Biomedical subjects
Publications and source records attributed to A S Morozova.
Pain-relieving and reinforcing effects of morphine after microinjections into brain structures have been studied. Reinforcing effects were revealed after administration into n. accumbens, while analgesic--after injections into periventricular area of the midbrain and dorsomedial hypothalamus. Data obtained demonstrate neurotopographic heterogeneity of two important effects of morphine.
Components of complex emotional reaction to nociceptive stimulation as well as antinociceptive effect of periaqueductal gray matter (PAG) electrical stimulation were determined in rats. Animals were treated with morphine hydrochloride or saline for 10 days. Morphine analgesic effect during subchronic dosage (50 mg/kg a day) was gradually decreased. The same was true for stimulation-produced analgesia (SPA). Naloxone (2 mg/kg) exerted a partially antagonistic effect in relation to SPA in saline-treated and failed to abolish SPA in morphine-treated rats. It is concluded that the opiate component of the antinociceptive system is of importance for the tolerance development to morphine-like drugs.
Analgesic and secondary reinforcing effects of morphine, bremazocine and phencyclidine microinjections into ventral tegmental area were studied in rats. The drugs under study failed to affect nociceptive reactions produced by thermal, mechanic and electrical stimuli. Morphine and phencyclidine have shown reinforcing properties in place preference paradigm. Ventral tegmental area seems to be a triggering zone of the reinforcing, and not analgesic effect of opioid agonists, with an important role of mu- and sigma-receptors revealed.
In experiments on rats with implanted electrode-cannules there were studied the effects of L-tryptophane (25 mg/kg intraperitoneally) and microinjections of serotonin (20 micrograms), dopamine (10 micrograms) and proserine (5 micrograms) into the area of periaqueductal central gray on the antinociceptive effect caused by stimulation of the same "points" of the midbrain. L-tryptophane, serotonine and proserine (in the presence of methylatropine) potentiated the effect of subthreshold antinociceptive stimulation which could be tested from the modifications of thresholds of the development of some complex pain reaction components under electrical stimulation of the rat tail. Dopamine did not have such an effect. The potentiating effect of serotonine is not eliminated by naloxone.
Comparative study of topographic and receptor selectivity of emotionally positive (place preference test) and analgetic (electrical and pressure nociceptive stimulation of the tail) effects of opioids was performed in rats. Morphine and selective agonists of mu-, kappa-, delta- and sigma-opiate receptors were administered through cannulae implanted into the periaqueductal grey and ventral tegmental area (VTA). Reinforcing effects of opioids in VTA was shown to be mediated mainly by mu-, delta- and sigma-receptors, while analgetic effect was realised with the aid of mu- and delta-opioid receptors.
It has been shown in rat experiments that repeated administration of morphine produces tolerance to the effect of stimulation analgesia (SA). In the control group, the same stimulation of the periaqueductal gray matter (PGM) failed to produce tolerance. Naloxone (2 mg/kg i.p.) exerted a partially antagonistic influence on SA in the control group and did not affect the antinociceptive action of PGM stimulation in morphine-treated animals.
In chronic experiments on rats it was established that electric stimulation of certain areas of the midbrain depresses pain reactions of different genesis. Morphine in subanalgetic doses (2--2.5 mg/kg) reveals and potentiates the antinociceptive effect of central stimulation shown first of all by depression of the complex highly integrated components of an emotionally behavioral conductive reaction to pain.