Effect of Anti-Norepinephrine Antibodies on the Development of Neuropathic Pain.

The study focuses on induction of autoantibodies directed against neurotransmitter norepinephrine during neuropathic pain syndrome and on the effect of immunization with norepinephrine-protein conjugated antigen on the development of this syndrome. The formation of anti-norepinephrine antibodies aggravated and prolonged neuropathic pain.

Analgesic Effect of Xenon in Rat Model of Inflammatory Pain.

The analgesic effects of inert gas xenon were examined on rats. The formalin model of inflammatory pain, tail-flick test, and hot-plate test revealed the antinociceptive effects of subanesthetizing doses of inhalation anesthetic xenon. Inhalation of 50/50 xenon/oxygen mixture moderated the nociceptive responses during acute and tonic phases of inflammatory pain.

[Analgesic effects of cannabinoids on central pain syndrome].

It was shown that cannabinoids anandamide, HU210 and WIN 55,212-2 inhibit both spontaneous episodes of pain and mechanical allodynia in rats with central pain syndrome caused by disturbance of inhibitory processes in the dorsal horns of lumbar spinal cord. The analgesic effect is most pronounced in the intrathecal route of administration. The intensity of analgesic actions of cannabinoids on the central pain syndrome in rats, depending on the drug is as follows: HU210 > WIN 55,212-2 > anandamide.

Role of cannabinoid receptor agonists in mechanisms of suppression of central pain syndrome.

We studied the effect of cannabinoid receptor agonists anandamide and WIN 55,212-2 on the central pain syndrome induced by intraspinal injection of penicillin sodium salt in rats. Cannabinoids suppressed allodynia and spontaneous attacks in rats with the central pain syndrome. The analgesic effect was most pronounced after intrathecal injection of cannabinoid receptor agonist in a dose of 100 microg in 10 microl. After systemic treatment the analgesic effect was produced by only WIN 55,212-2 in a dose of 1 mg/kg. WIN 55,212-2 was superior to anandamide by the duration and intensity of the effect on allodynia and spontaneous attacks.

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.

[Immunologic aspects of pathologic pain]. / Immunologicheskie aspekty patologicheskoi boli.

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.

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.

[Effect of dopamine antibodies on neuropathic pain syndrome in rats]. / Vliianie antitel k dopaminu na razvitie neiropaticheskogo bolevogo sindroma u krys.

Dopaminergic brain system plays an important role in regulation of pain sensitivity. However, the data on participation of antidopamine antibodies in the development of neurogenic pain are absent. This work was aimed at the study of the role of antidopamine antibodies in the development of pain syndrome induced by the injury of nn. ischiadic and saphenous in rats. It was shown that after the nerve injury, the behavioral reaction such as autotomy (self-injury) appeared as a feature of the experimental neuropathic pain syndrome. It was originally established that the development of neuropathic pain syndrome induced by the injury of peripheral nerves was accompanied by induction of dopamine autoantibodies. It was also shown that immunization of the animals with conjugated dopamine-protein autigen resulted in aninerease of autidopamine antibody level and an amplification of the experimental neuropathic pain syndrome, i.e., decrease in the latency of the first autotomy, increase in expression of autotomies, and increase in the number of animals with late autotomies.

[The effect of serotonin antibodies on the development of a neuropathic pain syndrome]. / Vliianie antitel k serotoninu na razvitie neiropaticheskogo bolevogo sindroma.

Serotoninergic and catecholaminergic neurotransmitter systems of the brain play an important role in the regulation of pain sensitivity. However, there are no data on the involvement of antibodies to the above neurotransmitters is the development of neuropathic pain syndromes. The authors' studies indicated that the development of neuropathic pain syndrome occurring after nerve damage is followed by the formation of serotonin antibodies and their enhanced induction caused by immunization of animals with serotonin-protein conjugated antigen aggravates the pain syndrome. Block and insufficiency of the serotoninergic antinociceptive system may be a cause of the progression of the pain syndrome due to serotonin antibodies.

[The effect of hydrocortisone on a neurogenic pain syndrome in rats]. / Vliianie gidrokortizona na neirogennyi bolevoi sindrome u krys.

The effect of hydrocortisone on the neurogenic pain syndrome induced by damage to the peripheral nerves was studied in 40 male Wistar rats. Intraperitoneal administration of 10 mg/kg of the drug caused both hyperalgesia and hypoalgesia. The direction of the hydrocortisone effect on the neurogenic pain syndrome depended on the time of administration: chronic administration before the damage to the nerves promoted the development and intensity of the syndrome; treatment applied after the nerve damage delayed the development of the syndrome. It is suggested that the mechanism of the hydrocortisone effect on the neurogenic pain syndrome may be realized via the central link through the effect of the hormone on the glucocorticoid receptors of the brain structures.

[Effect of hyperactivation of the somatosensory cortex on pain syndrome of spinal origin in rats]. / Vliianie giperaktivatsii somatosensornoi kory na bolevoi sindrom spinal'nogo proiskhozhdeniia u krys.

The cortical effects were studied in rats with abnormal pain. The spinal pain syndrome was induced by a generator of abnormally enhanced excitation in spinal dorsal cord. Hyperactivation of the somatosensory cortex was caused with penicillin. Cortical hyperactivation was shown to lead to the suppression of the pain syndrome.

[The effect of catecholamine and serotonin antibodies on pain sensitivity and the development of morphine tolerance in experimental drug addiction]. / Vliianie antitel k katekholaminam i serotoninu na bolevuiu chuvstvitel'nost' i razvitie tolerantnosti k morfinu pri éksperimental'noi narkomanii.

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.

[Epileptiform activity in the somatosensory cortex of rats with trigeminal neuralgia]. / Epileptiformnaia aktivnost' v somatosensornoi oblasti kory u krys c trigeminal'noi nevralgiei.

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.

[Effects of C-terminal fragment of substance P-CP 5-11 on the activity of neurons of the dorsal raphe nucleus]. / Vliianie C-kontsevogo fragmenta substantsii P-CP 5-11 na aktivnost' neironov dorsal'nogo iadra shva.

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.

[Microcirculatory changes in experimental trigeminal neuralgia in rats]. / Izmeneniia mikrotsirkuliatsii pri éksperimental'noi trigeminal'noi nevralgii u krys.

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.