scholarly journals Estimation of Synaptic Activity during Neuronal Oscillations

Mathematics ◽  
2020 ◽  
Vol 8 (12) ◽  
pp. 2153
Author(s):  
Catalina Vich ◽  
Rafel Prohens ◽  
Antonio E. Teruel ◽  
Antoni Guillamon
Keyword(s):  
Time Course ◽  
Mathematical Proof ◽  
Brain Connectivity ◽  
Synaptic Activity ◽  
Synaptic Conductance ◽  
Period Function ◽  
Voltage Trace ◽  
Local Functional ◽  
Time Trace ◽  
Synaptic Conductances

In the study of brain connectivity, an accessible and convenient way to unveil local functional structures is to infer the time trace of synaptic conductances received by a neuron by using exclusively information about its membrane potential (or voltage). Mathematically speaking, it constitutes a challenging inverse problem: it consists in inferring time-dependent parameters (synaptic conductances) departing from the solutions of a dynamical system that models the neuron’s membrane voltage. Several solutions have been proposed to perform these estimations when the neuron fluctuates mildly within the subthreshold regime, but very few methods exist for the spiking regime as large amplitude oscillations (revealing the activation of complex nonlinear dynamics) hinder the adaptability of subthreshold-based computational strategies (mostly linear). In a previous work, we presented a mathematical proof-of-concept that exploits the analytical knowledge of the period function of the model. Inspired by the relevance of the period function, in this paper we generalize it by providing a computational strategy that can potentially adapt to a variety of models as well as to experimental data. We base our proposal on the frequency versus synaptic conductance curve (f−gsyn), derived from an analytical study of a base model, to infer the actual synaptic conductance from the interspike intervals of the recorded voltage trace. Our results show that, when the conductances do not change abruptly on a time-scale smaller than the mean interspike interval, the time course of the synaptic conductances is well estimated. When no base model can be cast to the data, our strategy can be applied provided that a suitable f−gsyn table can be experimentally constructed. Altogether, this work opens new avenues to unveil local brain connectivity in spiking (nonlinear) regimes.

scholarly journals Tone-Evoked Excitatory and Inhibitory Synaptic Conductances of Primary Auditory Cortex Neurons

2004 ◽  
Vol 92 (1) ◽  
pp. 630-643 ◽  
Author(s):  
Andrew Y. Y. Tan ◽  
Li I. Zhang ◽  
Michael M. Merzenich ◽  
Christoph E. Schreiner
Keyword(s):  
Auditory Cortex ◽  
Time Course ◽  
Frequency Tuning ◽  
Primary Auditory Cortex ◽  
Cell Voltage ◽  
Synaptic Conductance ◽  
Synaptic Excitation ◽  
Tone Intensity ◽  
Synaptic Conductances

In primary auditory cortex (AI) neurons, tones typically evoke a brief depolarization, which can lead to spiking, followed by a long-lasting hyperpolarization. The extent to which the hyperpolarization is due to synaptic inhibition has remained unclear. Here we report in vivo whole cell voltage-clamp measurements of tone-evoked excitatory and inhibitory synaptic conductances of AI neurons of the pentobarbital-anesthetized rat. Tones evoke an increase of excitatory synaptic conductance, followed by an increase of inhibitory synaptic conductance. The synaptic conductances can account for the gross time course of the typical membrane potential response. Synaptic excitation and inhibition have the same frequency tuning. As tone intensity increases, the amplitudes of synaptic excitation and inhibition increase, and the latency of synaptic excitation decreases. Our data indicate that the interaction of synaptic excitation and inhibition shapes the time course and frequency tuning of the spike responses of AI neurons.

scholarly journals Background Synaptic Conductance and Precision of EPSP-Spike Coupling at Pyramidal Cells

2005 ◽  
Vol 93 (6) ◽  
pp. 3248-3256 ◽  
Author(s):  
Veronika Zsiros ◽  
Shaul Hestrin
Keyword(s):  
Time Course ◽  
Pyramidal Cells ◽  
Spike Timing ◽  
Synaptic Activity ◽  
Synaptic Conductance ◽  
Temporal Precision ◽  
Voltage Dependent ◽  
Cortical Slices

The temporal precision of converting excitatory postsynaptic potentials (EPSPs) into spikes at pyramidal cells is critical for the coding of information in the cortex. Several in vitro studies have shown that voltage-dependent conductances in pyramidal cells can prolong the EPSP time course resulting in an imprecise EPSP-spike coupling. We have used dynamic-clamp techniques to mimic the in vivo background synaptic conductance in cortical slices and investigated how the ongoing synaptic activity may affect the EPSP time course near threshold and the EPSP spike coupling. We report here that background synaptic conductance dramatically diminished the depolarization related prolongation of the EPSPs in pyramidal cells and improved the precision of spike timing. Furthermore, we found that background synaptic conductance can affect the interaction among action potentials in a spike train. Thus the level of ongoing synaptic activity in the cortex may regulate the capacity of pyramidal cells to process temporal information.

Altered desensitization produces enhancement of EPSPs in neocortical neurons

1994 ◽  
Vol 72 (2) ◽  
pp. 1032-1036 ◽  
Author(s):  
M. R. Pelletier ◽  
J. J. Hablitz
Keyword(s):  
Nmda Receptors ◽  
Time Course ◽  
Glutamate Release ◽  
Epileptiform Activity ◽  
Brain Slices ◽  
Synaptic Activity ◽  
Membrane Properties ◽  
Repetitive Firing ◽  
Resting Membrane Potential ◽  
Bath Application

1. Neocortical brain slices were prepared from rats (35–50 days of age) and maintained in vitro. Intracellular recordings were obtained from neurons in cortical layers II/III. The effect of bath application of cyclothiazide (CYZ), a potent blocker of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor desensitization, on evoked synaptic activity and passive membrane properties was investigated. 2. Bath application of CYZ did not significantly affect resting membrane potential, input resistance, or repetitive firing. CYZ increased both the amplitude and duration of evoked excitatory postsynaptic potentials (EPSPs). Polysynaptic responses were also augumented. These effects persisted after the blockade of N-methyl-D-aspartate (NMDA) receptors with D-2-amino-5-phosphonovaleric acid (D-APV). The magnitude of these effects appeared to vary directly with stimulation intensity and presumably, amount of glutamate release. 3. Epileptiform activity was induced by bath application of bicuculline methiodide. The amplitude and duration of evoked paroxysmal discharges were increased by CYZ. Similar results were seen in presence of D-APV. 4. These results indicate that CYZ has significant effects on synaptic transmission. Desensitization of non-NMDA receptors may be an important mechanism for determining the time course of EPSPs and in curtailing epileptiform responses in the rat neocortex.

scholarly journals Calculating Event-Triggered Average Synaptic Conductances From the Membrane Potential

2007 ◽  
Vol 97 (3) ◽  
pp. 2544-2552 ◽  
Author(s):  
Martin Pospischil ◽  
Zuzanna Piwkowska ◽  
Michelle Rudolph ◽  
Thierry Bal ◽  
Alain Destexhe
Keyword(s):  
Membrane Potential ◽  
Cortical Neurons ◽  
Time Course ◽  
Spike Generation ◽  
Nonlinear Contribution ◽  
Central Neurons ◽  
Time Courses ◽  
Model Subject ◽  
Synaptic Conductances

The optimal patterns of synaptic conductances for spike generation in central neurons is a subject of considerable interest. Ideally such conductance time courses should be extracted from membrane potential ( Vm) activity, but this is difficult because the nonlinear contribution of conductances to the Vm renders their estimation from the membrane equation extremely sensitive. We outline here a solution to this problem based on a discretization of the time axis. This procedure can extract the time course of excitatory and inhibitory conductances solely from the analysis of Vm activity. We test this method by calculating spike-triggered averages of synaptic conductances using numerical simulations of the integrate-and-fire model subject to colored conductance noise. The procedure was also tested successfully in biological cortical neurons using conductance noise injected with dynamic clamp. This method should allow the extraction of synaptic conductances from Vm recordings in vivo.

scholarly journals Current injection and receptor-mediated excitation produce similar maximal firing rates in hypoglossal motoneurons

2016 ◽  
Vol 115 (3) ◽  
pp. 1307-1313 ◽  
Author(s):  
Hilary E. Wakefield ◽  
Ralph F. Fregosi ◽  
Andrew J. Fuglevand
Keyword(s):  
Time Course ◽  
Input Resistance ◽  
Current Injection ◽  
Synaptic Activity ◽  
High Concentration ◽  
Membrane Potential Change ◽  
Firing Rates ◽  
Whole Cell Patch Clamp ◽  
Patch Clamp Electrophysiology ◽  
High Firing

The maximum firing rates of motoneurons (MNs), activated in response to synaptic drive, appear to be much lower than that elicited by current injection. It could be that the decrease in input resistance associated with increased synaptic activity (but not current injection) might blunt overall changes in membrane depolarization and thereby limit spike-frequency output. To test this idea, we recorded, in the same cells, maximal firing responses to current injection and to synaptic activation. We prepared 300 μm medullary slices in neonatal rats that contained hypoglossal MNs and used whole-cell patch-clamp electrophysiology to record their maximum firing rates in response to triangular-ramp current injections and to glutamate receptor-mediated excitation. Brief pressure pulses of high-concentration glutamate led to significant depolarization, high firing rates, and temporary cessation of spiking due to spike inactivation. In the same cells, we applied current clamp protocols that approximated the time course of membrane potential change associated with glutamate application and with peak current levels large enough to cause spike inactivation. Means (SD) of maximum firing rates obtained in response to glutamate application were nearly identical to those obtained in response to ramp current injection [glutamate 47.1 ± 12.0 impulses (imp)/s, current injection 47.5 ± 11.2 imp/s], even though input resistance was 40% less during glutamate application compared with current injection. Therefore, these data suggest that the reduction in input resistance associated with receptor-mediated excitation does not, by itself, limit the maximal firing rate responses in MNs.

scholarly journals Inhibitory-excitatory synaptic balance is shifted toward increased excitation in magnocellular neurosecretory cells of heart failure rats

2011 ◽  
Vol 106 (3) ◽  
pp. 1545-1557 ◽  
Author(s):  
Evgeniy S. Potapenko ◽  
Vinicia C. Biancardi ◽  
Renea M. Florschutz ◽  
Pan D. Ryu ◽  
Javier E. Stern
Keyword(s):  
Heart Failure ◽  
Ampa Receptor ◽  
Time Course ◽  
Neurosecretory Cell ◽  
Brain Slices ◽  
Synaptic Strength ◽  
Neurosecretory Cells ◽  
Synaptic Function ◽  
Synaptic Activity ◽  
Excitatory Drive

Despite the well-established contribution of neurohumoral activation to morbidity and mortality in heart failure (HF) patients, relatively little is known about the underlying central nervous system mechanisms. In this study, we aimed to determine whether changes in GABAergic inhibitory and glutamatergic excitatory synaptic function contribute to altered hypothalamic magnocellular neurosecretory cell (MNC) activity in HF rats. Patch-clamp recordings were obtained from MNCs in brain slices from sham and HF rats. Glutamate excitatory (EPSCs) and GABAergic inhibitory postsynaptic currents (IPSCs) were simultaneously recorded, and changes in their strengths, as well as their interactions, were evaluated. We found a diminished GABAergic synaptic strength in MNCs of HF rats, reflected as faster decaying IPSCs and diminished mean IPSC charge transfer. Opposite changes were observed in glutamate EPSC synaptic strength, resulting in a shift in the GABA-glutamate balance toward a relatively stronger glutamate influence in HF rats. The prolongation of glutamate EPSCs during HF was mediated, at least in part, by an enhanced contribution of AMPA receptor desensitization to the EPSC decay time course. EPSC prolongation, and consequently increased unitary strength, resulted in a stronger AMPA receptor-mediated excitatory drive to firing discharge in MNCs of HF rats. Blockade of GABAA synaptic activity diminished the EPSC waveform variability observed among events in sham rats, an effect that was blunted in HF rats. Together, our results suggest that opposing changes in postsynaptic properties of GABAergic and glutamatergic synaptic function contribute to enhanced magnocellular neurosecretory activity in HF rats.

Minor Contribution of Principal Excitatory Pathways to Hippocampal LFPs in the Anesthetized Rat: A Combined Independent Component and Current Source Density Study

2010 ◽  
Vol 104 (1) ◽  
pp. 484-497 ◽  
Author(s):  
A. Korovaichuk ◽  
J. Makarova ◽  
V. A. Makarov ◽  
N. Benito ◽  
O. Herreras
Keyword(s):  
Time Course ◽  
Specific Activity ◽  
Current Source ◽  
Current Source Density ◽  
Independent Component ◽  
Synaptic Activity ◽  
Population Activity ◽  
Neuronal Populations ◽  
Source Density ◽  
Sparse Population

Analysis of local field potentials (LFPs) helps understand the function of the converging neuronal populations that produce the mixed synaptic activity in principal cells. Recently, using independent component analysis (ICA), we resolved ongoing hippocampal activity into several major contributions of stratified LFP-generators. Here, using pathway-specific LFP reconstruction, we isolated LFP-generators that describe the activity of Schaffer-CA1 and Perforant-Dentate excitatory inputs in the anesthetized rat. First, we applied ICA and current source density analysis to LFPs evoked by electrical subthreshold stimulation of the pathways. The results showed that pathway specific activity is selectively captured by individual components or LFP-generators. Each generator matches the known distribution of axonal terminal fields in the hippocampus and recovers the specific time course of their activation. Second, we use sparse weak electrical stimulation to prime ongoing LFPs with activity of a known origin. Decomposition of ongoing LFPs yields a few significant LFP-generators with distinct spatiotemporal characteristics for the Schaffer and Perforant inputs. Both pathways convey an irregular temporal pattern in bouts of population activity of varying amplitude. Importantly, the contribution of Schaffer and Perforant inputs to the power of raw LFPs in the hippocampus is minor (7 and 5%, respectively). The results support the hypothesis on a sparse population code used by excitatory populations in the entorhino-hippocampal system, and they validate the separation of LFP-generators as a powerful tool to explore the computational function of neuronal circuits in real time.

Activation and Deactivation of Voltage-Dependent K+ Channels During Synaptically Driven Action Potentials in the MNTB

2006 ◽  
Vol 96 (3) ◽  
pp. 1547-1555 ◽  
Author(s):  
Achim Klug ◽  
Laurence O. Trussell
Keyword(s):  
Action Potentials ◽  
Time Course ◽  
Low Voltage ◽  
Multiple Roles ◽  
Synaptic Activity ◽  
Leak Current ◽  
Medial Nucleus ◽  
Voltage Dependent ◽  
Spike Waveforms ◽  
Trapezoid Body

K+ channels shape individual action potentials and determine their pattern of firing. In auditory relays, both high- and low-voltage–activated K+ channels (HVA and LVA) are critical for preservation of auditory timing cues. We examined how these channels participate in firing in the medial nucleus of the trapezoid body. Principal cells at physiological temperature were voltage clamped using spike waveforms previously recorded in response to calyceal firing. Current components were isolated by digital subtraction of traces recorded in the channel antagonists dendrotoxin-I or tetraethylammonium. During orthodromic spikes delivered at 300 and 600 Hz, both currents activated with a slight delay, peaking just after the crest of the spike. The decay of HVA was sufficiently fast to match the time course of the spike. By contrast, with 300-Hz stimuli, LVA continued to decay after the spikes reached a stable interspike potential. Although LVA currents partially inactivate during prolonged voltage steps, their peak amplitudes remained stable or increased during trains of spikelike stimuli. At 600 Hz, LVA did not fully deactivate between the spikes and therefore generated a leak current. To determine the effect of blocking LVA channels on spiking, prerecorded postsynaptic conductances were injected, with and without dendrotoxin-I. After block of LVA channels, strong synaptic conductances produced broader spikes, greater spike jitter, and prolonged depolarized states. HVA blockade with tetraethylammonium also broadened spikes but led to less error in timing. These results reveal multiple roles for LVA channels in spike repolarization and timing during synaptic activity.

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