PubMed Health⌕ Search

Biomedical subjects

I G Sil'kis

Publications and source records attributed to I G Sil'kis.

At least 19 recordsLinked to original sources
PubMed2006

Possible mechanisms of the involvement of dopaminergic cells and cholinergic interneurons in the striatum in the conditioned-reflex selection of motor activity.

A possible mechanism for the involvement of cholinergic interneurons in the striatum and dopaminergic cells in the substantia nigra in the selection from among several types of motor activity during learning is proposed. Selection is triggered by simultaneous increases in the activity of dopaminergic neurons and a pause in the activity of cholinergic interneurons in response to the conditioned signal. The appearance of the pause may facilitate activation of GABAergic interneurons in the striatum and the action of dopamine on D2 receptors on cholinergic interneurons. Differently directed changes in dopamine and acetylcholine levels synergistically modulate the efficiency of corticostriatal inputs, such that the rules for modulation of the "strong" and "weak" inputs are opposite in sign. The subsequent reorganization of neuron activity in the cortex-basal ganglia-thalamus-cortex circuit leads to increased activity in those cortical neurons providing "strong" innervation to the striatum with simultaneous decreases in the activity of neurons providing "weak" innervation to the striatum, which may underlie the selection of the movement reaction, in which the neocortex is involved. It follows from this model that if the delay between the conditioned and unconditioned stimuli is not longer than the latent period of the reactions of dopaminergic and cholinergic cells (about 100 msec), selection of movement activity in response to the conditioned signal and learning is hindered.

Acetylcholine↗
PubMed2006

A possible mechanism for the effect of modifiable lateral inhibition in the striatum on the selection of conditioned reflex motor responses.

A mechanism is proposed for the effects of striatal dopamine-modifiable lateral inhibition on the selection of conditioned reflex motor responses. According to this mechanism, activation of dopamine D1 (D2) receptors on strionigral (striopallidal) neurons facilitates long-term depression (potentiation) of the inhibitory inputs simultaneously with potentiation (depression) of the excitatory inputs, of sufficient strength to open NMDA channels. For " weak" excitation, insufficient to open NMDA channels, the modification rules were of the opposite sign. Activation of presynaptic D2 (D1) receptors leads to decreases (increases) in GABA release from strionigral (striopallidal) axon terminals innervating strionigral (striopallidal) cells. As a result, dopamine-modifiable lateral inhibition simultaneously increases both the potentiation (depression) of the excitatory inputs to "strongly" activated strionigral (striopallidal) neurons, increasing (decreasing) their activity, and increases the depression (potentiation) of the excitatory inputs to the "weakly" activated strionigral (striopallidal) neurons, decreasing (increasing) their activity. Subsequent reorganization of neuron activity in the cortex-basal ganglia-thalamus-cortex circuit facilitates selection of conditioned reflex motor responses by further increasing (decreasing) the activity of those motor cortex neurons which were "strongly" ("weakly") excited by the striatum in conditions of dopamine release in response to the conditioned stimulus.

Animals↗
PubMed2004

[Potential mechanisms of effects of endogenous neuromodulators on the interdependent activity of neurons in various nuclei of the basal ganglia].

A possible mechanism of influence of neuromodulators on interdependent activity of neurons in the diverse basal ganglia nuclei is suggested. According to modulation rules, an activation of postsynaptic Gs- or Gq/11-(Gi/0-) protein coupled receptors promotes induction of long-term potentiation (depression) of excitatory inputs to different neurons and augmentation (lowering) of their activity; an activation of presynaptic Gs- or Gq/11-(Gi/0-) protein coupled receptors promotes a rise (decrease) of release of GABA and co-peptides from striatal terminals and glutamate release from subthalamic terminals in the globus pallidus and output nuclei. It follows from the modulation rules that, since identical receptors are present on striatal neuron and their axon terminals, effects of neuromodulator action in diverse basal ganglia nuclei can be summarized. Neuromodulators released from striato-nigral and striato-pallidal fibers could promote interdependent activity of neurons in "direct" and "indirect" pathways through the basal ganglia due to convergence of these fibers on cholinergic interneurons and pallido-striatal cells.

Animals↗
PubMed2004

[Possible mechanisms of firing patterns reorganization of the neurons of the output nuclei basal ganglia].

Previously proposed unitary modification rules and known experimental data were used for understanding possible mechanisms of reorganization of firing patterns of neurons in the output basal ganglia nuclei. According to the suggested mechanism, a switch from regular-spiking to bursting activity evoked by systemic inactivation of N-methyl-d-aspartate (NMDA) receptors or dopaminic receptors mainly depends on modifications of cortico-striatal synapses whereas the opposite effect of inactivation of the same receptors directly on the output basal ganglia cells is less effective. We hypothesized that some of the output basal ganglia nuclei neurons which can generate bursting discharges due to inactivation of NMDA and dopaminic receptors are glutamatergic or cholinergic cells.

Animals↗
PubMed2003

The involvement of dopamine in strengthening cortical signals activating NMDA receptors in the striatum (a hypothetical mechanism).

A possible mechanism is proposed for the enhancement/weakening of those cortical signals in the cortex-basal ganglia-thalamus-cortex neural network which induce/do not induce opening of NMDA channels in the spiny neurons of the striatum and which can be regarded as "strong"/"weak" in terms of this measure. The mechanism is based on the modulatory influences of dopamine on changes in the efficiency of corticostriatal inputs. In the absence of dopamine, relative increases in the intensity of "strong" ("weak") cortical signals can lead to the induction of long-term potentiation (depression) of corticostriatal synapses. In this case, because of the differently directed influences on thalamic cells of signals passing via strionigral and striopallidal cells, "strong" signals at the output of the thalamus are weakened, while "weak" signals are strengthened. Activation of dopamine D1 (D2) receptors on strionigral (striopallidal) neurons may facilitate increases in the extent of long-term potentiation/depression (decreases in the extent of long-term potentiation/depression or induction of long-term potentiation/depression). The consequence of this is that "strong" signals at the output of the thalamus can be strengthened synergistically, while "weak" signals can be weakened synergistically. Background cortical signals evoking tonic release of dopamine in the striatum can decrease strengthening because of weakening of the modulatory influence of dopamine on the modification of corticostriatal synapses.

Animals↗
PubMed2003

A possible mechanism for the effect of neuromodulators and modifiable inhibition on long-term potentiation and depression of the excitatory inputs to hippocampal principal cells.

A postsynaptic mechanism for the influences of various neuromodulators and modifiable disynaptic inhibition on long-term potentiation and depression of the excitatory inputs to granule and pyramidal neurons in the hippocampus is described. According to this mechanism, facilitation of the induction of long-term depression/potentiation at the excitatory input to the inhibitory interneuron induced by the action of a neuromodulator on a receptor bound to a G(i/0)/(Gs or G(q/11)) protein can lead to decreases/increases in GABA release, weakening/strengthening of the inhibitory action on the target cell, and improvement in the conditions for induction of long-term potentiation/depression of the excitatory input to this cell. In the absence of inhibition, the same neuromodulator, activating the same type of receptors on the target cell, would facilitate induction of long-term depression/potentiation in that cell. The resultant effect of the action of the neuromodulator on the target cell depends on the ratio of the "strengths" of the excitatory and inhibitory inputs to the cell, on the presence on the interneuron and the target cell of the same or different types of receptors sensitive to this neurumodulator, and on the concentration of the neurumodulator, because of its different affinities for the receptors through which its differently directed effects on postsynaptic processes are mediated. Predictions based on this mechanism are in agreement with known experimental data.

Animals↗
PubMed2002

[Possible mechanism of cannabinoid-mediated modulation of signal transduction through the basal ganglia].

A possible mechanism of cannabinoid-mediated akinesia is suggested. This effect is proposed to be the consequence of a decrease in LTD/LTP in cortical inputs to striatopallidal/striatonigral cells in the matrix due to CB1 receptor activation. In addition, cannabinoids can attenuate locomotor activity due to a reducing of glutamate/GABA release from axon terminals of subthalamic nucleus/striatonigral cells of matrix and subsequent decrease/increase in the activity of neurons of globus pallidus/substantia nigra pars reticulata. Cannabinoid-mediated rise of dopamine release might be a result of a decrease of dopamine neuron inhibition by striatonigral cells of striosomes. It follows from the suggested mechanism that an inactivation (activation) of CB1 receptors leading to rise (lowering) of the motor activity can be useful for treatment of Parkinson (Huntington) disease.

Animals↗
PubMed2001

[Mechanisms of effects of adenosine and dopamine on modification of synapses in striato-nigral and striato-pallidal neurons].

On the basis of earlier suggested unitary mechanism of synaptic plasticity opposite effects of adenosine and dopamine on the cAMP concentration in striatal spinal cells can emphasize the well known antagonistic interactions between A2A and D2 receptors on striatopallidal cells and between A1 and D1 receptors on striatonigral cells. This is due to that both the dopamine agonist and adenosine antagonist must promote the induction of long-term potentiation/depression of efficacy of excitatory cortical inputs to striatopallidal/striatonigral cells. This modification must lead to synergistic disinhibition of thalamic cells via "direct" and "indirect" pathways through basal ganglia and subsequent strengthening of motor activity.

Adenosine↗
PubMed2001

[Involvement of dopamine in amplification of cortical signals activating NMDA-receptors in the striatum (hypothetic mechanism)].

Possible mechanisms of amplification/attenuation of cortical signals opening or not opening NMDA-channels in striatal spine cells while passing through basal ganglio-thalamocortical network and relegated to either "strong" or "weak" signals, are considered. In absence of dopamine, a relative increase in intensity of the "strong" or "weak" cortical signals should result in the LTP/LTD on both striatonigral and striatopallidal cells, the thalamic cells being affected in the opposite way. Activation of the dopamine receptors on the striatonigral (striatopallidal) cells prompts the LTP/LTD expression. Thereof, the "strong" cortical signals are synergistically amplified whereas the "weak" signals are synergistically attenuated at the thalamic output.

Corpus Striatum↗
PubMed2000

[Interconnected biochemical processes in striatal neurons induced by activation of excitatory, inhibitory, and dopamine inputs].

Postsynaptic processes induced by glutamate, GABA, and dopamine in dendritic spines of inhibitory striatal neurones, were studied. Some functional features were revealed in striatal neurones activation of two protein kinases, cAMP-dependent PKA and cGMP-dependent PKG; presence of calcium/calmodulin-independent adenylate cyclase; bidirectional changes of the cAMP concentration with dopamine. Rise of the cGMP concentration in striatum seems to be a result of activation of the membrane-bound guanylate cyclase via the GABAb receptors. The findings suggest that the active protein kinases/phosphatases ratio is affected by calcium influx through the NMDA-channels.

Adenylyl Cyclases↗
PubMed2000

[Unified postsynaptic mechanism of plasticity in the striatum, neocortex, hippocampus, and cerebellum].

The unitary postsynaptic mechanism of plasticity in striatum, neocortex, hippocampus and cerebellum involves the LTP/LTD excitation as result of AMPA and NMDA receptor phosphorylation/dephosphorylation, while the LTP/LTD of inhibition is the result of the GABA receptor phosphorylation/dephosphorylation. It follows from this mechanism that when NMDA channels are closed, the determinant role in receptor phosphorylation is played by the PKG. When the NMDA channels are open, the determinant role in receptor phosphorylation is played by the PKC and CaMKII.

Animals↗
PubMed1998

[Effect of high frequency cortical microstimulation on the interhemisphere synchronization in the rat motor cortex].

Long-term posttetanic changes of callosal neurons' synchronisation was studied in the rat motor cortex. Following tetanisation, the synchronisation of previously active cells decreased whereas the cells that became active were mostly synchronised. Ultra "narrow" peaks appeared in callosal interactions and correlated with "intermediate" (30-80 ms) those.

Action Potentials↗
PubMed1998

[Characteristics and mechanisms of the interhemisphere synchronization in the rat motor cortex].

Synchronised activity of the callosal cells was studied in the rat motor cortex. Cross-correlation analysis revealed narrow symmetrical peaks (less than 20 ms) and intermediate ones (30-80 ms). Common neuron(s) located in one hemisphere reciprocally connected callosal cells can play the role of a "common input" that synchronises discharges of the cells in both hemispheres. The narrow and intermediate peaks seem to be mediated by mono- and polysynaptic connections, resp.

Action Potentials↗
PubMed1979

[Feedback inhibition in microsegments of the visual cortex].

Interaction between 3-4 neighbouring neurons in the visual cortex of awakening cats was examined using a cross-correlation analysis. In some microsystems neurons revealed a tendency towards synchronized activity indicating a shared excitatory input. In other microsystems asymmetrical interaction was observed: neurons with larger spike amplitudes exhibited excitatory effect on neurons with smaller spike amplitudes (latent period about 5 ms) and neurons with small spike amplitudes inhibited neurons with large spike amplitudes (latent period 1-8 ms, duration of inhibition 30-200 ms). Suggestions were made about the existence of recurrent inhibition and inhibitory interneurons in microsystems of the visual cortex.

Animals↗