Synaptic Interactions in a Passive Dendritic Tree

1998 ◽  
Author(s):  
Christof Koch
Keyword(s):  
Nervous System ◽  
Dendritic Tree ◽  
Extreme Case ◽  
Pyramidal Cells ◽  
Inhibitory Synapses ◽  
Dendritic Trees ◽  
Central Processing ◽  
Voltage Dependent ◽  
Dendritic Spikes ◽  
Spatial Positioning

Nerve cells are the targets of many thousands of excitatory and inhibitory synapses. An extreme case are the Purkinje cells in the primate cerebellum, which receive between one and two hundred thousand synapses onto dendritic spines from an equal number of parallel fibers (Braitenberg and Atwood, 1958; Llinas and Walton, 1998). In fact, this structure has a crystalline-like quality to it, with each parallel fiber making exactly one synapse onto a spine of a Purkinje cell. For neocortical pyramidal cells, the total number of afferent synapses is about an order of magnitude lower (Larkman, 1991). These numbers need to be compared against the connectivity in the central processing unit (CPU) of modern computers, where the gate of a typical transistor usually receives input from one, two, or three other transistors or connects to one, two, or three other transistor gates. The large number of synapses converging onto a single cell provide the nervous system with a rich substratum for implementing a very large class of linear and nonlinear neuronal operations. As we discussed in the introductory chapter, it is only these latter ones, such as multiplication or a threshold operation, which are responsible for “computing” in the nontrivial sense of information processing. It therefore becomes crucial to study the nature of the interaction among two or more synaptic inputs located in the dendritic tree. Here, we restrict ourselves to passive dendritic trees, that is, to dendrites that do not contain voltage-dependent membrane conductances. While such an assumption seemed reasonable 20 or even 10 years ago, we now know that the dendritic trees of many, if not most, cells contain significant nonlinearities, including the ability to generate fast or slow all-or-none electrical events, so-called dendritic spikes. Indeed, truly passive dendrites may be the exception rather than the rule in the nervous In Sec. 1.5, we studied this interaction for the membrane patch model. With the addition of the dendritic tree, the nervous system has many more degrees of freedom to make use of, and the strength of the interaction depends on the relative spatial positioning, as we will see now. That this can be put to good use by the nervous system is shown by the following experimental observation and simple model.

Passive Dendritic Trees

1998 ◽  
Author(s):  
Christof Koch
Keyword(s):  
Nervous System ◽  
Morphological Structure ◽  
Pyramidal Cells ◽  
Quantitative Relationship ◽  
Cell Types ◽  
Dendritic Morphology ◽  
Granule Cell Layer ◽  
Dendritic Trees ◽  
A Cell ◽  
The Brain

The previous chapter dealt with the solution of the cable equation in response to current pulses and steps within a single unbranched cable. However, real nerve cells possess highly branched and extended dendritic trees with quite distinct morphologies. Figure 3.1 illustrates the fantastic variety of dendritic trees found throughout the animal kingdom, ranging from neurons in the locust to human brain cells and cells from many different parts of the nervous system. Some of these cells are spatially compact, such as retinal amacrine cells, which are barely one-fifth of a millimeter across, while some cells have immense dendritic trees, such as α motoneurones in the spinal cord extending across several millimeters. Yet, in all cases, neurons are very tightly packed: in vertebrates, peak density appears to be reached in the granule cell layer of the human cerebellum with around 5 million cells per cubic millimeter (Braitenberg and Atwood, 1958) while the packing density of the cells filling the 0.25 mm3 nervous system of the housefly Musca domestica is around 1.2 million cells per cubic millimeter (Strausfeld, 1976). The dendritic arbor of some cell types encompasses a spherical volume, such as for thalamic relay cells, while other cells, such as the cerebellar Purkinje cell, fill a thin slablike volume with a width less than one-tenth of their extent. Different cell types do not appear at random in the brain but are unique to specific parts of the brain. By far the majority of excitatory cells in the cortex are the pyramidal cells. Yet even within this class, considerable diversity exists. But why this diversity of shapes? To what extent do these quite distinct dendritic architectures reflect differences in their roles in information processing and computation? What influence does the dendritic morphology have on the electrical properties of the cell, or, in other words, what is the relationship between the morphological structure of a cell and its electrical function? One of the few cases where a quantitative relationship between form and some aspect of neuronal function has been established is the retinal neurons.

Amplification and linearization of distal synaptic input to cortical pyramidal cells

1994 ◽  
Vol 72 (6) ◽  
pp. 2743-2753 ◽  
Author(s):  
O. Bernander ◽  
C. Koch ◽  
R. J. Douglas
Keyword(s):  
Pyramidal Cell ◽  
Synaptic Input ◽  
Striate Cortex ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Synaptic Efficacy ◽  
Induced Voltage ◽  
Apical Tuft ◽  
Voltage Dependent ◽  
The Relationship

1. Computer simulations were used to study the effect of voltage-dependent calcium and potassium conductances in the apical dendritic tree of a pyramidal cell on the synaptic efficacy of apical synaptic input. The apical tuft in layers 1 and 2 is the target of feedback projections from other cortical areas. 2. The current, Isoma, flowing into the soma in response to synaptic input was used to assess synaptic efficacy. This measure takes full account of all the relevant nonlinearities in the dendrities and can be used during spiking activity. Isoma emphasizes current flowing in response to synaptic input rather than synaptically induced voltage change. This measure also permits explicit characterization of the input-output relationship of the entire neuron by computing the relationship between presynaptic input and postsynaptic output frequency. 3. Simulations were based on two models. The first was a biophysically detailed 400-compartment model of a morphologically characterized layer 5 pyramidal cell from striate cortex of an adult cat. In this model eight voltage-dependent conductances were incorporated into the somatic membrane to provide the observed firing behavior of a regular spiking cell. The second model was a highly simplified three-compartment equivalent electrical circuit. 4. If the dendritic tree is entirely passive, excitatory synaptic input of the non-N-methyl-D-aspartate (non-NMDA) type to layers 1, 2, and 3 saturate at very moderate input rates, because of the high input impedance of the apical tuft. Layers 1 and 2 together can deliver only 0.25 nA current to the soma. This modest effect is surprising in view of the important afferents that synapse on the apical tuft and is inconsistent with experimental data indicating a more powerful effect. 5. We introduced in a controlled manner a voltage-dependent potassium conductance in the apical tuft, gK, to prevent saturation of the synaptic response. This conductance was designed to linearize the relationship between presynaptic input frequency and the somatic current. We also introduced a voltage-dependent calcium conductance along the apical trunk, gCa, to amplify the apical signal, i.e., the synaptic current reaching the soma. 6. To arrive at a specific relationship between the presynaptic input rate and the somatic current delivered by the synaptic input, we derived the activation curves of gK and gCa either analytically or numerically. The resultant voltage-dependent behavior of both conductances was similar to experimentally measured activation curves.(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Dendritic branch structure compartmentalizes voltage-dependent calcium influx in cortical layer 2/3 pyramidal cells

2022 ◽  
Author(s):  
Andrew Tyler Landau ◽  
Pojeong Park ◽  
David Wong-Campos ◽  
Tian He ◽  
Adam Ezra Cohen ◽  
...  
Keyword(s):  
Calcium Influx ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Cortical Layer ◽  
Calcium Signals ◽  
Local Reduction ◽  
Layer 2 ◽  
Voltage Dependent ◽  
Dendritic Branches ◽  
Kinetics Of

Back-propagating action potentials (bAPs) regulate synaptic plasticity by evoking voltage-dependent calcium influx throughout dendrites. Attenuation of bAP amplitude in distal dendritic compartments alters plasticity in a location-specific manner by reducing bAP-dependent calcium influx. However, it is not known if neurons exhibit branch-specific variability in bAP-dependent calcium signals, independent of distance-dependent attenuation. Here, we reveal that bAPs fail to evoke calcium influx through voltage-gated calcium channels (VGCCs) in a specific population of dendritic branches in cortical layer 2/3 pyramidal cells, despite evoking substantial VGCC-mediated calcium influx in sister branches. These branches contain VGCCs and successfully propagate bAPs in the absence of synaptic input; nevertheless, they fail to exhibit bAP-evoked calcium influx due to a branch-specific reduction in bAP amplitude. We demonstrate that these branches have more elaborate branch structure compared to sister branches, which causes a local reduction in electrotonic impedance and bAP amplitude. Finally, we show that bAPs still amplify synaptically-mediated calcium influx in these branches because of differences in the voltage-dependence and kinetics of VGCCs and NMDA-type glutamate receptors. Branch-specific compartmentalization of bAP-dependent calcium signals may provide a mechanism for neurons to diversify synaptic tuning across the dendritic tree.

Distribution of neurons expressing α1G subunit mRNA of T-type voltage-dependent calcium channel in adult rat central nervous system

1999 ◽  
Vol 268 (2) ◽  
pp. 77-80 ◽  
Author(s):  
Masahiko Kase ◽  
Shingo Kakimoto ◽  
Satoru Sakuma ◽  
Takeshi Houtani ◽  
Hitoshi Ohishi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Calcium Channel ◽  
Adult Rat ◽  
Subunit Mrna ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent

Electrical Properties and Anion Permeability of Doubly Rectifying Junctions in the Leech Central Nervous System

1988 ◽  
Vol 137 (1) ◽  
pp. 1-11
Author(s):  
Susan E. Acklin
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
T Cell ◽  
Action Potentials ◽  
Sodium Pump ◽  
Current Flow ◽  
Cell Movement ◽  
Voltage Dependent ◽  
Electrical Connections

A study has been made of the electrical connections between touch sensory (T) neurones in the leech central nervous system (CNS) which display remarkable double rectification: depolarization spreads in both directions although hyperpolarization spreads poorly. Tests were made to determine whether this double rectification was a property of the junctions themselves or whether it resulted from changes in the length constants of processes intervening between the cell body and the junctions. Following trains of action potentials, T cells and their fine processes within the neuropile became hyperpolarized through the activity of an electrogenie sodium pump. When any T cell was hyperpolarized by 25 mV by repetitive stimulation, hyperpolarization failed to spread to the T cells to which it was electrically coupled. Further evidence for double rectification of junctions linking T cells was provided by experiments in which Cl− was injected electrophoretically. Cl− injection into one T cell caused inhibitory potentials recorded in it to become reversed. After a delay, Cl− spread to reverse IPSPs in the coupled T cell. Movement of Cl−, like current flow, was dependent on membrane potential. When the T cell into which Cl− was injected was kept hyperpolarized, Cl− failed to move into the adjacent T cell. Upon release of the hyperpolarization in the injected T cell, Cl− moved and reversed IPSPs in the coupled T cell. Together these results indicate that the gating properties of channels linking T cells are voltage-dependent, such that depolarization of either cell allows channels to open whereas hyperpolarization causes them to close.

The Golgi Material of the Neurones of the Central Nervous System of Sheep Infected with Louping-Ill

1947 ◽  
Vol s3-88 (1) ◽  
pp. 55-63
Author(s):  
R. A. R. GRESSON ◽  
I. ZLOTNIK
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Purkinje Cells ◽  
Medulla Oblongata ◽  
Motor Nerve ◽  
Pyramidal Cells ◽  
Cell Processes ◽  
The Central Nervous System ◽  
Louping Ill

1. The Golgi material of the pyramidal cells of the cerebral cortex, the Purkinje cells of the cerebellum, and the multipolar cells of the medulla oblongata and ventral horns of the spinal cord of the sheep is present as filaments and as irregularly shaped bodies. In some of the cells, particularly in the lamb (Sheep V), the Golgi material has the appearance of a network. As it is frequently present as separate bodies it is suggested that it may always consist of discrete Golgi elements which are sometimes situated in close proximity or in contact with one another. Filamentous Golgi elements are present in the basal part of the cell processes. 2. An examination of neurones from the corresponding regions of the central nervous system of sheep infected experimentally with louping-ill showed that the Golgi material undergoes changes consequent upon the invasion of the cells by the virus. The Golgi material undergoes hypertrophy, and at the same time there is a reduction in the number of filamentous Golgi elements and a reduction in the amount of Golgi substance present in the cell processes. These changes are followed by fragmentation. All the neurones of a particular region are not affected equally at the same time. The Golgi material of the Purkinje cells tends to form groups in the cytoplasm prior to fragmentation. In the multipolar cells of the medulla oblongata the hypertrophy of the Golgi material is not as great as in the other regions of the central nervous system. The Golgi material of the motor nerve-cells of the ventral horns of the spinal cord undergoes considerable hypertrophy which is followed by a grouping of the Golgi elements and fragmentation.

Hippocampal pyramidal cells: significance of dendritic ionic conductances for neuronal function and epileptogenesis

1979 ◽  
Vol 42 (2) ◽  
pp. 476-496 ◽  
Author(s):  
R. D. Traub ◽  
R. Llinas
Keyword(s):  
Hot Spots ◽  
Potassium Conductance ◽  
Pyramidal Cells ◽  
Calcium Currents ◽  
Membrane Properties ◽  
Repetitive Firing ◽  
Published Data ◽  
Neuronal Responses ◽  
Voltage Dependent ◽  
Hippocampal Pyramidal Cells

1. Starting with published data derived mainly from hippocampal slice preparations, we have used computer-modeling techniques to study hippocampal pyramidal cells (HPCs). 2. The dendrites of the HPC apparently have a short electrotonic length. Calcium spikes are apparently generated by a voltage-dependent mechanism whose kinetics are slow in comparison with those generating sodium spikes of the soma. Inward calcium currents are assumed to trigger a long-lasting potassium conductance. This slow calcium-potassium system, which in our model is located predominantly on the dendrites, provides a heuristic model to describe the mechanism for a) the after-depolarization following an HPC soma (sodium) spike, b) the long afterhyperpolarization following repetitive firing, c) bursts of spikes that sometimes occur after orthodromic or antidromic stimulation, and d) the buildup of the "depolarizing shift" during the strong synaptic input presumed to occur during seizures. 3. Fast prepotentials or d-spikes are shown to arise most probably from dendritic "hot spots" of sodium-regenerative membrane. The limited amplitude and short duration of these prepotentials imply that the hot spots are located on small dendrites. 4. Dendritic electroresponsiveness, first postulated for the HPC by Spencer and Kandel (52), is analyzed quantitatively here and is shown to provide rich integrative possibilities for this cell. Our model suggests that, for these nerve cells, alterations in specific membrane properties, particularly calcium electroresponsiveness, can lead to bursting behavior that resembles epileptogenic neuronal responses.

scholarly journals Factors affecting the appearance of the hump charge movement component in frog cut twitch fibers.

1991 ◽  
Vol 98 (2) ◽  
pp. 315-347 ◽  
Author(s):  
C S Hui
Keyword(s):  
Time Course ◽  
Extreme Case ◽  
Complete Recovery ◽  
Creatine Phosphate ◽  
Boltzmann Distribution ◽  
Distribution Functions ◽  
Charge Movement ◽  
Factors Affecting ◽  
Gap Technique ◽  
Voltage Dependent

Charge movement was measured in frog cut twitch fibers with the double Vaseline gap technique. Five manipulations listed below were applied to investigate their effects on the hump component (I gamma) in the ON segments of TEST minus CONTROL current traces. When external Cl-1 was replaced by MeSO3- to eliminate Cl current, I gamma peaked earlier due to a few millivolts shift of the voltage dependence of I gamma kinetics in the negative direction. The Q-V plots in the TEA.Cl and TEA.MeSO3 solutions were well fitted by a sum of two Boltzmann distribution functions. The more steeply voltage-dependent component (Q gamma) had a V approximately 6 mV more negative in the TEA.MeSO3 solution than in the TEA.Cl solution. These voltage shifts were partially reversible. When creatine phosphate in the end pool solution was removed, the I gamma hump disappeared slowly over the course of 20-30 min, partly due to a suppression of Q gamma. The hump reappeared when creatine phosphate was restored. When 0.2-1.0 mM Cd2+ was added to the center pool solution to block inward Ca current, the I gamma hump became less prominent due to a prolongation in the time course of I gamma but not to a suppression of Q gamma. When the holding potential was changed from -90 to -120 mV, the amplitude of I beta was increased, thereby obscuring the I gamma hump. Finally, when a cut fiber was stimulated repetitively, I gamma lost its hump appearance because its time course was prolonged. In an extreme case, a 5-min resting interval was insufficient for a complete recovery of the waveform. In general, a stimulation rate of once per minute had a negligible effect on the shape of I gamma. Of the five manipulations, MeSO3- has the least perturbation on the appearance of I gamma and is potentially a better substitute for Cl- than SO2-(4) in eliminating Cl current if the appearance of the I gamma hump is to be preserved.

Electrophysiological evidence from glutamate microapplications for local excitatory circuits in the CA1 area of rat hippocampal slices

1988 ◽  
Vol 59 (1) ◽  
pp. 110-123 ◽  
Author(s):  
E. P. Christian ◽  
F. E. Dudek
Keyword(s):  
Hippocampal Neurons ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Inhibitory Synapses ◽  
Excitatory Synapses ◽  
Recording Site ◽  
Postsynaptic Potentials ◽  
Inhibitory Postsynaptic Potentials ◽  
Ca1 Area ◽  
Transverse Slice

1. Evidence for local excitatory synaptic connections in CA1 of the rat hippocampus was obtained by recording excitatory postsynaptic potentials (EPSPs) intracellularly from pyramidal cells during local microapplications of glutamate. 2. Experiments were performed in hippocampal slices cut parallel to (transverse slice) or perpendicular to (longitudinal slice) alvear fibers. In normal solutions, glutamate microdrops (10–20 mM, 10–20 micron diam) applied in CA1 within 400 micron of recorded cells sometimes increased the frequency of inhibitory postsynaptic potentials for 5–10 s in both transverse and longitudinal slices. Increases in EPSP frequency were also occasionally observed, but only in transverse slices. Tetrodotoxin (1 microgram/ml) blocked glutamate-induced increases in PSP frequency, thus indicating that they were not caused by subthreshold effects on presynaptic terminals. Increases in PSP frequency were interpreted to result from glutamate activation of hippocampal neurons with inhibitory and excitatory connections to recorded neurons. 3. In both slice orientations, local excitatory circuits were studied in more isolated conditions by surgically separating CA1 from CA3 (transverse slices) and by blocking GABAergic inhibitory synapses with picrotoxin (5–10 microM). Microdrops were systematically applied at 200 and 400 micron on each side of the recording site. Significant glutamate-induced increases in EPSP frequency were observed in neurons from both slice orientations to microdrops in at least one of the locations. This provided evidence that excitatory synapses are present in both transverse and longitudinal slices. 4. Substantial increases in EPSP frequency only occurred in neurons from longitudinal slices when glutamate was microapplied 200 micron or less from the recording site. In transverse slices, however, large increases in EPSP frequency were observed to glutamate microapplications at 200 or 400 micron. These data suggest that CA1 local excitatory connections project for longer distances in the transverse than in the longitudinal plane of section. 5. Increases in EPSP frequency, averaged across cells, did not differ significantly in the four microapplication sites in either transverse or longitudinal slices. Thus local excitation in CA1 does not appear to be asymmetrically arranged in the way suggested for CA3. 6. The densities of local excitatory circuits in CA1 versus CA3 were studied by quantitatively comparing glutamate-induced increases in EPSP frequency.(ABSTRACT TRUNCATED AT 400 WORDS)

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