries lead to "lost" roots; difficulties associated with these can be avoided by making small changes to the lengths of affected segments. Complicated cells, such as a CA1 pyramid, produce many closely spaced time constants in the range of interest. Models with large somatic shunts and dendrites of unequal electrotonic lengths can produce large amplitude waveform components with surprisingly slow time constants. This analytic solution should complement existing passive neurone modeling techniques.     

Spatial Localization of Synapses Required for Supralinear Summation of Action Potentials and EPSPs

Although the supralinear summation of synchronizing excitatory postsynaptic potentials (EPSPs) and backpropagating action potentials (APs) is important for spike-timing-dependent synaptic plasticity (STDP), the spatial conditions of the amplification in the divergent dendritic structure have yet to be analyzed. In the present study, we simulated the coincidence of APs with EPSPs at randomly determined synaptic sites of a morphologically reconstructed hippocampal CA1 pyramidal model neuron and clarified the spatial condition of the amplifying synapses. In the case of uniform conductance inputs, the amplifying synapses were localized in the middle apical dendrites and distal basal dendrites with small diameters, and the ratio of synapses was unexpectedly small: 8-16% in both apical and basal dendrites. This was because the appearance of strong amplification requires the coincidence of both APs of 3-30 mV and EPSPs of over 6 mV, both of which depend on the dendritic location of synaptic sites. We found that the localization of amplifying synapses depends on A-type K+ channel distribution because backpropagating APs depend on the A-type K+ channel distribution, and that the localizations of amplifying synapses were similar within a range of physiological synaptic conductances. We also quantified the spread of membrane amplification in dendrites, indicating that the neighboring synapses can also show the amplification. These findings allowed us to computationally illustrate the spatial localization of synapses for supralinear summation of APs and EPSPs within thin dendritic branches where patch clamp experiments cannot be easily conducted.     

Asymmetry of motor impulses and neuromuscular synapses produced in crayfish claws by unilateral immobilization

Summary The fast axon supplying the closer muscle in crayfish (Procambarus clarkii) normally fires few impulses and generates large excitatory postsynaptic potentials (EPSPs) that fatigue rapidly with repeated stimulation. When the dactyl of one claw is immobilized in the closed position, impulse production in the fast axon decreases on the immobilized side and increases on the contralateral side. On the immobilized side, EPSPs become larger but more readily depressed with repeated stimulation, while converse changes occur on the contralateral side.In order to establish whether the smaller number of impulses on the immobilized side was responsible for the changes in EPSPs, extra impulses were generated in the fast axon of immobilized claws by implanting electrodes in the claw. Raising the impulse production to equal or exceed that of the contralateral side did not prevent the changes in EPSPs produced by immobilization. Thus, it is probable that changes in the level of synaptic input to central parts of the fast closer excitor neuron are mainly responsible for altered physiological properties of peripheral synapses, rather than the fast axon's impulse traffic per se.     

Transient Response in a Dendritic Neuron Model for Current Injected at One Branch

Mathematical expressions are obtained for the response function corresponding to an instantaneous pulse of current injected to a single dendritic branch in a branched dendritic neuron model. The theoretical model assumes passive membrane properties and the equivalent cylinder constraint on branch diameters. The response function when used in a convolution formula enables one to compute the voltage transient at any specified point in the dendritic tree for an arbitrary current injection at a given input location. A particular numerical example, for a brief current injection at a branch terminal, illustrates the attenuation and delay characteristics of the depolarization peak as it spreads throughout the neuron model. In contrast to the severe attenuation of voltage transients from branch input sites to the soma, the fraction of total input charge actually delivered to the soma and other trees is calculated to be about one-half. This fraction is independent of the input time course. Other numerical examples, which compare a branch terminal input site with a soma input site, demonstrate that, for a given transient current injection, the peak depolarization is not proportional to the input resistance at the injection site and, for a given synaptic conductance transient, the effective synaptic driving potential can be significantly reduced, resulting in less synaptic current flow and charge, for a branch input site. Also, for the synaptic case, the two inputs are compared on the basis of the excitatory post-synaptic potential (EPSP) seen at the soma and the total charge delivered to the soma.     

Ultrastructure of synapses and cellular relationships in the oculomotor nucleus of the rhesus monkey

Summary The fine structure of synapses and of cellular relations was examined in the somatic efferent portion of the oculomotor nucleus of the adult rhesus monkey. Axosomatic and axodendritic synapses are characterized by distinct synaptic clefts which usually measure 20–30 nm between pre- and postsynaptic membranes. Cytoplasmic thickenings of pre- and postsynaptic membranes are often observed. Subjunctional bodies are present at both axosomatic and axodendritic synapses. Somatic and dendritic spine synapses are present. Serial synapses are also found, suggesting the operation of presynaptic inhibition in this nucleus. At some synapses the extracellular gap between pre- and postsynaptic membranes is reduced to 5–9 nm. However, junctions similar to the latter are also present between neurons and glia, and at the junctions between adjacent glial elements. The present results provide no evidence for a clear morphological substrate for electrotonic transmission in the somatic efferent portion of the primate oculomotor nucleus.Supported in part by grants from the National Institutes of Health (NS-15320), the Kroc Foundation, and by the Medical Research Service of the Veterans Administration (to S.G.W.), and from the National Science Foundation (BNS 77-28493) and the Muscular Dystrophy Association of America (to G.D.P.)