Biomedical subjects

Maxim Volgushev

Publications and source records attributed to Maxim Volgushev.

10 recordsLinked to original sources

PubMed2006

Precise long-range synchronization of activity and silence in neocortical neurons during slow-wave oscillations [corrected].

Slow-wave sleep is characterized by alternating periods of activity and silence in corticothalamic networks. Both activity and silence are stable network states, but the mechanisms of their alternation remain unknown. We show, using simultaneous multisite intracellular recordings in cats, that slow rhythm involves all neocortical neurons and that both activity and silence started almost synchronously in cells located up to 12 mm apart. Activity appeared predominantly at the area 5/7 border and spread in both anterior and posterior directions. The activity started earlier in fast-spiking cells and intrinsically bursting cells than in regular-spiking neurons. These results provide direct evidence for two mechanisms of active state generation: spread of activity from a local focus and synchronization of weaker activity, originating at multiple locations. Surprisingly, onsets of silent states were synchronized even more precisely than the onsets of activity, showing no latency bias for location or cell type. This most intriguing finding exposes a major gap in understanding the nature of state alternation. We suggest that it is the synchronous termination of activity and occurrence of silent states of the neuronal network that makes the EEG picture during slow-wave sleep so characteristic. Synchronous onset of silence in distant neurons cannot rely exclusively on properties of individual cells and synapses, such as adaptation of neuronal firing or synaptic depression; instead, it implies the existence of a network mechanism. Revealing this yet unknown large-scale mechanism, which switches network activity to silence, will aid our understanding of the origin of brain rhythms in normal function and pathology.

Action Potentials↗

PubMed2006

Unique features of action potential initiation in cortical neurons.

Neurons process and encode information by generating sequences of action potentials. For all spiking neurons, the encoding of single-neuron computations into sequences of spikes is biophysically determined by the cell's action-potential-generating mechanism. It has recently been discovered that apparently minor modifications of this mechanism can qualitatively change the nature of neuronal encoding. Here we quantitatively analyse the dynamics of action potential initiation in cortical neurons in vivo, in vitro and in computational models. Unexpectedly, key features of the initiation dynamics of cortical neuron action potentials--their rapid initiation and variable onset potential--are outside the range of behaviours described by the classical Hodgkin-Huxley theory. We propose a new model based on the cooperative activation of sodium channels that reproduces the observed dynamics of action potential initiation. This new model predicts that Hodgkin-Huxley-type dynamics of action potential initiation can be induced by artificially decreasing the effective density of sodium channels. In vitro experiments confirm this prediction, supporting the hypothesis that cooperative sodium channel activation underlies the dynamics of action potential initiation in cortical neurons.

Action Potentials↗

PubMed2006

Detection of active and silent states in neocortical neurons from the field potential signal during slow-wave sleep.

Oscillations of the local field potentials (LFPs) or electroencephalogram (EEG) at frequencies below 1 Hz are a hallmark of the slow-wave sleep. However, the timing of the underlying cellular events, which is an alternation of active and silent states of thalamocortical network, can be assessed only approximately from the phase of slow waves. Is it possible to detect, using the LFP or EEG, the timing of each episode of cellular activity or silence? With simultaneous recordings of the LFP and intracellular activity of 2-3 neocortical cells, we show that high-gamma-range (20-100 Hz) components in the LFP have significantly higher power when cortical cells are in active states as compared with silent-state periods. Exploiting this difference we have developed a new method, which uses the LFP signal to detect episodes of activity and silence of neocortical neurons. The method allows robust, reliable, and precise detection of timing of each episode of activity and silence of the neocortical network. It works with both surface and depth EEG, and its performance is affected little by the EEG prefiltering during recording. These results open new perspectives for studying differential operation of neural networks during periods of activity and silence, which rapidly alternate on the subsecond scale.

Action Potentials↗

PubMed2005

Adaptation at synaptic connections to layer 2/3 pyramidal cells in rat visual cortex.

Neocortical synapses express differential dynamic properties. When activated at high frequencies, the amplitudes of the subsequent postsynaptic responses may increase or decrease, depending on the stimulation frequency and on the properties of that particular synapse. Changes in the synaptic dynamics can dramatically affect the communication between nerve cells. Motivated by this question, we studied dynamic properties at synapses to layer 2/3 pyramidal cells with intracellular recordings in slices of rat visual cortex. Synaptic responses were evoked by trains of test stimuli, which consisted of 10 pulses at different frequencies (5-40 Hz). Test stimulation was applied either without any adaptation (control) or 2 s after an adaptation stimulus, which consisted of 4 s stimulation of these same synapses at 10, 25, or 40 Hz. The synaptic parameters were then assessed from fitting the data with a model of synaptic dynamics. Our estimates of the synaptic parameters in control, without adaptation are broadly consistent with previous studies. Adaptation led to pronounced changes of synaptic transmission. After adaptation, the amplitude of the response to the first pulse in the test train decreased for several seconds and then recovered back to the control level with a time constant of 2-18 s. Analysis of the data with extended models, which include interaction between different pools of synaptic vesicles, suggests that the decrease of the response amplitude was due to a synergistic action of two factors, decrease of the release probability and depletion of the available transmitter. After a weak (10 Hz) adaptation, the decrease of the response amplitude was accompanied by and correlated with the decrease of the release probability. After a strong adaptation (25 or 40 Hz), the depletion of synaptic resources was the main cause for the reduced response amplitude. Adaptation also led to pronounced changes of the time constants of facilitation and recovery, however, these changes were not uniform in all synapses, and on the population level, the only consistent and significant effect was an acceleration of the recovery after a strong adaptation. Taken together, our results suggest, that apart from decreasing the amplitude of postsynaptic responses, adaptation may produce synapse-specific effects, which could result in a kind of re-distribution of activity within neural networks.

Adaptation, Physiological↗

PubMed2004

Dependence of calcium influx in neocortical cells on temporal structure of depolarization, number of spikes, and blockade of NMDA receptors.

Increase of intracellular [Ca(2+)] evoked by action potentials in a cell can induce long-term synaptic plasticity even without concomitant presynaptic stimulation. We used optical recording of the fluorescence of a Ca(2+)-indicator Oregon Green to investigate whether differences in results obtained with modifications of that purely postsynaptic induction protocol could be due to differential Ca(2+) influx. We compared changes of the somatic [Ca(2+)] in layer II-III pyramidal cells in slices of rat visual cortex evoked by bursts of depolarization pulses and long depolarizing steps. During weak depolarizations, the Ca(2+) influx was proportional to the amplitude and duration of the depolarization. With suprathreshold depolarizations, the Ca(2+) influx was proportional to the number of action potentials. Because the burst depolarizations evoked more spikes than did the long duration steps, this burst protocol led to a larger Ca(2+) influx. With all stimulation protocols, the spike-induced Ca(2+) influx was reduced during blockade of N-methyl-D-aspartate (NMDA) receptors. Differences in intracellular [Ca(2+)] increases thus may be one reason for differential effects of purely postsynaptic challenges on synaptic transmission.

Action Potentials↗

PubMed2004

Probability of transmitter release at neocortical synapses at different temperatures.

The probability of transmitter release at synaptic terminals is one of the key characteristics of communication between nerve cells because it determines both the strength and dynamic properties of synaptic connections. To assess the distribution of the release probabilities at excitatory synapses on supragranular pyramidal cells in rat visual cortex, we have used the MK-801, a blocker of the open N-methyl-d-aspartate (NMDA) receptor-gated channels. With this method, the release probability can be calculated from the time course of the blockade of NMDA-receptor mediated postsynaptic currents in the presence of MK-801. At temperatures >32 degrees C, the distribution of release probabilities covered the range from 0.05 to 0.43 [mean: 0.171 +/- 0.012 (SE), n = 65], being skewed toward low values. When estimated at room temperature (22-25 degrees C), the release probabilities were significantly lower (mean: 0.123 +/- 0.009, n = 54), and almost the whole distribution was restricted to values <0.2. Furthermore, warming from room temperature to >32 degrees C led to a pronounced overshooting increase of the release probability. Taken together, the results of the present study show that release probabilities at synapses formed onto layer 2/3 pyramidal cells in the visual cortex vary significantly, but values >0.3 are rare and the results obtained either at room or variable temperature differ significantly from those made under conditions of constant temperature in the physiological range.

Animals↗

PubMed2004

Nitric oxide synthase in rat visual cortex: an immunohistochemical study.

The aim of the present study was to identify the distribution of two isoforms of the nitric oxide synthase (NOS), the neuronal (nNOS) and the endothelial (eNOS) form, in rat visual cortex. Immunohistochemical localisation of each NOS isoform was studied with three tissue-processing protocols. In the first one, immunohistochemical reactions were made on 30-microm-thick sections with membrane detergents, Triton or Saponin, used to increase the permeability of the tissue for the antibodies. In the second protocol, we excluded these detergents from all solutions to avoid a destruction of the cellular membrane. In the third protocol, we used thin paraffin sections (5 microm thick) to assure delivery of the antibodies to intracellular structures. Our data demonstrate, that both neuronal and endothelial isoforms of the NOS are present in the visual cortex. Among the neurones labelled by the antibodies against eNOS or nNOS, some excitatory cells were definitely present. nNOS immunopositive were neurones and a dense network of fibres, presumably axons. Some of the neurones were heavily labelled in a Golgi-like manner, while others showed only weak labelling. eNOS immunopositivity was found in the blood vessels and in neurones. eNOS positive neurones were much more numerous than nNOS-containing cells, and represent about 60% of the cortical cells. However, with antibodies against eNOS, we never observed neurone-specific cell features. The NOS-containing cells found in our present study represent a possible morphological substrate for production of nitric oxide (NO).

Animals↗

PubMed2003

Gamma-frequency fluctuations of the membrane potential and response selectivity in visual cortical neurons.

Fluctuations at frequencies of 25-70 Hz is an inherent property of cortical activity. These rapid, gamma-range fluctuations are apparent in the local field potentials, in spiking of cells and cell groups, and in the membrane potential of neurons. To investigate stimulus dependence of the gamma-frequency fluctuations of the membrane potential, we have recorded intracellularly responses of cells in cat visual cortex to presentation of moving gratings. We found gamma-range fluctuations of the membrane potential in both simple and complex cells. The strength of the gamma-frequency fluctuations correlated with the stimulus optimality. Furthermore, the amplitude of the gamma-frequency fluctuations correlated with the phase of stimulus-imposed slow changes of the membrane potential. The combination of these features makes cortical neurons capable of encoding the slow changes in the visual world in a kind of amplitude modulation of the high frequency fluctuations. This assures reliable transformation of the membrane potential changes into spike responses without compromising the temporal resolution of visual information encoding in the low frequency range.

Action Potentials↗

PubMed2003

Independence of visuotopic representation and orientation map in the visual cortex of the cat.

The representations of visual space and stimulus orientation were mapped in the cat primary visual cortex using electrophysiological recordings supplemented with intrinsic signal optical imaging. The majority of units displaced up to 600 micro m laterally had overlapping RFs both in orientation domains and around singularities of the orientation map. Quantitative comparison of these units revealed only a weak, positive correlation between the difference in their preferred orientations and RF separations (area 17: r = 0.09; area 18: r = 0.15). The occurrence of nonoverlapping RFs could be accounted for by random RF position scatter rather than by orientation difference between the units. Monte Carlo analysis showed that our findings are compatible with a locally smooth and linear representation of visual space that is not coupled to the representation of stimulus orientation. An important functional implication of the above map relationships is that positional information captured by the retina is faithfully transmitted into the cortex.

Animals↗

PubMed2002

A novel mechanism of response selectivity of neurons in cat visual cortex.

The spiking of cortical neurons critically depends on properties of the afferent stimuli. In the visual cortex, neurons respond selectively to the orientation and direction of movement of an object. The orientation and direction selectivity is improved upon transformation of the membrane potential changes into trains of action potentials. To address the question of whether the transformation of the membrane potential changes into spiking of a cell depends on the stimulus orientation and the direction of movement, we made intracellular recordings from the cat visual cortex in vivo during presentation of moving gratings of different orientations. We found that the relationship between the membrane polarization and the firing rate (input-output transfer function) depended on the stimulus orientation. The input-output transfer function was steepest during responses to the optimal stimulus; membrane depolarization of a given amplitude led to generation of more action potentials when evoked by an optimal stimulus than during non-optimal stimulation. The threshold for the action potential generation did not depend on stimulus orientation, and thus could not account for the observed difference in the transfer function. Oscillations of the membrane potential in the gamma-frequency range (25-70 Hz) were most pronounced during optimal stimulation and their strength changed in parallel with the changes in the transfer function, suggesting a possible relationship between the two parameters. We suggest that the improved input-output relationship of neurons during optimal stimulation represents a novel mechanism that may contribute to the final sharp orientation selectivity of spike responses in the cortical cells.

Action Potentials↗