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It was found that the absence of the analgesic effect of morphine, as determined by the tail-flick test, in morphine-resistant and morphine-tolerant rats, as well as in naloxane blockade of morphine analgesia in morphine-sensitive rats was attended with a four- to eight-fold increase in morphine antibodies in the plasma, as determined by the ELISA method. It is suggested that a pharmacokinetic factor mediated through immune reactions of morphine antibodies formation is one of the mechanisms of such conditions.

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Rat experiments revealed a dose-dependent and naloxone-dependent analgetic effect of cocaine (0.5-3.0 mg/kg), evaluated by the tail-flick test. The cocaine-sensitive animals were morphine-sensitive and the cocaine-insensitive ones were morphine-insensitive. In some cocaine-insensitive rats, the use of cocaine led to that the first phase characterized by the lack of changes in nociception was followed by a hyperalgesic phase. It is suggested that cocaine produces an analgetic effect mainly via the delta-opioid mechanism.

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The paper reviews the data available in the literature and the authors own data demonstrating the differences in the levels of endogenous opioids and in the effects of enkephalinase inhibitor and naloxone in morphine-responsive and morphine-resistant and -tolerant animals. In the morphine-tolerant animals, a single administration of enkephalinase inhibitor or some doses of naloxone was found to produce an analgesic effect leading to a short-term analgesic effect of morphine. Chronic administration of naloxone causing a gradual decrease in and subsequent cessation of its analgesic effect leads to recovery of morphine's analgesic effect in the drug-resistant and -tolerant animals. It is suggested that the morphine-resistant animals have a congenital high activity of enkephalinase, while the drug-tolerant ones have its acquired high activity. Naloxone in certain doses with the high activity of enkephalinase act as its inhibitor, but in high doses acts as its opioid antagonist.

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In morphine-sensitive (s.c. 1.5 mg/kg) Wistar rats (60%) i.p. inoculation of 300-600 mg/kg d-Phenylalanine (d-Pha) did not change the nociception (tail-flick test), but in morphine-resistant rats (40%) evoked a dose-dependent analgetic effect. In morphine-sensitive rats (40%) chronic morphine administration induced the tolerance and d-Pha injection evoked analgetic effect. Morphine injection just after d-Pha analgesia was over evoked analgetic effect in morphine-resistant and -tolerant rats. It is suggested that morphine-resistant rats have a congenital and morphine-tolerant rats an acquired high level of enkephalinase activity which blocked the morphine analgetic action.

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In morphine-sensitive (s. c. 1.5 mg/kg) Wistar rats i.p. injection of 0.3 mg/kg naloxone either did not change nociception (tail-flick test) or induced hyperalgesia. In morphine-resistant rats 0.2-0.7 mg/kg naloxone injection induced analgetic effect but 1.0 mg/kg induced hyperalgesia. In morphine-sensitive rats chronic morphine administration induced the tolerance and naloxone injection evoked analgetic effect. Morphine inoculation just after naloxone analgesia was over induced analgetic effect. In morphine-resistant and -tolerant rats chronic naloxone administration induced gradual decrease and subsequent disappearance of its analgetic effect and subsequent morphine injections induced analgetic effect for some days. It is suggested that naloxone in morphine-resistant and -tolerant rats with high level of enkephalinase activity functions as its inhibitor. Chronic naloxone administration evoked progressive inhibition of enkephalinase activity that induced the morphine analgetic effect in morphine-resistant and -tolerant rats.

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Preliminary neurotropin administration improved subsequent conditioned avoidance learning of rats in a shuttle-box: increased the number of conditioned avoidance reactions and decreased their latency in comparison with the control but did not change the number of intertrial responses. "The demolition" (5 series of negative reinforcements applied despite of avoidance occurrence) caused behavioural stress reactions and inhibited the conditioned and unconditioned avoidance learned reactions. Neurotropin injection before the demolition abolished such disturbances, that having been done after the demolition restored conditioned avoidance. The positive effects of neurotropin were suggested to be due to its antistress property and ability to improve the formation of a result of an acceptor of action.

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In rats anaesthetized with +-chloralose the changes in extracellular pH and K+ in spinal cord dorsal horn were studied using pH and K+ ion-selective electrodes. The addition of 20% CO2 into inhaled air decreased the basal level of [pH]0 from 7.35 +/- 0.01 to 6.78 +/- 0.09 pH units and increased the basal level of [K+]0 from 3.1 +/- 0.1 to 5.14 +/- 0.8 mM. Electrocutaneous supramaximal (10 mA) simulation of both hind paws with the frequency 30 and 100 Hz induced the shift in the concentration of H+ and K+ by 0.15-0.2 unit and 2-2.5 mM, respectively. Under hypercapnia this shift of pH decreased by 36.9 +/- 8.5% at 30 Hz frequency of electrocutaneous stimulation and by 41.9 +/- 6.1% at 100 Hz frequency. The K+ shift decreased by 11.5 +/- 1.3% and by 17.3 +/- 1.5% under similar conditions. Hypercapnia induced by addition of 20% CO2 into inhaled air decreased also the focal potential amplitude by 16.8 +/- 4%. Thus, hypercapnia induces the increase of [K+]0 and [pH]0 and the decrease of recorded indicators in response to electrocutaneous stimulation. Total depression of synaptic transmission and analgetic effect occur due to these changes of ions distribution.

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In unanaesthetized acupuncture-sensitive rabbit d-phenylalanine injection didn't change the EP in response to tooth pulp electrostimulation, but prolonged the analgetic effect of auriculo-acupuncture stimulation 15 Hz expressed by decreasing of the amplitude of N1P2 component EP. In acupuncture-resistant rabbit d-phenylalanine injection induced analgetic effect which was enhanced and prolonged by auriculo-acupuncture stimulation. It's suggested that the recovery of pain sensibility after acupuncture analgesia is determined by enkephalinase's mechanism activation which is activated permanently in acupuncture-resistant rabbits.

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In experiments of albino rats neurotropin injection was shown to increase the latency of the tail-flick test in response to the nociceptive thermal stimulus and didn't change the threshold of the test in response to the nociceptive electroskin stimulus. The administration of the antiserum to beta-endorphin lowered the threshold and the latency of the tail-flick test in response to both stimuli. The preliminary administration of neurotropin reduced the hyperalgesic effect of the antiserum on both nociceptive stimuli.

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Clinical studies and animal experiments have demonstrated an antinociceptive effect of auricular electrostimulation (AE), 15 Hz, 300 microA, 25 min, on toothache. Perceptual and emotional vegetative components of the painful reaction were reduced by AE in 60 percent of patients and 64 percent of animals. Intravenous naloxone (0.2 mg/kg) abolished AE analgetic effect. The absence of AE analgetic effect in 40 percent of patients and 36 percent of animals can be explained by individual features of the endogenic opioid system functioning. Prospects of AE clinical application with various stimulation frequencies are discussed.

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In unanaesthetized rabbits auriculo-acupuncture electrostimulation with frequency of 15 Hz decreased the amplitude of somatosensory EP second component in response to the tooth pulp electrostimulation which was blocked by intravenous injection of naloxone but not by intraventricular injection of saralasin. The same effect of auriculo-acupuncture electrostimulation with frequency 100 Hz was blocked by saralasin, was increased by angiotensin II, was diminished by methysergide but wasn't changed by naloxone. It's suggested that there is angiotensinergic antinociceptive mechanism of dental pain which is activated by auriculo-acupuncture electrostimulation with frequency 100 Hz.

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Intravenous injection of beta-endorphin antiserum lowered the threshold of the tail-shock reaction to nociceptive electrocutaneous stimulation in rats in the first 1-2 days and raised it in the following 2-3 months. Naloxone injection reversed the analgesic effect of antiserum to beta-endorphin. Administration of normal serum did not change the threshold of the nociceptive reaction and naloxone failed to alter its effect. It is suggested that the secondary protracted effect of antiserum to beta-endorphin is a result of activation of the endogenous opioid system as a rebound-effect to diminished liberation of beta-endorphin in the first phase of the action of its antiserum.

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In rats beta-endorphin antiserum systemic injection decreased during 1-2 days the threshold of tail-shock and latency of tail-flick tests, and during subsequent 85 days increased the threshold of tail shock, but not changed the latency of tail-flick tests. Naloxone injection blocked the increasing of thresholds, but not changed the latency of tail tests. It is suggested that antiserum evokes the first inhibition and the second selective activation of endogenous antinociceptive opioid system with affinity to electric nociception.

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In non-anesthesized rabbits intraventricular injection of angiotensin II reduced the amplitude of somatosensory evoked potential to nociceptive tooth pulp, but not to nociceptive electrocutaneous stimulation. The same injection of bombesin induced the contrary analgetic effect. The systemic naloxone (0.1 mg/kg) injection didn't reverse the peptides analgetic effects. It's suggested that selective analgetic effects of angiotensin II and bombesin are determined by the presence of the specific different peptide mechanisms for nociception with the different pain genesis.

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In experiments on unanesthetized rabbits it was found that the effects of ketamine and kalipsol were characterized by a decrease of the negative phase amplitude of the primary response (PR) of evoked potentials (EP) and the secondary positive deviation of EP of the cortical somatosensory region.

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