Correlation between the amplitude of action potentials and the rate of conduction along axons of the output cells of the sensomotor cortex

Antidromic responses of neighbouring neurones in micro-areas of the sensorimotor cortex to the stimulation of fibers of the pyramidal tract as well as of the red nucleus and thalamic nuclei VPL and MGB, were studied in acute experiments on unanesthetized immobilized cats. Depending on the velocity of conduction along the axon, the neurones of all the categories were divided into fast and slow cells. When examining the two neuronal groups most differing in AP amplitude (N1 and N3), it was found that N1 neurones were mainly fast-conducting and N3 neurones-- slow-conducting. The conclusion is made that at multineuronal recording, each of the examined categories of the output neurones is characterized by positive correlation between AP amplitude and the axon conduction velocity and consequently, the size of the cell.     

Plant virus infection development as affected by heavy metal stress

The work was focused on the investigation of possible dependencies between the development of viral infection in plants and the presence of high heavy metal concentrations in soil. Field experiments have been conducted in order to study the development of systemic tobacco mosaic virus (TMV) infection in Lycopersicon esculentum L. cv. Miliana plants under effect of separate salts of heavy metals Cu, Zn and Pb deposited in soil. As it is shown, simultaneous effect of viral infection and heavy metals in tenfold maximum permissible concentration leads to decrease of total chlorophyll content in experiment plants mainly due to the degradation of chlorophyll a. The reduction of chlorophyll concentration under the combined influence of both stress factors was more serious comparing to the separate effect of every single factor. Plants' treatment with toxic concentrations of lead and zinc leaded to slight delay in the development of systemic TMV infection together with more than twofold increase of virus content in plants that may be an evidence of synergism between these heavy metal's and virus' effects. Contrary, copper although decreased total chlorophyll content but showed protective properties and significantly reduced amount of virus in plants.     

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.     

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.     

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.     

Interrelated modification of excitatory and inhibitory synaptic connections in the olivary-cerebellar neuronal network

The model of simultaneous interrelated modification in the efficacy of synaptic inputs to different neurons of the olivary-cerebellar network is developed. The model is based on the following features of the network: simultaneous activation of the input layer (granule) cells and the output layer (deep cerebellar nuclei) cells by mossy fibers; simultaneous activation of Purkinje cells and cerebellar cells of the input and output layers by climbing fibers and their collaterals; the existence of local feedback excitatory, inhibitory, and disinhibitory circuits. The rise (decrease) of posttetanic Ca2+ concentration in reference to the level produced by previous stimulation causes the decrease (increase) in cGMP-dependent protein kinase G activity, and increase (decrease) inprotein phosphatase 1 activity. Subsequent dephosphorylation (phosphorylation) of ionotropic receptors results in simultaneous LTD (LTP) of the excitatory input together with the LTP (LTD) of the inhibitory input to the same neuron. The character of interrelated modifications of synapses at different cerebellar levels strongly depends on the olivary cell activity. In the presence (absence) of the signal from the inferior olive LTD (LTP) of the output cerebellar signal can be induced.     

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.     

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.     

A unified postsynaptic mechanism for the effect of various neuromodulators on modification of potentiated and depressed inputs to hippocampal cells (hypothesis)

The unitary postsynaptic mechanism underlying the influence of diverse neuromodulators on modification of excitatory and inhibitory inputs to granule, pyramidal and inhibitory hippocampal cells is suggested. According to this mechanism, the effect of dopamine, adenosine, acetylcholine, noradrenaline, serotonin, somatostatin, galanin, opioids, cannabinoids, neuropeptide Y on postsynaptic receptors, bound to Gi/0 proteins, should promote LTD of excitatory inputs and LTP of inhibitory inputs. The effect of dopamine, adenosine, acetylcholine, noradrenaline, serotonin, vasopressin, tachykinin, histamine on postsynaptic receptors, bound to Gs and Gq/11 proteins, should oppositively modulate the same inputs. Only synaptically activated excitatory and inhibitory inputs can by influenced by neuromodulators. The character of neuromodulatory influence on modification of hippocampal synaptic efficacy, implying from the suggested mechanism is in accordance with known experimental data.