Armen Sargsyan

L. A. Orbeli Institute of Physiology NAS RA, Ayrivan, Yerevan, Armenia

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Publications (4)7.95 Total impact

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    ABSTRACT: We suggest a new method for calculation of extracellular field potentials generated by a large population of pyramidal cells (PCs), using a single PC compartmental model. Similar methods described earlier use the assumption that the intracellular potential or current distributions of the cells within the population are much alike as a result of simultaneous activation at about the same longitudinal location (i.e., all the PCs in the population are located on the same level and are ideally synchronized). However, the degree of synchronization of natural firing even during synchronized rhythmic discharges in the cortex is not as high. We introduce the possibility to vary the degree of synchronization of the PCs' activity in the population, thus taking into account disperse timing of cortical pyramidal cells' firing. The temporal variability in cell firing is described by a Gaussian distribution, the width of which defines the degree of synchronization/desynchronization. In addition, the suggested method allows for certain spatial spread of PCs in the population along longitudinal axis of the PCs. The method was applied to test the assumption that the transition from sleep spindles to rhythmic spike and wave discharges (SWDs) observed in absence epilepsy may occur due to an increase in pyramidal cells' firing synchronization. We show that in case of weak synchronization of PC firing in the population, the shape of field potential during rhythmic thalamic input is similar to the oscillations during a sleep spindle, while at stronger synchronization of PCs, it looks much more as a SWD, with clear expressed spikes and waves. This suggests that in large population of pyramidal cells the changes in the degree of synchronization of cell firing may explain the changes in the shape of field potential from spindle oscillations to SWDs and vice versa.
    Journal of Neuroscience Methods 09/2007; 164(1):161-76. · 1.96 Impact Factor
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    ABSTRACT: Activity-dependent synaptic plasticity has important implications for network function. The previously developed model of the hippocampal CA1 area, which contained pyramidal cells (PC) and two types of interneurons involved in feed-forward and recurrent inhibition, respectively, and received synaptic inputs from CA3 neurons via the Schaffer collaterals, was enhanced by incorporating dynamic synaptic connections capable of changing their weights depending on presynaptic activation history. The model output was presented as field potentials, which were compared with those derived experimentally. The parameters of Schaffer collateral-PC excitatory model synapse were determined, with which the model successfully reproduced the complicated dynamics of train-stimulation sequential potentiation/depression observed in experimentally recorded field responses. It was found that the model better reproduces the time course of experimental field potentials if the inhibitory synapses on PC are also made dynamic, with expressed properties of frequency-dependent depression. This finding supports experimental evidence that these synapses are subject to activity-dependent depression. The model field potentials in response to various randomly generated and real (derived from recorded CA3 unit activity) long stimulating trains were calculated, illustrating that short-term plasticity with the observed characteristics could play specific roles in frequency processing in hippocampus and thus providing a new tool for the theoretical study of activity-dependent synaptic plasticity.
    Journal of Neuroscience Methods 06/2004; 135(1-2):175-91. · 1.96 Impact Factor
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    ABSTRACT: We propose a general computer model of a synapse, which incorporates mechanisms responsible for the realization of both short- and long-term synaptic plasticity-the two forms of experimentally observed plasticity that seem to be very significant for the performance of neuronal networks. The model consists of a presynaptic part based on the earlier 'double barrier synapse' model, and a postsynaptic compartment which is connected to the presynaptic terminal via a feedback, the sign and magnitude of which depend on postsynaptic Ca(2+) concentration. The feedback increases or decreases the amount of neurotransmitter which is in a ready for release state. The model adequately reproduced the phenomena of short- and long-term plasticity observed experimentally in hippocampal slices for CA3-CA1 synapses. The proposed model may be used in the investigation of certain real synapses to estimate their physiological parameters, and in the construction of realistic neuronal networks.
    Neural Networks 11/2003; 16(8):1161-77. · 2.08 Impact Factor
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    ABSTRACT: A computer model of the hippocampal CA1 area, which receives synaptic inputs from CA3 neurons via the Schaffer collaterals, was constructed. Pyramidal cells (PC) and two types of interneurons were represented by compartmental models, and mechanisms of feed-forward inhibition (FFI) and recurrent inhibition were incorporated. Four types of receptor mediated synaptic conductances were used in the model: those of AMPA, GABA(A), GABA(B) and N-methyl-D-aspartate (NMDA). The output of the model, i.e. the field potential calculated at various points in space, was able to qualitatively reproduce the main features of field potentials, which were recorded in hippocampal slices maintained in vitro for both subthreshold and suprathreshold stimulation. In both the experiments and the model, the influence of NMDA and GABA synaptic currents affected mostly the late, decaying phase of evoked field potentials. The modeled interaction of NMDA and GABA components could explain the enhancement of the field potential late phase, which was observed experimentally during paired-pulse stimulation.
    Journal of Neuroscience Methods 02/2001; 104(2):143-53. · 1.96 Impact Factor

Publication Stats

24 Citations
7.95 Total Impact Points


  • 2003–2007
    • L. A. Orbeli Institute of Physiology NAS RA
      Ayrivan, Yerevan, Armenia
  • 2001
    • University of Patras
      • School of Medicine
      PatrĂ­s, Kentriki Makedonia, Greece