scholarly journals Frequency Dependence of Spike Timing Reliability in Cortical Pyramidal Cells and Interneurons

2001 ◽  
Vol 85 (4) ◽  
pp. 1782-1787 ◽  
Author(s):  
J.-M. Fellous ◽  
A. R. Houweling ◽  
R. H. Modi ◽  
R.P.N. Rao ◽  
P.H.E. Tiesinga ◽  
...  
Keyword(s):  
Cortical Neurons ◽  
Phase Locking ◽  
Pyramidal Cells ◽  
Limited Range ◽  
Spike Timing ◽  
Current Injection ◽  
Constant Current ◽  
Intrinsic Frequency ◽  
Spike Threshold ◽  
Subthreshold Oscillations

Pyramidal cells and interneurons in rat prefrontal cortical slices exhibit subthreshold oscillations when depolarized by constant current injection. For both types of neurons, the frequencies of these oscillations for current injection just below spike threshold were 2–10 Hz. Above spike threshold, however, the subthreshold oscillations in pyramidal cells remained low, but the frequency of oscillations in interneurons increased up to 50 Hz. To explore the interaction between these intrinsic oscillations and external inputs, the reliability of spiking in these cortical neurons was studied with sinusoidal current injection over a range of frequencies above and below the intrinsic frequency. Cortical neurons produced 1:1 phase locking for a limited range of driving frequencies for fixed amplitude. For low-input amplitude, 1:1 phase locking was obtained in the 5- to 10-Hz range. For higher-input amplitudes, pyramidal cells phase-locked in the 5- to 20-Hz range, whereas interneurons phase-locked in the 5- to 50-Hz range. For the amplitudes studied here, spike time reliability was always highest during 1:1 phase-locking, between 5 and 20 Hz for pyramidal cells and between 5 and 50 Hz for interneurons. The observed differences in the intrinsic frequency preference between pyramidal cells and interneurons have implications for rhythmogenesis and information transmission between populations of cortical neurons.

scholarly journals Rapid Temporal Modulation of Synchrony by Competition in Cortical Interneuron Networks

2004 ◽  
Vol 16 (2) ◽  
pp. 251-275 ◽  
Author(s):  
P.H.E. Tiesinga ◽  
T. J. Sejnowski
Keyword(s):  
Cortical Neurons ◽  
Pyramidal Neurons ◽  
Background Activity ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Network Activity ◽  
Local Networks ◽  
Rapid Changes ◽  
Asynchronous State ◽  
The Impact

The synchrony of neurons in extrastriate visual cortex is modulated by selective attention even when there are only small changes in firing rate (Fries, Reynolds, Rorie, & Desimone, 2001). We used Hodgkin-Huxley type models of cortical neurons to investigate the mechanism by which the degree of synchrony can be modulated independently of changes in firing rates. The synchrony of local networks of model cortical interneurons interacting through GABAA synapses was modulated on a fast timescale by selectively activating a fraction of the interneurons. The activated interneurons became rapidly synchronized and suppressed the activity of the other neurons in the network but only if the network was in a restricted range of balanced synaptic background activity. During stronger background activity, the network did not synchronize, and for weaker background activity, the network synchronized but did not return to an asynchronous state after synchronizing. The inhibitory output of the network blocked the activity of pyramidal neurons during asynchronous network activity, and during synchronous network activity, it enhanced the impact of the stimulus-related activity of pyramidal cells on receiving cortical areas (Salinas & Sejnowski, 2001). Synchrony by competition provides a mechanism for controlling synchrony with minor alterations in rate, which could be useful for information processing. Because traditional methods such as cross-correlation and the spike field coherence require several hundred milliseconds of recordings and cannot measure rapid changes in the degree of synchrony, we introduced a new method to detect rapid changes in the degree of coincidence and precision of spike timing.

Role of Axonal NaV1.6 Sodium Channels in Action Potential Initiation of CA1 Pyramidal Neurons

2008 ◽  
Vol 100 (4) ◽  
pp. 2361-2380 ◽  
Author(s):  
Michel Royeck ◽  
Marie-Therese Horstmann ◽  
Stefan Remy ◽  
Margit Reitze ◽  
Yoel Yaari ◽  
...  
Keyword(s):  
Action Potential ◽  
Cortical Neurons ◽  
Pyramidal Neurons ◽  
Voltage Dependence ◽  
Pyramidal Cells ◽  
Spike Threshold ◽  
Ca1 Pyramidal Cells ◽  
Gated Channel ◽  
Spike Initiation

In many neuron types, the axon initial segment (AIS) has the lowest threshold for action potential generation. Its active properties are determined by the targeted expression of specific voltage-gated channel subunits. We show that the Na+ channel NaV1.6 displays a striking aggregation at the AIS of cortical neurons. To assess the functional role of this subunit, we used Scn8a med mice that are deficient for NaV1.6 subunits but still display prominent Na+ channel aggregation at the AIS. In CA1 pyramidal cells from Scn8a med mice, we found a depolarizing shift in the voltage dependence of activation of the transient Na+ current ( INaT), indicating that NaV1.6 subunits activate at more negative voltages than other NaV subunits. Additionally, persistent and resurgent Na+ currents were significantly reduced. Current-clamp recordings revealed a significant elevation of spike threshold in Scn8a med mice as well as a shortening of the estimated delay between spike initiation at the AIS and its arrival at the soma. In combination with simulations using a realistic computer model of a CA1 pyramidal cell, our results imply that a hyperpolarized voltage dependence of activation of AIS NaV1.6 channels is important both in determining spike threshold and localizing spike initiation to the AIS. In addition to altered spike initiation, Scn8a med mice also showed a strongly reduced spike gain as expected with combined changes in persistent and resurgent currents and spike threshold. These results suggest that NaV1.6 subunits at the AIS contribute significantly to its role as spike trigger zone and shape repetitive discharge properties of CA1 neurons.

Analysis of repetitive transient response of lobster motor axons

1960 ◽  
Vol 199 (2) ◽  
pp. 367-372
Author(s):  
W. J. Adelman ◽  
E. Pautler ◽  
S. Epstein
Keyword(s):  
Repetitive Sequence ◽  
Spike Timing ◽  
Constant Current ◽  
Intensity Increase ◽  
Transient Phase ◽  
Intensity Data ◽  
Probability Level ◽  
Excitation Process ◽  
Excitatory State ◽  
Repetitive Discharge

An analysis was made to determine the relation between spike timing and the intensity of a constant current evoking a repetitive discharge in the single lobster motor axon. Accurate measurements of repetition intervals during the transient phase showed that an intensity increase of about 10–3 rheobase units produces a significantly different change in spike interval timing at the 0.005 probability level. Applications of excitation theory to the latency-intensity data have produced an equation which predicts the latency to the nth spike in a repetitive sequence as a function of stimulus intensity. The equation implies that the excitation process producing the nth spike is similar to the process producing the first spike in the repetitive sequence. Influences of supernormality and refractoriness were incorporated into the analysis. Also repeated stimulation at a fixed intensity indicated an inherent variability in the timing of the repetitive response which was shown to be a function of the magnitude of the latency. To explain this result a fixed uncertainty in the level of the initiating excitatory state was postulated.

scholarly journals Subthreshold membrane potential dynamics of posterior parietal cortical neurons coupled with hippocampal ripples

2021 ◽  
Author(s):  
Y. Sato ◽  
H. Mizuno ◽  
N. Matsumoto ◽  
Y. Ikegaya
Keyword(s):  
Local Field ◽  
Cortical Neurons ◽  
Posterior Parietal Cortex ◽  
Pyramidal Cells ◽  
Membrane Potentials ◽  
High Frequency Oscillations ◽  
Neocortical Neurons ◽  
Field Activity ◽  
Posterior Parietal ◽  
Post Hoc

AbstractDuring behavioral states of immobility, sleep, and anesthesia, the hippocampus generates high-frequency oscillations called ripples. Ripples occur simultaneously with synchronous neuronal activity in the neocortex, known as slow waves, and contribute to memory consolidation. During these ripples, various neocortical regions exhibit modulations in spike rates and local field activity irrespective of whether they receive direct synaptic inputs from the hippocampus. However, little is known about the subthreshold dynamics of the membrane potentials of neocortical neurons during ripples. We patch-clamped layer 2/3 pyramidal cells in the posterior parietal cortex (PPC), a neocortical region that is involved in allocentric spatial representation of behavioral exploration and sequential series of relevant action potentials during ripples. We simultaneously monitored the membrane potentials of post hoc-identified PPC neurons and the local field potentials of the hippocampus in anesthetized mice. More than 50% of the recorded PPC neurons exhibited significant depolarizations and/or hyperpolarizations during ripples. Histological inspections of the recorded neurons revealed that the ripple-modulated PPC neurons were distributed in the PPC in a spatially non-biased fashion. These results suggest that hippocampal ripples are widely but selectively associated with the subthreshold dynamics of the membrane potentials of PPC neurons even though there is no monosynaptic connectivity between the hippocampus and the PPC.

scholarly journals Dopaminergic Neuromodulation of Spike Timing Dependent Plasticity in Mature Adult Rodent and Human Cortical Neurons

2021 ◽  
Vol 15 ◽  
Author(s):  
Emma Louise Louth ◽  
Rasmus Langelund Jørgensen ◽  
Anders Rosendal Korshoej ◽  
Jens Christian Hedemann Sørensen ◽  
Marco Capogna
Keyword(s):  
Learning And Memory ◽  
Cortical Neurons ◽  
Synaptic Depression ◽  
Spike Timing ◽  
Therapeutic Interventions ◽  
Spike Timing Dependent Plasticity ◽  
Mature Adult ◽  
Dependent Plasticity ◽  
Cortical Synapses

Synapses in the cerebral cortex constantly change and this dynamic property regulated by the action of neuromodulators such as dopamine (DA), is essential for reward learning and memory. DA modulates spike-timing-dependent plasticity (STDP), a cellular model of learning and memory, in juvenile rodent cortical neurons. However, it is unknown whether this neuromodulation also occurs at excitatory synapses of cortical neurons in mature adult mice or in humans. Cortical layer V pyramidal neurons were recorded with whole cell patch clamp electrophysiology and an extracellular stimulating electrode was used to induce STDP. DA was either bath-applied or optogenetically released in slices from mice. Classical STDP induction protocols triggered non-hebbian excitatory synaptic depression in the mouse or no plasticity at human cortical synapses. DA reverted long term synaptic depression to baseline in mouse via dopamine 2 type receptors or elicited long term synaptic potentiation in human cortical synapses. Furthermore, when DA was applied during an STDP protocol it depressed presynaptic inhibition in the mouse but not in the human cortex. Thus, DA modulates excitatory synaptic plasticity differently in human vs. mouse cortex. The data strengthens the importance of DA in gating cognition in humans, and may inform on therapeutic interventions to recover brain function from diseases.

scholarly journals Density of voltage-gated potassium channels is a bifurcation parameter in pyramidal neurons

2015 ◽  
Vol 113 (2) ◽  
pp. 537-549 ◽  
Author(s):  
Hugo Zeberg ◽  
Hugh P. C. Robinson ◽  
Peter Århem
Keyword(s):  
Outward Current ◽  
Pyramidal Cells ◽  
Theoretical Work ◽  
K Channel ◽  
Threshold Dynamics ◽  
Bifurcation Parameter ◽  
Channel Density ◽  
Subthreshold Oscillations

Several types of intrinsic dynamics have been identified in brain neurons. Type 1 excitability is characterized by a continuous frequency-stimulus relationship and, thus, an arbitrarily low frequency at threshold current. Conversely, Type 2 excitability is characterized by a discontinuous frequency-stimulus relationship and a nonzero threshold frequency. In previous theoretical work we showed that the density of Kv channels is a bifurcation parameter, such that increasing the Kv channel density in a neuron model transforms Type 1 excitability into Type 2 excitability. Here we test this finding experimentally, using the dynamic clamp technique on Type 1 pyramidal cells in rat cortex. We found that increasing the density of slow Kv channels leads to a shift from Type 1 to Type 2 threshold dynamics, i.e., a distinct onset frequency, subthreshold oscillations, and reduced latency to first spike. In addition, the action potential was resculptured, with a narrower spike width and more pronounced afterhyperpolarization. All changes could be captured with a two-dimensional model. It may seem paradoxical that an increase in slow K channel density can lead to a higher threshold firing frequency; however, this can be explained in terms of bifurcation theory. In contrast to previous work, we argue that an increased outward current leads to a change in dynamics in these neurons without a rectification of the current-voltage curve. These results demonstrate that the behavior of neurons is determined by the global interactions of their dynamical elements and not necessarily simply by individual types of ion channels.

scholarly journals Sparse bursts optimize information transmission in a multiplexed neural code

2018 ◽  
Vol 115 (27) ◽  
pp. E6329-E6338 ◽  
Author(s):  
Richard Naud ◽  
Henning Sprekeler
Keyword(s):  
Firing Rate ◽  
Cortical Neurons ◽  
Neural Code ◽  
Spike Timing ◽  
Neural Ensemble ◽  
Multiple Input ◽  
Cortical Hierarchy ◽  
Connectivity Patterns ◽  
Rate Coding

Many cortical neurons combine the information ascending and descending the cortical hierarchy. In the classical view, this information is combined nonlinearly to give rise to a single firing-rate output, which collapses all input streams into one. We analyze the extent to which neurons can simultaneously represent multiple input streams by using a code that distinguishes spike timing patterns at the level of a neural ensemble. Using computational simulations constrained by experimental data, we show that cortical neurons are well suited to generate such multiplexing. Interestingly, this neural code maximizes information for short and sparse bursts, a regime consistent with in vivo recordings. Neurons can also demultiplex this information, using specific connectivity patterns. The anatomy of the adult mammalian cortex suggests that these connectivity patterns are used by the nervous system to maintain sparse bursting and optimal multiplexing. Contrary to firing-rate coding, our findings indicate that the physiology and anatomy of the cortex may be interpreted as optimizing the transmission of multiple independent signals to different targets.

Sodium-potassium pump inhibitors increase neuronal excitability in the rat hippocampal slice: role of a Ca2+-dependent conductance

1987 ◽  
Vol 57 (2) ◽  
pp. 496-509 ◽  
Author(s):  
M. McCarren ◽  
B. E. Alger
Keyword(s):  
Hippocampal Slice ◽  
Neuronal Excitability ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Extracellular Potassium ◽  
Gamma Aminobutyric Acid ◽  
Extracellular Potassium Concentration ◽  
Spike Threshold ◽  
Pump Activity ◽  
Voltage Dependent

We have used the rat hippocampal slice preparation as a model system for studying the epileptogenic consequences of a reduction in neuronal Na+-K+ pump activity. The cardiac glycosides (CGs) strophanthidin and dihydroouabain were used to inhibit the pump. These drugs had readily reversible effects, provided they were not applied for longer than 15-20 min. Hippocampal CA1 pyramidal cells were studied with intracellular recordings; population spike responses and changes in extracellular potassium concentration ([K+]o) were also measured in some experiments. This investigation focused on the possibility that intrinsic neuronal properties are affected by Na+-K+ pump inhibitors. The CGs altered the CA1 population response evoked by an orthodromic stimulus from a single spike to an epileptiform burst. Measurements of [K+]o showed that doses of CGs sufficient to cause bursting were associated with only minor (less than 1 mM) changes in resting [K+]o. However, the rate of K+ clearance from the extracellular space was moderately slowed, confirming that a decrease in pump activity had occurred. Intracellular recording indicated that CG application resulted in a small depolarization and apparent increase in resting input resistance of CA1 neurons. Although CGs caused a decrease in fast gamma-aminobutyric acid mediated inhibitory postsynaptic potentials (IPSPs), CGs could also enhance the latter part of the epileptiform burst induced by picrotoxin, an antagonist of these IPSPs. Since intrinsic Ca2+ conductances comprise a significant part of the burst, this suggested the possibility that Na+-K+ pump inhibitors affected an intrinsic neuronal conductance. CGs decreased the threshold for activation of Ca2+ spikes (recorded in TTX and TEA) without enhancing the spikes themselves, indicating that a voltage-dependent subthreshold conductance might be involved. The action of CGs on Ca2+ spike threshold could not be mimicked by increasing [K+]o up to 10 mM. A variety of K+ conductance antagonists, including TEA, 4-AP, Ba2+ (in zero Ca2+), and carbachol were ineffective in preventing the CG-induced threshold shift of the Ca2+ spike. The shift was also seen in the presence of a choline-substituted low Na+ saline. Enhancement of a slow inward Ca2+ current is a possible mechanism for the decrease in Ca2+ spike threshold; however, it is impossible to use the Ca2+ spike as an assay when testing the effects of blocking Ca2+ conductances. Therefore, we studied the influence of CGs on the membrane current-voltage (I-V) curve, since persistent voltage-dependent conductances appear as nonlinearities in the I-V plot obtained under current clamp.(ABSTRACT TRUNCATED AT 400 WORDS)

Possible Effects of Depolarizing GABAA Conductance on the Neuronal Input–Output Relationship: A Modeling Study

2005 ◽  
Vol 93 (6) ◽  
pp. 3504-3523 ◽  
Author(s):  
Kenji Morita ◽  
Kunichika Tsumoto ◽  
Kazuyuki Aihara
Keyword(s):  
Firing Rate ◽  
Cortical Neurons ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Resting Potential ◽  
Input Output ◽  
Wide Range ◽  
The Relationship

Recent in vitro experiments revealed that the GABAA reversal potential is about 10 mV higher than the resting potential in mature mammalian neocortical pyramidal cells; thus GABAergic inputs could have facilitatory, rather than inhibitory, effects on action potential generation under certain conditions. However, how the relationship between excitatory input conductances and the output firing rate is modulated by such depolarizing GABAergic inputs under in vivo circumstances has not yet been understood. We examine herewith the input–output relationship in a simple conductance-based model of cortical neurons with the depolarized GABAA reversal potential, and show that a tonic depolarizing GABAergic conductance up to a certain amount does not change the relationship between a tonic glutamatergic driving conductance and the output firing rate, whereas a higher GABAergic conductance prevents spike generation. When the tonic glutamatergic and GABAergic conductances are replaced by in vivo–like highly fluctuating inputs, on the other hand, the effect of depolarizing GABAergic inputs on the input–output relationship critically depends on the degree of coincidence between glutamatergic input events and GABAergic ones. Although a wide range of depolarizing GABAergic inputs hardly changes the firing rate of a neuron driven by noncoincident glutamatergic inputs, a certain range of these inputs considerably decreases the firing rate if a large number of driving glutamatergic inputs are coincident with them. These results raise the possibility that the depolarized GABAA reversal potential is not a paradoxical mystery, but is instead a sophisticated device for discriminative firing rate modulation.

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