scholarly journals Distinct dendritic Ca2+ spike forms produce opposing input-output transformations in rat CA3 pyramidal cells

2021 ◽  
Author(s):  
Ádám Magó ◽  
Noémi Kis ◽  
Balázs Lükó ◽  
Judit K Makara
Keyword(s):  
Action Potentials ◽  
Dendritic Structure ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Afferent Input ◽  
Male Rats ◽  
Input Output ◽  
Single Action ◽  
Na Currents ◽  
Ca3 Pyramidal Cells

Proper integration of different inputs targeting the dendritic tree of CA3 pyramidal cells (CA3PCs) is critical for associative learning and recall. Dendritic Ca2+ spikes have been proposed to perform associative computations in other PC types, by detecting conjunctive activation of different afferent input pathways, initiating afterdepolarization (ADP) and triggering burst firing. Implementation of such operations fundamentally depends on the actual biophysical properties of dendritic Ca2+ spikes; yet little is known about these properties in dendrites of CA3PCs. Using dendritic patch-clamp recordings and two-photon Ca2+ imaging in acute slices from male rats we report that, unlike CA1PCs, distal apical trunk dendrites of CA3PCs exhibit distinct forms of dendritic Ca2+ spikes. Besides ADP-type global Ca2+ spikes, a majority of dendrites expresses a novel, fast Ca2+ spike type that is initiated locally without backpropagating action potentials, can recruit additional Na+ currents, and is compartmentalized to the activated dendritic subtree. Occurrence of the different Ca2+ spike types correlates with dendritic structure, indicating morpho-functional heterogeneity among CA3PCs. Importantly, ADPs and dendritically initiated spikes produce opposing somatic output: bursts versus strictly single action potentials, respectively. The uncovered variability of dendritic Ca2+ spikes may underlie heterogeneous input-output transformation and bursting properties of CA3PCs, and might specifically contribute to key associative and non-associative computations performed by the CA3 network.

scholarly journals Distinct dendritic Ca2+ spike forms produce opposing input-output transformations in rat CA3 pyramidal cells

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Ádám Magó ◽  
Noémi Kis ◽  
Balázs Lükő ◽  
Judit K Makara
Keyword(s):  
Dendritic Structure ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Afferent Input ◽  
Male Rats ◽  
Input Output ◽  
Single Action ◽  
Two Photon ◽  
Ca3 Pyramidal Cells ◽  
Output Transformation

Proper integration of different inputs targeting the dendritic tree of CA3 pyramidal cells (CA3PCs) is critical for associative learning and recall. Dendritic Ca2+ spikes have been proposed to perform associative computations in other PC types by detecting conjunctive activation of different afferent input pathways, initiating afterdepolarization (ADP), and triggering burst firing. Implementation of such operations fundamentally depends on the actual biophysical properties of dendritic Ca2+ spikes; yet little is known about these properties in dendrites of CA3PCs. Using dendritic patch-clamp recordings and two-photon Ca2+ imaging in acute slices from male rats, we report that, unlike CA1PCs, distal apical trunk dendrites of CA3PCs exhibit distinct forms of dendritic Ca2+ spikes. Besides ADP-type global Ca2+ spikes, a majority of dendrites expresses a novel, fast Ca2+ spike type that is initiated locally without bAPs, can recruit additional Na+ currents, and is compartmentalized to the activated dendritic subtree. Occurrence of the different Ca2+ spike types correlates with dendritic structure, indicating morpho-functional heterogeneity among CA3PCs. Importantly, ADPs and dendritically initiated spikes produce opposing somatic output: bursts versus strictly single-action potentials, respectively. The uncovered variability of dendritic Ca2+ spikes may underlie heterogeneous input-output transformation and bursting properties of CA3PCs, and might specifically contribute to key associative and non-associative computations performed by the CA3 network.

Evidence from simultaneous intracellular recordings in rat hippocampal slices that area CA3 pyramidal cells innervate dentate hilar mossy cells

1994 ◽  
Vol 72 (5) ◽  
pp. 2167-2180 ◽  
Author(s):  
H. E. Scharfman
Keyword(s):  
Pyramidal Cell ◽  
Action Potentials ◽  
Granule Cells ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Probability Of Failure ◽  
Mossy Cells ◽  
Mossy Cell ◽  
Ca3 Pyramidal Cells ◽  
Area Ca3

1. Simultaneous intracellular recordings of area CA3 pyramidal cells and dentate hilar “mossy” cells were made in rat hippocampal slices to test the hypothesis that area CA3 pyramidal cells excite mossy cells monosynaptically. Mossy cells and pyramidal cells were differentiated by location and electrophysiological characteristics. When cells were impaled near the border of area CA3 and the hilus, their identity was confirmed morphologically after injection of the marker Neurobiotin. 2. Evidence for monosynaptic excitation of a mossy cell by a pyramidal cell was obtained in 7 of 481 (1.4%) paired recordings. In these cases, a pyramidal cell action potential was followed immediately by a 0.40 to 6.75 (mean, 2.26) mV depolarization in the simultaneously recorded mossy cell (mossy cell membrane potentials, -60 to -70 mV). Given that pyramidal cells used an excitatory amino acid as a neurotransmitter (Cotman and Nadler 1987; Ottersen and Storm-Mathisen 1987) and recordings were made in the presence of the GABAA receptor antagonist bicuculline (25 microM), it is likely that the depolarizations were unitary excitatory postsynaptic potentials (EPSPs). 3. Unitary EPSPs of mossy cells were prone to apparent “failure.” The probability of failure was extremely high (up to 0.72; mean = 0.48) if the effects of all presynaptic action potentials were examined, including action potentials triggered inadvertently during other spontaneous EPSPs of the mossy cell. Probability of failure was relatively low (as low as 0; mean = 0.24) if action potentials that occurred during spontaneous activity of the mossy cell were excluded. These data suggest that unitary EPSPs produced by pyramidal cells are strongly affected by concurrent synaptic inputs to the mossy cell. 4. Unitary EPSPs were not clearly affected by manipulation of the mossy cell's membrane potential. This is consistent with the recent report that area CA3 pyramidal cells innervate distal dendrites of mossy cells (Kunkel et al. 1993). Such a distal location also may contribute to the high incidence of apparent failures. 5. Characteristics of unitary EPSPs generated by pyramidal cells were compared with the properties of the unitary EPSPs produced by granule cells. In two slices, pyramidal cell and granule cell inputs to the same mossy cell were compared. In other slices, inputs to different mossy cells were compared. In all experiments, unitary EPSPs produced by granule cells were larger in amplitude but similar in time course to unitary EPSPs produced by pyramidal cells. Probability of failure was lower and paired-pulse facilitation more common among EPSPs triggered by granule cells.(ABSTRACT TRUNCATED AT 400 WORDS)

On the synchronous activity induced by 4-aminopyridine in the CA3 subfield of juvenile rat hippocampus

1993 ◽  
Vol 70 (3) ◽  
pp. 1018-1029 ◽  
Author(s):  
M. Avoli ◽  
C. Psarropoulou ◽  
V. Tancredi ◽  
Y. Fueta
Keyword(s):  
Nmda Receptor ◽  
Gabaa Receptor ◽  
Action Potentials ◽  
Hippocampal Slices ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Occurrence Rate ◽  
Gamma Aminobutyric Acid ◽  
Synchronous Activity ◽  
Ca3 Pyramidal Cells

1. Extracellular field potential and intracellular recordings were made in the CA3 subfield of hippocampal slices obtained from 10- to 24-day-old rats during perfusion with artificial cerebrospinal fluid (ACSF) containing the convulsant 4-aminopyridine (4-AP, 50 microM). 2. Three types of spontaneous, synchronous activity were recorded in the presence of 4-AP by employing extracellular microelectrodes positioned in the CA3 stratum (s.) radiatum: first, inter-ictal-like discharges that lasted 0.2-1.2 s and had an occurrence rate of 0.3-1.3 Hz; second, ictal-like events (duration: 3-40 s) that occurred at 4-38 x 10(-3) Hz; and third, large-amplitude (up to 8 mV) negative-going potentials that preceded the onset of the ictal-like events and thus appeared to initiate them. 3. None of these synchronous activities was consistently modified by addition of antagonists of the N-methyl-D-aspartate (NMDA) receptor to the ACSF. In contrast, the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 2-10 microM) reversibly blocked interictal- and ictallike discharges. The only synchronous, spontaneous activity recorded in this type of medium consisted of the negative-going potentials that were abolished by the GABAA receptor antagonists bicuculline methiodide (5-20 microM) or picrotoxin (50 microM). Hence they were mediated through the activation of the GABAA receptor. 4. Profile analysis of the 4-AP-induced synchronous activity revealed that the gamma-aminobutyric acid (GABA)-mediated field potential had maximal negative amplitude in s. lacunosum-moleculare, attained equipotentiality at the border between s. radiatum and s. pyramidale, and became positive-going in s. oriens. These findings indicated that the GABA-mediated field potential presumably represented a depolarization occurring in the dendrites of CA3 pyramidal cells. 5. This conclusion was supported by intracellular analysis of the 4-AP-induced activity. The GABA-mediated potential was reflected by a depolarization of the membrane of CA3 pyramidal cells that triggered a few variable-amplitude, fractionated spikes or fast action potentials. By contrast, the ictal-like discharge was associated with a prolonged depolarization during which repetitive bursts of action potentials occurred. Short-lasting depolarizations with bursts of action potentials occurred during each interictal-like discharge. 6. The GABA-mediated potential recorded intracellularly in the presence of CNQX consisted of a prolonged depolarization (up to 12 s) that was still capable of triggering a few fast action potentials and/or fractionated spikes.(ABSTRACT TRUNCATED AT 400 WORDS)

Complex Blockade of TTX-Resistant Na+ Currents by Lidocaine and Bupivacaine Reduce Firing Frequency in DRG Neurons

1998 ◽  
Vol 79 (4) ◽  
pp. 1746-1754 ◽  
Author(s):  
Andreas Scholz ◽  
Noboru Kuboyama ◽  
Gunter Hempelmann ◽  
Werner Vogel
Keyword(s):  
Spinal Anesthesia ◽  
Action Potentials ◽  
Sensory Information ◽  
Firing Frequency ◽  
Drg Neurons ◽  
Patch Clamp Technique ◽  
Single Action ◽  
Na Currents ◽  
Frequency Of Action Potentials ◽  
Frequency Of Stimulation

Scholz, Andreas, Noboru Kuboyama, Gunter Hempelmann, and Werner Vogel. Complex blockade of TTX-resistant Na+ currents by lidocaine and bupivacaine reduce firing frequency in DRG neurons. J. Neurophysiol. 79: 1746–1754, 1998. Mechanisms of blockade of tetrodotoxin-resistant (TTXr) Na+ channels by local anesthetics in comparison with the sensitivity of tetrodotoxin-sensitive (TTXs) Na+ channels were studied by means of the patch-clamp technique in neurons of dorsal root ganglions (DRG) of rat. Half-maximum inhibitory concentration (IC50) for the tonic block of TTXr Na+ currents by lidocaine was 210 μmol/l, whereas TTXs Na+ currents showed five times lower IC50 of 42 μmol/l. Bupivacaine blocked TTXr and TTXs Na+ currents more potently with IC50 of 32 and 13 μmol/l, respectively. In the inactivated state, TTXr Na+ channel block by lidocaine showed higher sensitivities (IC50 = 60 μmol/l) than in the resting state underlying tonic blockade. The time constant τ1 of recovery of TTXr Na+ channels from inactivation at −80 mV was slowed from 2 to 5 ms after addition of 10 μmol/l bupivacaine, whereas the τ2 value of ∼500 ms remained unchanged. The use-dependent block of TTXr Na+ channels led to a progressive reduction of current amplitudes with increasing frequency of stimulation, which was ≤53% block at 20 Hz in 10 μmol/l bupivacaine and 81% in 100 μmol lidocaine. The functional importance of the use-dependent block was confirmed in current-clamp experiments where 30 μmol/l of lidocaine or bupivacaine did not suppress the single action potential but clearly reduced the firing frequency of action potentials again with stronger potency of bupivacaine. Because it was found that TTXr Na+ channels predominantly occur in smaller sensory neurons, their blockade might underlie the suppression of the sensation of pain. Different sensitivities and varying proportions of TTXr and TTXs Na+ channels could explain the known differential block in spinal anesthesia. We suggest that the frequency reduction at low local anesthetic concentrations may explain the phenomenon of paresthesia where sensory information are suppressed gradually during spinal anesthesia.

Axon terminal hyperexcitability associated with epileptogenesis in vitro. I. Origin of ectopic spikes

1993 ◽  
Vol 70 (3) ◽  
pp. 961-975 ◽  
Author(s):  
S. F. Stasheff ◽  
M. Hines ◽  
W. A. Wilson
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Model Neuron ◽  
Extracellular Recording ◽  
Pyramidal Cells ◽  
Initiation Site ◽  
Electrographic Seizures ◽  
Ca3 Pyramidal Cells

1. Intracellular and extracellular recording techniques were used to study the increase in ectopic (i.e., nonsomatic) action-potential generation occurring among CA3 pyramidal cells during the kindling-like induction of electrographic seizures (EGSs) in this subpopulation of the hippocampal slice. Kindling-like stimulus trains (60 Hz, 2 s) were delivered to s. radiatum of CA3 at 10-min intervals. As EGSs developed, the frequency of ectopic firing increased markedly (by 10.33 +/- 3.29 spikes/min, mean +/- SE, P << 0.01). Several methods were applied to determine the initiation site for these action potentials within the cell (axons vs. dendrites). 2. Collision tests were conducted between known antidromic and orthodromic action potentials in CA3 cells to determine the critical period, c, for collision. Attempts were then made to collide ectopic spikes with known antidromic action potentials. At intervals less than c, ectopic spikes failed to collide with antidromic ones, in 5 of 10 cases. In these cells, this clearly indicates that the ectopic spikes were themselves of axonal origin. In the remaining five cases, ectopic spikes collided with antidromic action potentials at intervals approximately equal to c, most likely because of interactions within the complex system of recurrent axon collaterals in CA3. 3. Action potentials of CA3 pyramidal cells were simulated with the use of a compartmental computer model, NEURON. These simulations were based on prior models of CA3 pyramidal neurons and of the motoneuron action potential. Simulated action potentials generated in axonal compartments possessed a prominent inflection on their rising phase (IS-SD break), which was difficult to appreciate in those spikes generated in somatic or dendritic compartments. 4. An analysis of action potentials recorded experimentally from CA3 pyramidal cells also showed that antidromic spikes possess a prominent IS-SD break that is not present in orthodromic spikes. In addition to identified antidromic action potentials, ectopic spikes also possess such an inflection. Together with the predictions of computer simulations, this analysis also indicates that ectopic spikes originate in the axons of CA3 cells. 5. Tetrodotoxin (TTX, 50 microM) was locally applied by pressure injection while monitoring ectopic spike activity. Localized application of TTX to regions of the slice that could include the axons but not the dendrites of recorded cells abolished or markedly reduced the frequency of ectopic spikes (n = 5), further confirming the hypothesis that these action potentials arise from CA3 axons.(ABSTRACT TRUNCATED AT 400 WORDS)

Modulation of the input/output function of rat piriform cortex pyramidal cells

1994 ◽  
Vol 72 (2) ◽  
pp. 644-658 ◽  
Author(s):  
E. Barkai ◽  
M. E. Hasselmo
Keyword(s):  
Action Potentials ◽  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Current Injection ◽  
Resting Potential ◽  
Repetitive Firing ◽  
Output Function ◽  
Input Output ◽  
Cholinergic Agonist ◽  
Strong Adaptation

1. In transverse brain slice preparations of rat piriform cortex, we characterized the repetitive firing properties of layer II pyramidal cells in control conditions (n = 78) and during perfusion of the cholinergic agonist carbachol (n = 26), with the ultimate goal of developing realistic computational simulations of the cholinergic modulation of the input/output function of these neurons. The response of neurons to prolonged (1 s) intracellular current injections was examined at a full range of current injection amplitudes, providing three-dimensional plots of firing frequency versus current amplitude versus time. 2. All neurons showed adaptation in response to intracellular current injection, with repetitive generation of action potentials at frequencies that were highest at the onset of the pulse and that decreased considerably thereafter. Substantial differences were observed between cells with regard to their rates of adaptation and the maximal number of action potentials they could generate during the current pulse. 3. The adaptation characteristics of each neuron were quantified by plotting the number of action potentials generated in 1 s as a function of the normalized current injection amplitude and measuring the area beneath this plot of the number of spikes versus current injection amplitude (S-I plot). This value was termed S-I value and allowed neurons to be plotted on a continuum including neurons showing strong adaptation (S-I value < 8.0) and neurons showing weak adaptation (S-I value > 8.0). The group showing weak adaptation contained 36% of the cells in control solution and 93.8% of the cells in 20 microM carbachol. 4. Neurons showing strong adaptation did not differ significantly from neurons showing weak adaptation in control conditions in measurements of resting potential, input resistance, threshold, and spike amplitude. Only a small difference was found in frequencies of firing measured soon after pulse onset (after 100 ms). This implies that differences in S-I values are primarily due to different rates of adaptation in later parts of the response. 5. Perfusion with solution containing the cholinergic agonist carbachol (2–100 microM) or 0 Ca2+ and 200 microM cadmium resulted in a substantial increase in the S-I values of neurons showing strong adaptation but had only a small effect on their initial firing rates. The effect on weakly adapting cells was smaller. In the presence of 20 microM carbachol, neurons showed a distribution shifted predominantly toward weak adaptation (n = 26).(ABSTRACT TRUNCATED AT 400 WORDS)

scholarly journals Neuronal gain modulability is determined by dendritic morphology: a computational optogenetic study

2016 ◽  
Author(s):  
Sarah Jarvis ◽  
Konstantin Nikolic ◽  
Simon R Schultz
Keyword(s):  
Dendritic Tree ◽  
Gain Control ◽  
Pyramidal Cells ◽  
Dendritic Morphology ◽  
Inhibitory Input ◽  
List Type ◽  
Moderate Degree ◽  
Gain Modulation ◽  
Input Output

AbstractThe mechanisms by which the gain of the neuronal input-output function may be modulated have been the subject of much investigation. However, little is known of the role of dendrites in neuronal gain control. New optogenetic experimental paradigms based on spatial profiles or patterns of light stimulation offer the prospect of elucidating many aspects of single cell function, including the role of dendrites in gain control. We thus developed a model to investigate how competing excitatory and inhibitory input within the dendritic arbor alters neuronal gain, incorporating kinetic models of opsins into our modeling to ensure it is experimentally testable. To investigate how different topologies of the neuronal dendritic tree affect the neuron’s input-output characteristics we generate branching geometries which replicate morphological features of most common neurons, but keep the number of branches and overall area of dendrites approximately constant. We found a relationship between a neuron’s gain modulability and its dendritic morphology, with neurons with bipolar dendrites with a moderate degree of branching being most receptive to control of the gain of their input-output relationship. The theory was then tested and confirmed on two examples of realistic neurons: 1) layer V pyramidal cells - confirming their role in neural circuits as a regulator of the gain in the circuit in addition to acting as the primary excitatory neurons, and 2) stellate cells. In addition to providing testable predictions and a novel application of dual-opsins, our model suggests that innervation of all dendritic subdomains is required for full gain modulation, revealing the importance of dendritic targeting in the generation of neuronal gain control and the functions that it subserves. Finally, our study also demonstrates that neurophysiological investigations which use direct current injection into the soma and bypass the dendrites may miss some important neuronal functions, such as gain modulation.Author SummaryGain modulability indicated by dendritic morphologyPyramidal cell-like shapes optimally receptive to modulationAll dendritic subdomains required for gain modulation, partial illumination is insufficientComputational optogenetic models improve and refine experimental protocols

Propagation of Action Potentials in Dendrites Depends on Dendritic Morphology

2001 ◽  
Vol 85 (2) ◽  
pp. 926-937 ◽  
Author(s):  
Philipp Vetter ◽  
Arnd Roth ◽  
Michael Häusser
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Dendritic Morphology ◽  
Dopamine Neurons ◽  
Action Potential Propagation ◽  
Voltage Gated ◽  
Wide Range ◽  
Gated Channel

Action potential propagation links information processing in different regions of the dendritic tree. To examine the contribution of dendritic morphology to the efficacy of propagation, simulations were performed in detailed reconstructions of eight different neuronal types. With identical complements of voltage-gated channels, different dendritic morphologies exhibit distinct patterns of propagation. Remarkably, the range of backpropagation efficacies observed experimentally can be reproduced by the variations in dendritic morphology alone. Dendritic geometry also determines the extent to which modulation of channel densities can affect propagation. Thus in Purkinje cells and dopamine neurons, backpropagation is relatively insensitive to changes in channel densities, whereas in pyramidal cells, backpropagation can be modulated over a wide range. We also demonstrate that forward propagation of dendritically initiated action potentials is influenced by morphology in a similar manner. We show that these functional consequences of the differences in dendritic geometries can be explained quantitatively using simple anatomical measures of dendritic branching patterns, which are captured in a reduced model of dendritic geometry. These findings indicate that differences in dendritic geometry act in concert with differences in voltage-gated channel density and kinetics to generate the diversity in dendritic action potential propagation observed between neurons. They also suggest that changes in dendritic geometry during development and plasticity will critically affect propagation. By determining the spatial pattern of action potential signaling, dendritic morphology thus helps to define the size and interdependence of functional compartments in the neuron.

Synchronized excitation and inhibition driven by intrinsically bursting neurons in neocortex

1989 ◽  
Vol 62 (5) ◽  
pp. 1149-1162 ◽  
Author(s):  
Y. Chagnac-Amitai ◽  
B. W. Connors
Keyword(s):  
Action Potentials ◽  
Lower Layer ◽  
Single Cells ◽  
Pyramidal Cells ◽  
Synaptic Activity ◽  
Large Field ◽  
Repetitive Firing ◽  
Field Potentials ◽  
Single Neurons ◽  
Single Action

1. The cellular mechanisms of synchronous synaptic activity were studied in isolated slices of rat SmI neocortex in which gamma-aminobutyric acid (GABA)-mediated inhibition was slightly suppressed. Intracellular measurements were made from single neurons, and extracellular recordings monitored the timing and intensity of population events. 2. Neurons in cortical layers II-VI were classified by the attributes of their single action potentials and repetitive firing patterns during injection of intracellular current pulses. Regular-spiking (RS) cells occurred in all layers and had relatively long-duration spikes and strong frequency adaptation. Intrinsically bursting (IB) cells occurred only in layers IV and V and generated bursts of greater than or equal to 3 spikes; some IB cells of lower-layer V produced repetitive bursts during long depolarizing pulses. Fast-spiking (FS) cells had brief spikes and little or no adaptation and fired at high frequencies. 3. When GABAA-mediated inhibition was slightly reduced with low doses of bicuculline methiodide (BMI, 0.8-1.0 microM), synchronous events were evoked by stimulating layer VI with single shocks. Synchronous events were characterized by prominent, often all-or-none extracellular field potentials that propagated horizontally for variable distances up to several millimeters. Large field potentials were invariably correlated with excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) in single neurons. Both PSPs and field potentials often had long (up to 250 ms) and variable latencies, and sometimes two or more events were generated by single stimuli. In all cases the PSPs and field potentials were synchronous. Both field potentials and single cells sometimes generated short epochs (3-7 peaks) of rhythmic events at 20-50 Hz. 4. The physiological class of single neurons was correlated with the relative dominance of excitation and inhibition during each synchronous event. In phase with each synchronous event, most RS cells were very strongly inhibited with only small amounts of concurrent excitation. By contrast, IB cells were strongly and consistently excited, with relatively little inhibition. FS cells were also phasically excited. 5. Anatomic studies have identified RS and IB cells as pyramidal cells and FS cells as GABAergic nonpyramidal cells. This implies that, during the synchronous events of the present study, the majority of pyramidal cells were dominated by IPSPs. Synchronous excitation of FS cells, the presumed inhibitory interneurons, is consistent with this. Only a subset of the pyramidal neurons, almost all of them IB cells of the middle layers, displayed strong, synchronous excitation and clusters of action potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Synaptic Democracy in Active Dendrites

2006 ◽  
Vol 96 (5) ◽  
pp. 2307-2318 ◽  
Author(s):  
Clifton C. Rumsey ◽  
L. F. Abbott
Keyword(s):  
Action Potentials ◽  
Dendritic Tree ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Dominant Factor ◽  
Dependent Plasticity ◽  
Ca1 Pyramidal Cells ◽  
Active Dendrites ◽  
Hebbian Plasticity ◽  
The Impact

Given the extensive attenuation that can occur along dendritic cables, location within the dendritic tree might appear to be a dominant factor in determining the impact of a synapse on the postsynaptic response. By this reasoning, distal synapses should have a smaller effect than proximal ones. However, experimental evidence from several types of neurons, such as CA1 pyramidal cells, indicates that a compensatory strengthening of synapses counteracts the effect of location on synaptic efficacy. A form of spike-timing-dependent plasticity (STDP), called anti-STDP, combined with non-Hebbian activity-dependent plasticity can account for the equalization of synaptic efficacies. This result, obtained originally in models with unbranched passive cables, also arises in multi-compartment models with branched and active dendrites that feature backpropagating action potentials, including models with CA1 pyramidal morphologies. Additionally, when dendrites support the local generation of action potentials, anti-STDP prevents runaway dendritic spiking and locally balances the numbers of dendritic and backpropagating action potentials. Thus in multiple ways, anti-STDP eliminates the location dependence of synapses and allows Hebbian plasticity to operate in a more “democratic” manner.

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