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On cats, we studied the influence of stimulation of the Raphe nuclei (RN) on postsynaptic processes evoked in neurons of the somatosensory cortex by stimulation of nociceptive (intensive stimulation of the tooth pulp) and non-nociceptive (moderate stimulation of the ventroposteromedial--VPN--nucleus of the thalamus) afferent inputs. 6 cells, selectively excited by stimulation of nocciceptors and 9 cells, activated by both the above nociceptive and non-nociceptive influences (nociceptive and convergent neurons, respectively) were recorded intracellular. In neurons of both groups, responses to nociceptive stimulation (of sufficient intensity) looked like an EPSP-spike-IPSP (the letter of significant duration, up to 200-300 ms) compleх. Conditioning stimulation of the RN which preceded test stimulus applied to the tooth pulp or VPM nucleus by 100 to 800 ms, induced 40-60 % decrease of the IPSP amplitude only, while maхimal effect of influence, in both cases, was noted within intervals of 300-800 ms between conditioning and test stimulus. During stimulation of the RN, serotonin released via receptor and second messengers, provides postsynaptic modulation of GABAergic system, decreasing the IPSP amplitude which occurs after stimulation of both the tooth pulp and VPM thalamic nucleus. This process may be realized trough either pre- or postsynaptic mechanisms.

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Inversion of the early component of IPSPs in neurons of the sensorimotor cortex by artificial hyperpolarization of the membrane was demonstrated in cats immobilized by myorelaxants in acute experiments. The late component of IPSP was not inverted. Amplitudes of the early component of IPSPs were decreased by the membrane depolarization while the late component was completely reduced. The input resistance of the membrane which decreased during the early component of IPSPs was restored to the initial level during the late component.

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In acute experiments on immobilized cats intracellular injection of Ca+ decreased of IPSP and postburst hyperpolarization amplitudes in pyramidal neurons of the sensorimotor cortex. Intracellular injection of ethylene glycol tetraacetic acid had almost the same effect. This substance also reduced the late part of spike afterhyperpolarization, while the early part remained practically unchanged. It is concluded that Ca2+-dependent K+-conductance might play an important role in the genesis of IPSP, postburst and spike afterhyperpolarization in the membrane of pyramidal neurons of the cat sensorimotor cortex.

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Evoked potentials to stimulation of the ventrolateral and intralaminar thalamic nuclei, the surface of the sensomotor cortex, and the pyramidal pathways, derived from the same point, and also corresponding postsynaptic responses of pyramidal neurons were studied in acute experiments on cats anesthetized with ether or superficially with pentobarbital (25-30 mg/kg, intraperitoneally), and immobilized with muscle relaxants. Surface application of strychnine inhibits the slow negative potential arising in response to direct and primary responses, and the corresponding slow potentials of the IPSP. The action of iontophoretic application of strychnine on IPSP of pyramidal neurons and responses of cortical glial cells also were studied. Both methods of application of strychnine block mainly the early component of the IPSP, during which the input resistance is significantly lower than that during the late component, evidence of their different genesis. The results of the investigation show that slow negative potentials are a reflection of hyperpolarization of pyramidal neurons, and that the separate components of the responses have a common genesis.

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Intracellular correlates of evoked rhythmic cortical "spike-and-wave" potentials produced in sensorimotor cortex during 3/s stimulation of the thalamic relay nucleus (VPL) and of self-sustained "spike-and-wave" afterdischarges following 8-14/s stimulation of the same nucleus were studied in acute experiments on cats immobilized by myorelaxants. Intracellular recordings of pyramidal tract neurons revealed that different components of evoked "spike-and-wave" potentials, i. e. the spike-like negative wave and the long lasting negative wave, are postsynaptic in origin: the first is due to EPSPs with spike discharges, and the latter--to IPSPs of cortical neurons. Components of "spike-and-wave" afterdischarge mostly reflect the paroxysmal depolarizing shifts of the membrane potential of cortical neurons. After cessation of sustained "spike-and-wave" activity the long-lasting hyperpolarization accompanied by inhibition of spike discharges and subsequent recovery was observed in cortical neurons. It is presumed that the negative wave of the evoked "spike-and-wave" potential as well as slow negative potentials of direct cortical and primary responses reflect IPSPs of deeper parts of pyramidal tract neurons, while the waves of the sustained "spike-and-wave" afterdischarges are due to paroxysmal depolarizing shifts in cortical neurons.

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The intracellular activity of pyramidal tract neurons during electrical stimulation of ventro-lateral and ventro-postero-lateral nuclei of thalamus was studied in acute experiments on cats immobilized by myorelaxants. Both somatic and presumably dendritic spikes (d-spikes) were observed. The latter were characterized by relatively low and variable (5-60 mV) amplitude; d-spikes occurred both spontaneously and in response to single shock and tetanic (8-14/s) stimulation of the thalamus. They were also induced by intracellular depolarizing current pulses and thalamic stimulation following iontophoretic application of strychnine. Simultaneously generated somatic and d-spikes revealed no collision between each other. Intracellular hyperpolarizing current pulses abolished only somatic spikes, while d-spikes were not affected. Dendritic origin with multiple generation zones of these variable spikes is suggested. Possible functional role of d-spike is discussed.

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Inversion of the early component of IPSPs in pyramidal neurons of the sensorimotor cortex by intracellular injection of chloride ions was demonstrated in cats immobilized by myorelaxants in acute experiments under moderate composed anesthesia (40 mg/kg nembutal and 20 mg/kg chloralose intraperitoneally). The late component of IPSPs as well as the post-burst hyperpolarization in pyramidal neurons were not inverted. It is concluded that during the early component of IPSPs of both pyramidal and nonpyramidal neurons the membrane permeability is increased for chloride ions, while both the late component of IPSPs and the post-burst hyperpolarization in pyramidal neurons are less dependent on the chloride permeability.

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In acute unanesthetized immobilized cats a sequence of fast hyperpolarization and long-lasting depolarization was found in pyramidal tract neurons of the sensorimotor cortex during tetanic stimulation (8-14/s for 10 s) of the ventro-postero-lateral nucleus of the thalamus. During long-lasting depolarization after cessation of stimulation self-sustained rhythmic paroxysmal depolarizing membrane potential shifts appeared which were terminated by long-lasting hyperpolarization. In glial cells only depolarization was observed during stimulation as well as during self-sustained "spike-and-wave" rhythmic activity. Hyperpolarization in glial cells appeared only after its termination in neurons. It is suggested that the long-lasting changes in the membrane potential of cortical elements may play a particular role in formation and cessation of "spike-and-wave" rhythmical activity.

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In acute experiments on immobilized cats, potentials evoked by stimulation of the ventrolateral and intralaminar thalamic nuclei, of the surface of the sensorimotor cortex and pyramidal pathways as well as the corresponding postsynaptic responses of pyramidal neurons, were studied. A negative shift of potential in response to tetanic stimulation of the cortical surface or thalamic nucleus occurred on the cortical surface. Concominantly, intracellular recording of the glial-cell activity was performed. Superficial application of strychnine induced the suppression of the slow-negative potential arising during direct cortical and primary responses and the corresponding slow potentials of IPSP. The effects of iontophoretic application of strychnine on IPSP of pyramidal neurons and cortical glial-cell response were also studied. Both ways of application appeared to block mainly the early component of IPSP during which the input resistance was significantly lesser than that of the late component, pointing to the difference in their genesis. The findings indicate that slow-negative potentials reflect hyperpolarization of pyramidal neurons, while the separate components of responses have common genesis.

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In acute experiments on cats under light nembutal anaesthesia, immobilized by myorelaxants, superficial application of strychnine was shown to suppress the slow negative potentials (arising during direct and primary cortical responses) and IPSPs of the pyramidal neurons corresponding to the slow negative potentials. Iontophoretic application of strychnine blocks predominantly the early component of IPSP during which the input resistance is significantly less than that of the late component indicating their different genesis. It is concluded that individual components of evoked potentials have a common genesis, the slow negative potential is the reflection of the IPSP of pyramidal neurons whose early component seems to be generated by axo-somatic synapses while the late one by axo-dendritic inhibitory synapses. Neurotransmitters in these inhibitory synapses may be different.

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Intracellular neuronal and glial activity in response to tetanic stimulation of the cortical surface or thalamic nuclei and accompanying cortical surface negative potential shifts were recorded in lightly nembutalized curarized cats. Glial cells responded to such stimulation by slow depolarization which under certain conditions of stimulation was replaced by slow hyperpolarization. Neurons responded by hyperpolarization. No correlations between depolarization and hyperpolarization of glial cells as well as between neuronal hyperpolarization and negative surface potential shifts were shown at simultaneous recordings of such shifts and glial neuronal responses. It is suggested that the negative surface potential shift is of a complex origin and is produced by both glial and neuronal somatic and dendritic responses.

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Evoked responses of the motor cortex (dendritic and slow negative potentials) elicited by its direct electrical stimulation, primary, nonspecific and antidromic responses elicited by stimulation of ventrolateral and intralaminar thalamic nuclei and pyramidal pathways and the respective postsynaptic responses of neurons were studied in acute experiments on curarized cats. The potentials evoked during direct cortical stimulation, as well as during stimulation of specific and nonspecific thalamic nuclei and pyramidal pathways were recorded from one and the same point of the motor cortex, while the respective intracellular responses--from one and the same neuron. It is demonstrated that slow negative potentials evoked under these stimulation conditions and the corresponding IPSP follow an identical time-course. The results obtained indicate that the slow negative potential is the reflection of hyperpolarization of pyramidal neurons. The individual components of various evoked potentials recorded from the cortical surface are supposed to be of common genesis.

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