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Biomedical subjects

S I Igon'kina

Publications and source records attributed to S I Igon'kina.

At least 19 recordsLinked to original sources
PubMed2003

Role of 5-HT3 receptors in the mechanisms of central pain syndrome.

Electrophysiological and behavioral studies showed that spinal 5-HT3 receptors are involved in the regulation of pain sensitivity in rats. Intrathecal administration of the 5-HT3 receptor antagonist tropine (200 microg) produced allodynia, reduced the threshold, decreased the latency, and increased the number of spikes in the late component of the nociceptive flexion reflex. Intrathecal administration of 5-HT3 receptor agonist quipazine (200 mg) abolished nociceptive flexion reflex and alleviated spinal pain syndrome produced by impairment of GABAergic inhibition in the lumbar spinal segments. Our results indicate that spinal 5-HT3 receptors are involved in the modulation of pain sensitivity: activation of these receptors inhibits nociceptive reactions, while blockade of 5-HT3 receptors potentiates the nociceptive response via modulation of excitability of GABAergic interneurons.

Animals↗
PubMed2003

[Immunologic aspects of pathologic pain].

The scientific review is devoted to an analysis of neuro-immune aspects of the pathological pain and to the role of disregulation between the central nervous system (CNS) and the immune system in triggering the mechanisms of such pain. The importance of anti-inflammatory cytokines (interleukins, and tumor necrosis factor) as well as of autoantibodies to neuro-mediators in the pathogenesis of different forms of hyperalgetic conditions is evaluated. New data are discussed, which are related with the possibility of modulating the antibodies to neuro-transmitters (serotonin and catecholamines) of experimental neuropathic pain syndromes.

Humans↗
PubMed2001

Effect of antiserotonin antibodies on bioelectrical activity of sensorimotor cortex.

The effect of antiserotonin antibodies on basal electrocorticogram was studied in electrophysiological experiments on rats. Intracortical injection of 10 microg antiserotonin antibodies into the sensorimotor cortex induced epileptiform activity in this area. It is assumed that antiserotonin antibodies modulate activity of cortical neurons due to both binding serotonin molecules and interaction with serotonin receptors.

Animals↗
PubMed1993

[The effect of catecholamine and serotonin antibodies on pain sensitivity and the development of morphine tolerance in experimental drug addiction].

The effect of antibodies to catecholamine and serotonin on the thermal pain sensitivity and tolerance to morphine was studied in rats immunized by protein-conjugated neurotransmitters before chronic drug intoxication. The antibodies to catecholamine have been found to affect bifunctionally on the nociception bifunctionally: either accelerating or delaying the pain reaction to thermal irritation. The antibodies to serotonin were ineffective as modulators both of the pain sensitivity and tolerance to morphine development. In contrast, the antibodies to catecholamine suppressed the expression of tolerance to chronic morphine. Serotonin antibodies virtually produced no effects on pain sensitivity and the development of morphine tolerance.

Animals↗
PubMed1992

[Epileptiform activity in the somatosensory cortex of rats with trigeminal neuralgia].

It was shown in experiments on rats that penicillin 1 microliter microinjection (100 U) into the caudal nucleus of the spinal tract of the trigeminal nerve, accounting for formation of a generator of pathologically enhanced excitation (GREE), brings about in rats the pain syndrome with characteristic for trigeminal neuralgia behavioural manifestations and the emergence of epileptiform activity in the somatosensory cortex, especially pronounced in the contralateral hemisphere. The emergence of this activity reflects, on the one hand, the action of the GREE in the caudal nucleus of the trigeminal nerve and, on the other hand, the involvement of the somatosensory cortex taking over stimulation from the hyperactive caudal nucleus, into formation of a pathological algic system of this form of trigeminal neuralgia.

Animals↗
PubMed1991

[Effects of C-terminal fragment of substance P-CP 5-11 on the activity of neurons of the dorsal raphe nucleus].

The experiments on Wistar rats showed that microinjection of C-terminal fragment of substance P-CP5-11 (1 microgram) into one of the antinociceptive system structure--dorsal raphe nucleus, caused a prolonged (24 hours of observation) analgetic effect by the hot plate test. Neuronal activity of dorsal raphe nucleus simultaneously enhanced. The CP5-11 antinociceptive activity was higher than the CP1-11 one. The conclusion is that CP1-11 and in particular its C-terminal fragment CP5-11 play a role in activation of antinociceptive system.

Analgesics↗
PubMed1991

[The microcirculatory system in hamsters in a model of central pain syndromes].

Experimental models of central pain syndromes, namely, trigeminal neuralgia (TN) and a pain syndrome of spinal origin, were developed in Syrian hamsters. Microhemocirculatory disorders, increased venular permeability, and increased mast cell degranulation in the mucosa of the cheek pouches were revealed. The importance of studying microcirculation in the cheek pouches of hamsters, especially in experimental TN is discussed, because appraisal of microcirculation in both pouches allows the beginning of generalization disorders to be determined.

Animals↗
PubMed1991

[Microcirculatory changes in experimental trigeminal neuralgia in rats].

Biomicroscopic studies of mesentery in trigeminal neuralgia rats caused by creation of a generator of pathologically enhanced excitation in trigeminal nerve caudal nucleus (injection 0.25-1.0 DLM Tetanus toxin) have shown the microcirculatory disorders, venular permeability, mast cells degranulation, and an increase in lymphatic contractile activity. Microcirculatory disorders intensity and adaptation reaction appearance correlated with trigeminal neuralgia clinical picture.

Animals↗
PubMed1990

[Changes in electric activity of neurons of dorsal raphe nuclei in the development of generator of pathologically enhanced excitation in the nociceptive system].

In the experiments on rats it was proved by the method of extracellular registration of impulse neuron activity of dorsal raphe nucleus, that the formation of generator of pathologically enhanced excitation (GPEE) in nociceptive structures of spinal brain underlying the pain syndrome of spinal origin, results in a change of electric neuron activity of dorsal raphe nucleus. These changes are manifested by growing number of background nucleus neurons, the increase of middle frequency of discharges, and assuming pack character of impulse activity. These changes are greater marked in a ventral nucleus part, than in a dorsal one, which is evident of the activation of this antinociceptive system structure. The changes of electric activity of dorsal raphe neurons are stable for a long time after GPEE is formed in nociceptive system, and participate in suppression of GPEE and corresponding pain syndrome.

Animals↗
PubMed1990

[Effects of verapamil on behavioral and microcirculatory disorders in pain syndrome of spinal etiology].

In the experiments on Wistar rats with pain syndrome of spinal origin (PSSO) caused by the generator of pathologically enhanced excitation (GPEE) in dorsal horns of the spinal cord lumbosacral segments, it was shown that the intravenous verapamil injection (1.25 mg/kg) undoubtedly decreased behaviour response and improves the state of microcirculation. The compound of 10-fold decreased dose does not affect the behaviour response and microcirculation. When PSSO exists, the intravenous injection of analgin (150 mg/kg) produced an effect on the behaviour response and does not produce any action on microcirculation. When verapamil reaches the dorsal surface of the spinal cord (GPEE area) it decreases the behaviour response and microcirculation disorders created in PSSO. The obtained data make it clear that the GPEE depression caused by the verapamil calcium channel blocker weakens PSSO and normalizes the microcirculation.

Animals↗
PubMed1989

[The effect of substance P on the neuronal activity of the antinociceptive system].

The experiments on rats showed that the 1 micrograms substance P injection to dorsal raphe nucleus caused prolonged (24 hours of study) analgetic effect--it enhances the reaction latent period to thermal nociceptive stimulation, intensifies the background impulse activity, rises the middle frequency of neuron discharges and creates high-frequency neurons as well as the neurons with burst impulse activity. The supposition is being confirmed that the mechanism of antinociceptive structures activation leads to analgesia caused by substance P.

Animals↗
PubMed1988

[Effects of substance P and its fragments in physiological and pathological pain].

It has been shown that substance P and its fragments can produce under certain conditions an analgetic effect on both physiological and pathological pain (i.e. on pain syndrome of spinal origin). The data obtained give evidence that prolonged hypoalgesia is caused by the injection of substance P and its fragments to nucleus raphe dorsal--a structure of the antinociceptive system. This analgetic effect can be initiated by the activation of the antinociceptive system influenced by substance P and or its fragments.

Animals↗
PubMed1987

[Effect of the spinal pain syndrome on pain reactions caused by nociceptive thermal stimuli].

It has been shown that the reaction of both limbs to thermal pain stimulation was suppressed during spinal pain syndrome development caused by generators of pathologically enhanced excitation (GPEE) formed in the dorsal horns of the spinal cord lumbosacral segments on one side. The analgetic effect on physiological pain was retained long after pain syndrome disappearance (48 hours), the effect was bilateral and was independent of the type of agent producing GPEE. It was shown that neuronal activity in the antinociceptive system key structure (nucleus raphe dorsal) increases. It is assumed that physiological pain relief is caused by enhanced activity in antinociceptive system structures in pain syndrome.

Analgesia↗