Effect of sodium hydroxybutyrate in pain syndromes

It is shown that sodium hydroxybutyrate exerts a preventive and therapeutic effect on models of neuropathic pain syndrome and adjuvant arthritis. The effects of sodium hydroxybutyrate droxybutyrate are correlated with its ability to reduce hyperactivity of the neurons that are generators of pathologically enhanced excitation and to inhibit the pathological algetic system. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 121, No. 4, pp. 395–398, April, 1996 Presented by G. N. Kryzhanovskii, Member of the Russian Academy of Medical Sciences     

Implication of the hippocampus in the development of a pain syndrome in rats following sciatic nerve damage

Local destruction or electrostimulation of the hippocampus did not affect pain sensitivity thresholds in rats with intact sciatic nerve. In rats with transected sciatic nerve, local hippocampal damage accelerated the development of a pain syndrome considerably, while hippocampal electrostimulation delayed it so that 80% of the test rats did not appear to have been experiencing pain throughout the 45-day observation period. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 8, pp. 120–122, August, 1994     

Characteristics of pain syndromes developing in rats upon interaction of two generators of pathologically enhanced excitation

Using rat models of a neuropathic and a central spinal pain syndrome, each of which is based on the formation of a generator of pathologically enhanced excitation, the authors explored how these syndromes develop when the two respective generators of pathologically enhanced excitation interact, and found that the interaction results in accelerated development and increased clinical manifestations of both syndromes. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N^no 10, pp. 364–367, October, 1994     

Electrical activity in dorsal horns of the spinal cord and in sensorimotor cortex in rats with the spinal pain syndrome

In rats with the spinal pain syndrome caused by penicillin application to the dorsal surface of lumbar segments of the spinal cord, the following changes in evoked potentials were observed in the dorsal horn in L₅ segment at the side of penicillin application: a marked increase in primary response and disappearance of the secondary hyperpolarization wave with its replaument by a high-amplitude and long depolarizing wave. In addition to these changes, repetitive spontaneous burst discharges were recorded in the corresponding region of the sensorimotor cortex. Thus, the pathogenic basis of the pain syndrome is a pathological algetic system formed of altered structures that belong to nociceptive apparatus in dorsal horn and higher subdivision of the pain sensory system. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 125, No. 3, pp. 269–272, March, 1998     

Effects of α-tocopherol in rats with a neuropathic pain syndrome

The rat model of a neuropathic pain syndrome (transection of the sciatic nerve with encapsulation of its central end) was used to evaluate the efficacy of the antioxidant α-tocopherol in such syndromes. It was found that administration of α-tocopherol 3 days before nerve transection and then for 3 weeks thereafter it delayed the development of the pain syndrome, which subsequently tended to subside. In contrast, a 3-week α-tocopherol treatment started when the pain syndrome had already set in failed to influence its evolution. α-Tocopherol markedly reduced manifestations of inflammatory and degenerative processes in the denervated limb. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N ^o 8, pp. 123–125, August, 1994 Presented by G. N. Kryzhanovskii, Member of the Russian Academy of Medical Sciences     

Effect from prophylactic administration of pentoxyphylline (trental) on the development of neuropathic pain syndrome and on the associated microcirculatory disturbances

Prophylactic injection of pentoxyphylline into rats with a neuropathic pain syndrome produced by sciatic nerve transection delayed and weakened the development of this syndrome, improved the microcirculation and venular permeability, and reduced mast cell degranulation. The findings of this study recommend pentoxyphylline for clinical use in the multidrug treatment of neuropathic pain syndromes. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 119, N ^o 5, pp. 485–487, May, 1995 Presented by G. N. Kryzhanovskii, Member of the Russian Academy of Medical Sciences     

Analgesic effects of spinal cord peptide factors produced during the establishment and development of generators of pathologically enhanced excitation in the rat spinal cord

In rats with a pain syndrome caused by the production of a generator of pathologically enhanced excitation, substances of peptide nature with analgesic properties were found to be produced in the nociceptive system of the spinal cord. Spinal cord extracts derived from rats with such syndromes (pain syndrome of spinal origin or adjuvant arthritis) exerted analgesic effects when injected intraventricularly into recipient rats with a pain syndrome of spinal origin. The highest analgesic activity was displayed by extracts obtained from the region where the generator of pathologically enhanced excitation had been set up. The analgesic activity of the extracts was directly related to the severity and duration of the pain syndrome in the donor rats. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 118, N^no 10, pp. 374–377, October, 1994     

Effects of ischemia on the development of a deafferentation pain syndrome and on microcirculatory disturbances in rats

In a group of rats with transected sciatic nerve, ischemia of the operated limb produced by femoral artery ligation was found to result in an accelerated onset and increased severity of autotomy as compared to a similar group of rats without ischemia. Biomicroscopic examination of the mesenteric microcirculation showed that the ischemia also intensified disturbances of the terminal blood flow, made the venules more permeable, and increased the percentage of degranulated mast cells. The possible mechanisms by which ischemia promotes the development of chronic pain syndromes are discussed. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 117, N ^o 3, pp. 235–237, March, 1994 Presented by G. N. Kryzhanovskii, Member of the Russian Academy of Medical Sciences     

Pathological integrations in the central nervous system

Damage to the nervous system is a causal and conditioning event leading to the development of pathological processes mediated via such endogenous mechanisms as the formation of integrative complexes from damaged and secondary changed nervous structures that are pathological by their nature, mechanisms, and effects. At the level of neural relationships such pathological integrative complex (PIC) is formed by an aggregate of hyperactive neurons (generator of pathologically enhanced excitation, GPEE) producing uncontrollable ongoing flow of nerve impulses. At the systemic level, PIC is a new pathodynamic system composed of various subdivisions of the CNS, which acts as a pathological system. The subdivision of the CNS containing GPEE assumes the role of a pathological determinant due to its enhanced activity. This pathological determinant induces the formation of a pathological system and controls its activity at the early period of its genesis. Every neuropathological syndrome is a clinical or behavioral manifestation of pathological system activity. Pathological determinant and pathological system are general biological categories that fall outside the scope of nervous disorders. They can arise in various systems at the micro- and macroscopic levels and induce systemic pathology. Translated fromByulleten's Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 3, pp. 244–247, March, 1999 Original article submitted October 5, 1998     

Effect of antiserotonin antibodies on pain sensitivity in rats with adjuvant-induced arthritis

Active immunization with a serotonin—protein conjugate inducing the formation of antiserotonin antibodies exerts an analgesic effect in rats with adjuvant-induced arthritis and inhibits the development of arthritis in early stages after injection of Freund's complete adjuvant. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 9, pp. 292–295, September, 1997     

Effect of the somatosensory cortex on the development of the deafferentation pain syndrome

Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 115, N ^o 5, pp. 473–475, May, 1993     

Effect of L-arginine in central spinal pain syndrome

When applied in combination with penicillin (2000 U) to the dorsal surface of the spinal cord, L-arginine in a low concentration of 100 nmol had a pronociceptive effect, while being applied in concentrations of 65–130 μmol with penicillin or injected intramuscularly before penicillin (15,000 U) L-arginine exhibited an analgesic effect. The opposite effects of L-arginine as the precursor of NO and of opioid dipeptide kyotorphin are demonstrated. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 2, pp. 160–163, February, 1999     

Effect of parlodel on brain electrical activity in experimental depressive syndrome in rats

In rats with experimental MPTP-induced depressive syndrome, chronic administration of parlodel prevented epileptiform activity, an increase in δ-band and a decrease in α-band spectral powers in the caudate-putamen structures, and an increase in δ-band spectral power in the hippocampus. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 129, No. 2, pp. 152–155, February, 2000     

Effect of akatinol (Memantine) in central spinal pain syndrome

On the model of central spinal pain syndrome in rats induced by application of penicillin to the dorsal surface of the lumbar spinal cord, akatinol injected intraperitoneally at the peak of syndrome or applied locally simultaneously with penicillin produced a dose-dependent analgesic effect. Intraperitoneal injection of akatinol at the peak of pain syndrome inhibited neuronal activity in spinal dorsal horn: the amplitude of total evoked neuronal response significantly decreased and the duration of action potentials returned to normal. It is concluded that activation of NDMA receptors plays a significant role in the development of central spinal pain syndrome, in particular spontaneous pain attacks, hyperalgesia, and tactile allodynia. Akatinol can be an essential component of the complex pathogenetic therapy of central pains. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 129, No. 5, pp. 500–503, May, 2000     

Bioelectrical activity in the sensorimotor cortex in the rats with the spinal pain syndrome

Formation of allodynia and the spinal pain syndrome of different intensity by application of penicillin to the dorsal surface of lumbar segments of the spinal cord are accompanied by dose-dependent changes in spontaneous and evoked bioelectric activity in the sensorimotor cortex. Translated from Byulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 127, No. 1, pp. 35–38, January, 1999     

Effect of neurotropin on regional cerebral blood flow and systemic blood pressure

Experiments on rabbits show that neurotropin has no effect on regional cerebral flow and systemic blood pressure under normal conditions, but reduces regional cerebral flow in partial circulatory hypoxia (ischemia) and recirculation. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 125, No. 6, pp. 612–614, June, 1998