Synaptic integration in an excitable dendritic tree

1993 ◽  
Vol 70 (3) ◽  
pp. 1086-1101 ◽  
Author(s):  
B. W. Mel
Keyword(s):  
Pyramidal Cell ◽  
Neuronal Response ◽  
Dendritic Tree ◽  
Pattern Discrimination ◽  
Synaptic Activity ◽  
Visual Neurons ◽  
Voltage Dependent ◽  
Sum Of Products ◽  
Very High ◽  
Synaptic Drive

1. Compartmental modeling experiments were carried out in an anatomically characterized neocortical pyramidal cell to study the integrative behavior of a complex dendritic tree containing active membrane mechanisms. Building on a previously presented hypothesis, this work provides further support for a novel principle of dendritic information processing that could underlie a capacity for nonlinear pattern discrimination and/or sensory processing within the dendritic trees of individual nerve cells. 2. It was previously demonstrated that when excitatory synaptic input to a pyramidal cell is dominated by voltage-dependent N-methyl-D-aspartate (NMDA)-type channels, the cell responds more strongly when synaptic drive is concentrated within several dendritic regions than when it is delivered diffusely across the dendritic arbor. This effect, called dendritic "cluster sensitivity," persisted under wide-ranging parameter variations and directly implicated the spatial ordering of afferent synaptic connections onto the dendritic tree as an important determinant of neuronal response selectivity. 3. In this work, the sensitivity of neocortical dendrites to spatially clustered synaptic drive has been further studied with fast sodium and slow calcium spiking mechanisms present in the dendritic membrane. Several spatial distributions of the dendritic spiking mechanisms were tested with and without NMDA synapses. Results of numerous simulations reveal that dendritic cluster sensitivity is a highly robust phenomenon in dendrites containing a sufficiency of excitatory membrane mechanisms and is only weakly dependent on their detailed spatial distribution, peak conductances, or kinetics. Factors that either work against or make irrelevant the dendritic cluster sensitivity effect include 1) very high-resistance spine necks, 2) very large synaptic conductances, 3) very high baseline levels of synaptic activity, and 4) large fluctuations in level of synaptic activity on short time scales. 4. The functional significance of dendritic cluster sensitivity has been previously discussed in the context of associative learning and memory. Here it is demonstrated that the dendritic tree of a cluster-sensitive neuron implements an approximative spatial correlation, or sum of products operation, such as that which could underlie nonlinear disparity tuning in binocular visual neurons.

scholarly journals NMDA-Based Pattern Discrimination in a Modeled Cortical Neuron

1992 ◽  
Vol 4 (4) ◽  
pp. 502-517 ◽  
Author(s):  
Bartlett W. Mel
Keyword(s):  
Pyramidal Cell ◽  
Dendritic Tree ◽  
Pattern Discrimination ◽  
Information Storage ◽  
Processing Power ◽  
Excitatory Synaptic Input ◽  
Voltage Dependent ◽  
Nmda Channels ◽  
Pattern Information

Compartmental simulations of an anatomically characterized cortical pyramidal cell were carried out to study the integrative behavior of a complex dendritic tree. Previous theoretical (Feldman and Ballard 1982; Durbin and Rumelhart 1989; Mel 1990; Mel and Koch 1990; Poggio and Girosi 1990) and compartmental modeling (Koch et al. 1983; Shepherd et al. 1985; Koch and Poggio 1987; Rall and Segev 1987; Shepherd and Brayton 1987; Shepherd et al. 1989; Brown et al. 1991) work had suggested that multiplicative interactions among groups of neighboring synapses could greatly enhance the processing power of a neuron relative to a unit with only a single global firing threshold. This issue was investigated here, with a particular focus on the role of voltage-dependent N-methyl-D-asparate (NMDA) channels in the generation of cell responses. First, it was found that when a large proportion of the excitatory synaptic input to dendritic spines is carried by NMDA channels, the pyramidal cell responds preferentially to spatially clustered, rather than random, distributions of activated synapses. Second, based on this mechanism, the NMDA-rich neuron is shown to be capable of solving a nonlinear pattern discrimination task. We propose that manipulation of the spatial ordering of afferent synaptic connections onto the dendritic arbor is a possible biological strategy for pattern information storage during learning.

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)

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.

Nonequivalent cylinder models of neurons: interpretation of voltage transients generated by somatic current injection

1988 ◽  
Vol 60 (1) ◽  
pp. 125-148 ◽  
Author(s):  
P. K. Rose ◽  
A. Dagum
Keyword(s):  
Regional Differences ◽  
Dendritic Tree ◽  
Membrane Properties ◽  
Reliable Estimate ◽  
Voltage Response ◽  
Spinal Motoneurons ◽  
Membrane Resistivity ◽  
Voltage Dependent ◽  
Voltage Transients ◽  
Specific Membrane

1. Numerical methods were used to simulate the voltage responses to an intrasomatic current step of neuronal models that incorporated tapering dendrites, dendrites of unequal electrotonic length, nonlinear membrane properties, and regional differences in specific membrane resistivity (Rm). A "peeling" technique was used to estimate the time constants (tau 0 and tau 1) and coefficients (a0 and a1) of the first two exponential terms of the series of exponential terms whose sum represented the slope of the voltage response. 2. The electrotonic structure of models with a uniform Rm was calculated using equations derived by Rall or Johnston or Brown et al. The adequacy of these methods were tested using a wide variety of models that conformed to the equivalent cylinder approximation of Rall. Johnston's method provided the most reliable estimate of electrotonic length (L) and the ratio of the dendritic conductance to the somatic conductance (rho). However, if L exceeded 2 and rho was eight or larger, the equations derived by Johnston could frequently not be solved due to small errors in the peeled values of tau 0, tau 1, a0, and a1. Although the method suggested by Brown et al. could be applied to all models, this method invariably underestimated L and rho. These errors were particularly large for model neurons with L values of 1.5 or larger and rho values of four or larger. Estimates of L using Rall's method were only reliable if rho was large and L was two or less. 3. Changing the geometry of the dendritic tree (dendritic tapering or dendrites of unequal L) or the addition of a time- and voltage-dependent conductance designed to mimic a sag process commonly seen in spinal motoneurons caused systematic changes in tau 0, tau 1, a0, and a1. The sag process always led to an underestimate of tau 0 even after applying a correction procedure. On the other hand, the ratio, tau 0/tau 1, was not affected by the sag process or dendritic tapering.(ABSTRACT TRUNCATED AT 400 WORDS)

Excitability Increase Induced by β-Adrenergic Receptor-Mediated Activation of Hyperpolarization-Activated Cation Channels in Rat Cerebellar Basket Cells

2000 ◽  
Vol 84 (4) ◽  
pp. 2026-2034 ◽  
Author(s):  
Fumihito Saitow ◽  
Shiro Konishi
Keyword(s):  
Preceding Paper ◽  
Input Resistance ◽  
Ionic Currents ◽  
Synaptic Activity ◽  
Basket Cells ◽  
Camp Analogue ◽  
Voltage Dependent ◽  
Current Clamp Mode ◽  
Old Rats ◽  
Whole Cell Recordings

In the preceding paper, we showed that norepinephrine (NE) enhances the spontaneous spike firings in cerebellar interneurons, basket cells (BCs), resulting in an increase in the frequency of BC-spike-triggered inhibitory postsynaptic currents (IPSCs) in Purkinje cells (PCs), and that the effects of NE on GABAergic BCs are mediated by β2-adrenergic receptors. This study aimed to further examine the ionic mechanism underlying the β-adrenoceptor-mediated facilitation of GABAergic transmission at the BC-PC synapses. Using cerebellar slices obtained from 15- to 21-day-old rats and whole cell recordings, we investigated ionic currents in the BCs and the effects of the β-agonist isoproterenol (ISP) as well as forskolin on the BC excitability. Hyperpolarizing voltage steps from a holding potential of −50 mV elicited a hyperpolarization-activated inward current, I h, in the BC. This current exhibited voltage-dependent activation that was accelerated by strong hyperpolarization, displaying two time constants, 84 ± 6 and 310 ± 40 ms, at −100 mV, and was inhibited by 20 μM ZD7288. ISP and forskolin, both at 20 μM, enhanced I h by shifting the activation curve by 5.9 and 9.3 mV toward positive voltages, respectively. Under the current-clamp mode, ISP produced a depolarization of 7 ± 3 mV in BCs and reduced their input resistance to 74 ± 6%. ISP and a cAMP analogue, Rp-cAMP-S, increased the frequency of spontaneous spikes recorded from BCs using the cell-attached mode. The I h inhibitor ZD7288 decreased the BC spike frequency and abolished the ISP-induced increase in spike discharges. The results suggest that NE depolarizes the BCs through β-adrenoceptor-mediated cAMP formation linking it to activation of I h, which is, at least in part, involved in noradrenergic afferent-mediated facilitation of GABAergic synaptic activity at BC-PC connections in the rat cerebellum.

Activation of Embryonic Red and White Muscle Fibers During Fictive Swimming in the Developing Zebrafish

2002 ◽  
Vol 87 (3) ◽  
pp. 1244-1251 ◽  
Author(s):  
Robert R. Buss ◽  
Pierre Drapeau
Keyword(s):  
Muscle Activation ◽  
White Muscle ◽  
Developmental Stages ◽  
Muscle Fibers ◽  
Synaptic Activity ◽  
Body Movements ◽  
Early Developmental ◽  
Whole Cell Recordings ◽  
Myotomal Muscle ◽  
Synaptic Drive

Sub-threshold, motoneuron-evoked synaptic activity was observed in zebrafish embryonic red (ER) and white (EW) muscle fibers paralyzed with a dose of d-tubocurarine insufficient to abolish synaptic activity to determine whether muscle activation was coordinated to produce the undulating body movements required for locomotion. Paired whole-cell recordings revealed a synaptic drive that alternated between ipsilateral and contralateral myotomes and exhibited a rostral-caudal delay in timing appropriate for swimming. Both ER and EW muscle were activated during fictive swimming. However, at the fastest fictive swimming rates, ER fibers were de-recruited, whereas they could be active in isolation of EW fibers at the slowest fictive swimming rates. Prior to hatching, fictive swimming was preceded by a lower frequency, more robust and rhythmic synaptic drive resembling the “coiling” behavior of fish embryos. The motor activity observed in paralyzed zebrafish closely resembled the swimming and coiling behaviors observed in these developing fishes. At the early developmental stages examined in this study, myotomal muscle recruitment and coordination were similar to that observed in adult fishes during swimming. Our results indicate that the patterned activation of myotomal muscle is set from the onset of development.

scholarly journals Delta activity encodes taste information in the human brain

2018 ◽  
Author(s):  
Raphael Wallroth ◽  
Kathrin Ohla
Keyword(s):  
Human Brain ◽  
Neuronal Response ◽  
Pattern Discrimination ◽  
Nutrient Sensing ◽  
Response Patterns ◽  
Gustatory System ◽  
Rapid Responses ◽  
Delta Activity ◽  
Taste Discrimination ◽  
Eeg Recordings

The categorization of food via sensing nutrients or toxins is crucial to the survival of any organism. On ingestion, rapid responses within the gustatory system are required to identify the oral stimulus to guide immediate behaviour (swallowing or expulsion). The way in which the human brain accomplishes this task has so far remained unclear. Using multivariate analysis of 64-channel scalp EEG recordings obtained from 16 volunteers during tasting salty, sweet, sour, or bitter solutions, we found that activity in the delta-frequency range (1-4 Hz; delta power and phase) has information about taste identity in the human brain, with discriminable response patterns at the single-trial level within 130 ms of tasting. Importantly, the latencies of these response patterns predicted the point in time at which participants indicated detection of a taste by pressing a button. Furthermore, taste pattern discrimination was independent of motor-related activation and other taste features such as intensity and valence. On comparison with our previous findings from a passive (delayed) taste-discrimination task (Crouzet et al., 2015), taste-specific neural representations emerged earlier during this active (speeded) taste-detection task, suggesting a goal-dependent flexibility in gustatory response coding. Together, these findings provide the first evidence of a role of delta activity in taste-information coding in humans. Crucially, these neuronal response patterns can be linked to the speed of simple gustatory perceptual decisions, a vital performance index of nutrient sensing.

scholarly journals Voltage-based inhibitory synaptic plasticity: network regulation, diversity, and flexibility

2020 ◽  
Author(s):  
Victor Pedrosa ◽  
Claudia Clopath
Keyword(s):  
Synaptic Plasticity ◽  
Pyramidal Cell ◽  
Brain Regions ◽  
Postsynaptic Membrane ◽  
Network Activity ◽  
Inhibitory Neurons ◽  
Plasticity Model ◽  
Feedforward Network ◽  
Voltage Dependent ◽  
Homeostatic Mechanisms

AbstractNeural networks are highly heterogeneous while homeostatic mechanisms ensure that this heterogeneity is kept within a physiologically safe range. One of such homeostatic mechanisms, inhibitory synaptic plasticity, has been observed across different brain regions. Computationally, however, inhibitory synaptic plasticity models often lead to a strong suppression of neuronal diversity. Here, we propose a model of inhibitory synaptic plasticity in which synaptic updates depend on presynaptic spike arrival and postsynaptic membrane voltage. Our plasticity rule regulates the network activity by setting a target value for the postsynaptic membrane potential over a long timescale. In a feedforward network, we show that our voltage-dependent inhibitory synaptic plasticity (vISP) model regulates the excitatory/inhibitory ratio while allowing for a broad range of postsynaptic firing rates and thus network diversity. In a feedforward network in which excitatory and inhibitory neurons receive correlated input, our plasticity model allows for the development of co-tuned excitation and inhibition, in agreement with recordings in rat auditory cortex. In recurrent networks, our model supports memory formation and retrieval while allowing for the development of heterogeneous neuronal activity. Finally, we implement our vISP rule in a model of the hippocampal CA1 region whose pyramidal cell excitability differs across cells. This model accounts for the experimentally observed variability in pyramidal cell features such as the number of place fields, the fields sizes, and the portion of the environment covered by each cell. Importantly, our model supports a combination of sparse and dense coding in the hippocampus. Therefore, our voltage-dependent inhibitory plasticity model accounts for network homeostasis while allowing for diverse neuronal dynamics observed across brain regions.

scholarly journals Intracellular QX-314 Causes Depression of Membrane Potential Oscillations in Lamprey Spinal Neurons During Fictive Locomotion

2002 ◽  
Vol 87 (6) ◽  
pp. 2676-2683 ◽  
Author(s):  
Guo-Yuan Hu ◽  
Zoltán Biró ◽  
Russell H. Hill ◽  
Sten Grillner
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Dendritic Tree ◽  
Cell Voltage ◽  
Fictive Locomotion ◽  
Spinal Neurons ◽  
Potential Oscillations ◽  
Short Pulses ◽  
Voltage Dependent ◽  
Membrane Potential Oscillations

Spinal neurons undergo large cyclic membrane potential oscillations during fictive locomotion in lamprey. It was investigated whether these oscillations were due only to synaptically driven excitatory and inhibitory potentials or if voltage-dependent inward conductances also contribute to the depolarizing phase by using N-(2,6-dimethylphenyl carbamoylmethyl)triethylammonium bromide (QX-314) administered intracellularly during fictive locomotion. QX-314 intracellularly blocks inactivating and persistent Na+ channels, and in some neurons, effects on certain other types of channels have been reported. To detail the effects of QX-314 on Na+ and Ca2+ channels, we used dissociated lamprey neurons recorded under whole cell voltage clamp. At low intracellular concentrations of QX-314 (0.2 mM), inactivating Na+ channels were blocked and no effects were exerted on Ca2+ channels (also at 0.5 mM). At 10 mM QX-314, there was, however a marked reduction of I Ca. In the isolated spinal cord of the lamprey, fictive locomotion was induced by superfusing the spinal cord with Ringer's solution containing N-methyl-d-aspartate (NMDA), while recording the locomotor activity from the ventral roots. Simultaneously, identified spinal neurons were recorded intracellularly, while infusing QX-314 from the microelectrode. Patch electrodes cannot be used in the intact spinal cord, and therefore “sharp” electrodes were used. The amplitude of the oscillations was consistently reduced by 20–25% in motoneurons ( P < 0.05) and unidentified spinal neurons ( P < 0.005). The onset of the effect started a few minutes after impalement and reached a stable level within 30 min. These effects thus show that QX-314 causes a reduction in the amplitude of membrane potential oscillations during fictive locomotion. We also investigated whether QX-314 could affect glutamate currents by applying short pulses of glutamate from an extracellular pipette. No changes were observed. We also found no evidence for a persistent Na+ current in dissociated neurons, but these cells have a much-reduced dendritic tree. The results indicate that there is an inward conductance, which is sensitive to QX-314, during membrane potential oscillations that “boosts” the synaptic drive during fictive locomotion. Taken together, the results suggest that inactivating Na+ channels contribute to this inward conductance although persistent Na+channels, if present on dendrites, could possibly also contribute to shaping the membrane potential oscillations.

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