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. Key Words: hippocampus; pathological algetic system; neurogenic pain syndromeClinical and experimental studies have shown that limbic structures are involved not only in mediating physiological pain [1,9,11] but also in the development of pain syndromes [7,10,15,16]. It is not clear, however, what role in the mechanisms of physiological and pathological pains is played by the hippocampus, one of the central structures of the limbic system.The purpose of the present study was to examine how destruction and electrostimulation of the hippocampus might influence thresholds of physiological pain and the development of a neurogenic pain syndrome which arises in rats after transection of the sciatic nerve. MATERIALS AND METHODSFor the experiments, 110 male Wistar rats weighhag 180-200 g were used. To elicit a neurogenic pain syndrome, the sciatic nerve was transected under Hexenal anesthesia (30 mg/kg intraperitoneaUy) below the site of its ligation, and the central portion of the nerve was placed in a polyethylene capsule to prevent its regeneration. The animals were considered to have developed a pain syndrome when their behavior was altered, autotomies were observed on the operated hind paw, and pain sensitivity thresholds were lowered [3]. The severity of the syndrome was rated in points from 1 to 11 using our modification of a previously proposed scoring scale [12]. Autotomic damage to one claw was assigned 1 point; to 2-5 claws, 2-5 points, respectively; to a phalanx on one digit, 6 points; to phalanges on 2-5 digits, 7 to 10 points, respectively; and damage to metatarsal bones, 11 points. Pain sensitivity thresholds were estimated by the hot plate and tail flick tests: licking the hind paws in response to the application of a hot (55~ plate and flicking of the tail in response to focused radiant heat. The hippocampus was stimulated electrically and damaged locally on the side contralateral to sciatic nerve transection. Local hippocampal damage (areas CA1-CA3) was produced electrolytically -by passing a direct an-0007-4888/94/0008-0806512.50 9 1995 Plenum Publishing Corporation
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 lxmol 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. Key Words: L-arginine; nitric oxide; central spinal pain syndrome; kyotorphinThe central spinal pain syndrome (CSPS) is a neurogenic pain syndrome caused by the formation of an aggregate of hyperactive nociceptive neurons in the dorsal horn capable to generate long-lasting spontaneous ongoing discharges of nerve impulses [1]. Clinical manifestations of the neurogenic pain syndrome include allodynia, hyperalgesia, and spontaneous pain. In many respects these symptoms result from disturbed inhibitory control [1], increased tonetropic glutamate and activation of NDMA receptors [10] and enhanced production of NO, a new neuronal messenger [3] involved in both central and peripheral nociception [5]. Our aim was to study the effect of Larginine (L-Arg) on the development of CSPS.
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 L S 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 algetie system formed of altered structures that belong to nociceptive apparatus in dorsal horn and higher subdivisions of. the pain sensory system. Key Words: dorsal horns; sensorimotor cortex, generator of pathologically enhanced excitation; pathological algetic system; spinal pain syndrome; penicillinWe have shown that application of convulsants (tetanotoxin, penicillin, and strychnine)to various subdivisions of the noeiceptive system provokes pain syndromes [ 1,2,5]. In this work our aim was to study the pathophysiological mechanisms of spinal pain syndrome caused by application of penicillin to the dorsal surface (DS) of the spinal cord lumbar segments and to analyze the characteristic features of electrical activity both in the penicillin-affected primary nocieeptive relay (dorsal horn, DH) and in the corresponding area of the sensorimotor cortex. MATERIALS AND METHODSThe study was carried out on 24 male Wistar rats weighing 270-320 g in accordance to regulations for experimental pain investigations in animals [9] and to the principles of work with animals in neuroInstitute of General Pathology and Pathophysioiogy0 Russian Academy of Medical Sciences, Moscow physiological studies [10]. In group 1 rats, an agar plate [2] (6xl.5x2 mm) containing 25000 U/ml penicillin sodium chloride salt was applied to the DS of lumbar segments of spinal cord exposed under ether anesthesia. The wound was sutured, and the animals were observed during the development of pain syndrome.In group 2 rats, electrical activity was recorded in penicillin-affected DH and in the corresponding region of the sensorimotor cortex. Measurements were performed when the pain syndrome reached the maximum in group 1 rats. The rats were anesthetized by intraperitoneal urethane (1400 mg/kg), placed in a stereotaxic apparatus with rigid fixation of the head and spine, trepanized, laminectomized, immobilized with a muscle relaxant (Myo-Relaxin, 50 mg/kg intramuscularly), and artificially ventilated. Muscle tissue, skin, and the vertebral spinous processes in the stereotaxic fixation points were treated with 0.5% procaine. Evoked potentials (EP) in DH of the spinal cord and in the sensorimotor cortex were recorded
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