Experimental model of combined pain and depression status in rats.

Combined pain and depression status in rats was created by inducing experimental depressive syndrome (by subchronic injection of MPTP proneurotoxin) in animals with manifest and developing neurogenic pain syndrome induced by preliminary crossing of the sciatic nerve in the hind limb. The neurogenic pain syndrome augmented by some parameters the depressive symptoms and provoked manifestation of signs of depressive behavior in animals treated with saline.

Autoantibodies against glutamate, gamma-aminobutyric acid, and norepinephrine in mechanisms of neuropathic pain syndrome.

The production and role of autoantibodies against neurotransmitters glutamate, gamma-aminobutyric acid, and norepinephrine were studied in rats with experimental neuropathic pain syndrome induced by sciatic nerve transection. Nerve transection in rats was followed by behavioral reaction of autotomy (self-mutilation of the operated limb), which often accompanies neuropathic pain syndrome. The development of neuropathic pain syndrome was accompanied by increased production of autoantibodies against glutamate, gamma-aminobutyric acid, and norepinephrine. A negative correlation was found between the amount of autoantibodies against neurotransmitters and severity of neuropathic pain syndrome. Our results suggest that antibodies against glutamate and norepinephrine exhibit protective activity.

Peculiarities of the development of analgesic effect during transcutaneous dynamic electrical stimulation.

The effect of transcutaneous dynamic electrical neurostimulation on the development of analgesia was studied in behavioral and electrophysiological experiments on rats. A 30-min dynamic electrical stimulation elevated the nociception threshold in tail-flick and hot plate tests, increased the threshold of the late nociceptive flexor reflex, and decreased the number of bursts in the response. Intraperitoneal injection of naloxone (2 mg/kg) abolished the analgesic effect of dynamic electrical neurostimulation. It is concluded that the key role in reflex analgesia during dynamic electrical neurostimulation is played by the endogenous cerebral opioid system, which inhibits the nociceptive signals traveling to CNS via unmyelinated C-fiber afferents.

Experimental depressive-pain syndrome in rats with initial various anxiety-phobic levels: a behavioral study.

Modeling of neurogenic pain syndrome by sciatic nerve transection in rats with pronounced dopamine-deficiency-dependent 1-methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-induced experimental depressive syndrome forms a stable state of combined pain and depression, which can be considered as a model of the pain-depressive syndrome. The neurogenic pain syndrome prolongs the state of behavioral depression in rats irrespective of their initial anxiety level. The depressive symptoms can potentiate the severity of pain syndrome. By a number of indices, more pronounced behavioral changes during the development of pain-depressive syndrome occur in initially nonanxious rats.

[Effects of paracetamol and naproxen on pain syndromes of various genesis]. / Effekty paratsetamola i naproksena pri bolevykh sindromakh razlichnogo geneza.

A comparative study of the effects of two nonsteroidal antiinflammatory drugs paracetamol and naproxen on the pain syndrome models of various etiology showed that paracetamol is more effective in the case of spinal and neuropathic pain syndromes (in which the leading pathogenic mechanisms are related to the formation of hyperactive neuron aggregates in the central nociceptive structures). Naproxen was effective in the case of adjuvant arthritis, for which the main development mechanism is related to the accumulation of inflammation mediators in tissues. It is concluded that special features of the pathogenic therapy of various pain syndromes are determined by the character of prostaglandin participation in the pathological process.

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.

[The effects of L-arginine in chronic pain syndromes]. / Effekty L-arginina pri khronicheskikh bolevykh sindromakh.

The effect of L-arginine in long-term parenteral administration was studied on a model of neuropathic pain syndrome and adjuvant arthritis. L-arginine produced a preventive and therapeutic effect in the neuropathic pain syndrome. It weakened the development of adjuvant arthritis for the period of its administration. The factor underlying the effect of L-arginine is its double action as a precursor of nitrous oxide and kiotorphin, an endogenous antinociceptive dipeptide.

[The role of the NMDA-receptor blocker and stimulator ketamine and glycine in the development of a neuropathic pain syndrome]. / Rol' blokatora i stimuliatora retseptorov NMDA ketamina i glitsina v razvitii neiropaticheskogo bolevogo sindroma.

The effect of glycine, ketamine, and their combination in chronic oral administration was studied on a model of the neuropathic pain syndrome. Glycine failed to prevent the pain syndrome but had a therapeutic effect. Ketamine possessed a marked preventive and therapeutic effect. In combined administration the drugs mutually potentiated their action. The effect of glycine and ketamine is based on intensification of spinal glycinergic inhibition, differently directed effect on the NMDA receptors, and intensification of monoaminergic inhibition.

[The action of piracetam and its complex with sodium oxybutyrate in the neuropathic pain syndrome]. / Deistvie piratsetama i ego kompleksa s oksibutiratom natriia pri neiropaticheskom bolevom sindrome.

Effects of the pyracetam and its sodium hydroxybutyrate complex were studied on a model of the neuropathic pain syndrome. It was demonstrated that the pyracetam prevents the development of the neuropathic pain syndrome. The pyracetam relieves the pain syndrome. The sodium hydroxybutyrate appears to enhance preventive and medical effects of the pyracetam. Possible mechanisms of action of these drugs are discussed.

[The effects of mexidol in pain syndromes]. / Effekty meksidola pri bolevykh sindromakh.

Models of neuropathic pain syndrome and adjuvant arthritis were used to study the effect of mexidole, an antioxidant from the 3-hydroxypyridine group. Mexidole was indicated to produce no preventive effect in pain syndromes, but to exhibit a therapeutic one. The use of mexidole in combination with the agents activating the monoaminergic systems in the central nervous system showed the presence of their reciprocal effect in neuropathic pain syndrome and its absence in adjuvant arthritis. Possible mechanisms of action of mexidole were also discussed.

[The action of sodium valproate in central pain syndromes]. / Deistvie val'proata natriia pri tsentral'nykh bolevykh sindromakh.

A model of acute spinal and phantom pain syndromes caused by the formation of an abnormally increased excitation generator (AIEG) in the system of dorsal horns of the spine was used to study the effects of sodium valproate when used chronically in the phantom pain syndrome, when given in a single dose in the acute pain syndrome and when applied to the spine with disinhibitors inducing the pain syndrome. It was shown that during chronic administration sodium valproate produced a stress-preventive action, but failed to affect pain sensation and to prevent the development of the pain syndrome. When used in the acute pain syndrome, sodium valproate had a marked analgesic effect, and when applied to the spine it substantially reduced the manifestations of the pain syndrome. The action of sodium valproate on the AIEG can be accounted for by the higher GABA level that results in the hyperpolarization of neurons which are a part of AIEG. When the latter is formed and operates in acute and chronic pain syndromes there are differences in the functional activity of the neurochemical structures responsible for the realization of pain reaction components. This is suggested by varying effects of sodium valproate on pain sensation during acute and chronic experiments.