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R Tammiso

Publications and source records attributed to R Tammiso.

13 recordsLinked to original sources
PubMed1991

Effects of diazepam on nociception in rats.

Acute i.p. injection of diazepam (1 mg/kg) resulted in a moderate increase in the tail-flick latency in rats. Tolerance to this diazepam effect developed after 10 days of diazepam treatment (1 mg kg-1 day-1). The benzodiazepine antagonist Ro 15-3505 only partially reversed the effect of diazepam on nociception. Naloxone (5 mg/kg i.p.) failed to affect the effect of diazepam on nociception, while the kappa antagonist MR 2266 fully antagonized the diazepam-induced increase of the tail-flick latency. Diazepam injected intracerebroventricularly (1, 5, 20 micrograms/rat) did not alter basal nociceptive threshold, however, diazepam injected intrathecally (20 micrograms/rat) prolonged the tail-flick latency. Furthermore, intracerebroventricular injection of muscimol partially antagonized the i.p. diazepam-induced increase of the tail-flick latency. These results suggest that benzodiazepine receptor sites are partially involved in the effect of diazepam on nociception and indicate that an indirect kappa-opioid-receptor-mediated mechanism may be involved. The anatomical site of diazepam action on tail-flick latency seems to be at the spinal level. Descending axons to the spinal cord from brain areas reached by intracerebroventricular injection of muscimol seem to modulate the effect of diazepam effect on nociception.

Animals↗
PubMed1987

Zopiclone potentiates the antinociceptive effect of morphine in rats.

The antinociceptive effect of morphine, as determined by the tail-flick test, was dose-dependently increased by the intraperitoneal injection of zopiclone. The benzodiazepine antagonists Ro 15-1788 (flumazepil) and Ro 15-3505, when intraperitoneally injected, significantly antagonized the effect of intraperitoneal injection of zopiclone on morphine antinociception. Intrathecal injection of zopiclone potentiated morphine antinociception, while the intracerebroventricular injection of zopiclone failed to enhance morphine antinociception and the intracerebroventricular injection of flumazepil to antagonize the intraperitoneal-zopiclone-induced increase in morphine antinociception. These results suggest that benzodiazepine sites are specifically involved in the potentiating effect of zopiclone on morphine antinociception. The anatomical locations of the receptors involved seem to be at the spinal level.

Animals↗
PubMed1986

Reversal of the effect of centrally-administered diazepam on morphine antinociception by specific (Ro 15-1788 and Ro 15-3505) and non-specific (bicuculline and caffeine) benzodiazepine antagonists.

Diazepam, injected into the lateral ventricles reduced the antinociceptive effect of morphine in rats, as measured by the tail-flick method. Specific antagonists of diazepam (Ro 15-1788 and Ro 15-3505) had no effect themselves but prevented inhibition by diazepam of morphine antinociception. Furthermore, the action of diazepam was partially reversed by intracerebroventricular injection of bicuculline or caffeine. These findings support the view that the depressant effect of diazepam on morphine antinociception is specific and GABAergic in nature and that some actions of diazepam are also mediated via the purinergic system.

Animals↗
PubMed1984

Purine involvement in morphine antinociception.

The effects of a series of adenosine derivatives on morphine antinoceptive effect were investigated in rats by the 'tail-flick' method. 2-Chloroadenosine (CADO) and L-N6-phenylisopropyladenosine (L-PIA), given intraperitoneally, caused decreased morphine antinociception. Intracerebroventricular injections of CADO, L-PIA and 5'-N-ethylcarboxamide adenosine (NECA), but not of 2'-deoxyadenosine, antagonized morphine antinociception. The effects of both central and peripheral injections of CADO and L-PIA on morphine antinociception were partially reversed by caffeine. Intracerebroventricular injection of dibutyryl-cyclic 3', 5' adenosine monophosphate (db cyclic AMP) had no effect on morphine antinociception. These data indicate that adenosine plays a role in morphine-induced antinociception. The results are discussed in terms of postulated effects of adenosine derivatives on adenylate cyclase.

2-Chloroadenosine↗
PubMed1982

Modification of the antinociceptive effect of morphine by centrally administered diazepam and midazolam.

1 Intracerebroventricular administration of diazepam or midazolam decreased the antinociceptive effect of morphine in rats as measured by the "tail flick" method. 2 Midazolam, injected into the periaqueductal grey matter (PAG) antagonized the analgesic effect of morphine. The action of midazolam was partially reversed by bicuculline. 3 These findings support the view that the effect of benzodiazephines on morphine antinociception may be mediated through gamma-aminobutyric acid receptors.

Analgesics↗
PubMed1981

Effects of some GABA-mimetic drugs on the antinociceptive activity of morphine and beta-endorphin in rats.

Intracerebroventricular administration of muscimol, a potent GABA-receptor agonist, counteracted the antinociceptive effect of morphine or beta-endorphin in rats as measured by the "tail flick" method. Muscimol's activity was reversed by bicuculline. Isoguvacine, another GABA agonist, as well as nipecotic acid and guvacine, two inhibitors of neuronal and glial uptake of GABA, also antagonized morphine's antinociceptive effect. A role of the central GABA-ergic system in mediating opiate antinociception is proposed.

Analgesics↗
PubMed1980

Estrogenic absorption through the skin: an experimental study.

Our results show in an unquestionable way that both the steroid (ethinylestradiol) and non-steroid (Ralone) estrogens studied by us were absorbed percutaneously by the rat. They also demonstrate that both estrogens affected target organs in a quite similar way being proportionally dependent upon the 1-to-1,000 ratio existing between them, as established on the basis of a known activity parameter. When one of the two estrogens is given for therapeutical purposes its systemic effects are of a dose-related type.

Animals↗
PubMed1979

Muscimol antagonism of morphine analgesia in rats.

1 Muscimol, a gamma-aminobutyric acid (GABA) receptor agonist, when injected intraventricularly antagonizes the antinociceptive effect of morphine given either subcutaneously or intraventricularly. The antagonistic effect of muscimol on morphine analgesia appears to be linearly related. 2 This finding provides support for the view that a GABA-ergic system is involved in morphine analgesia.

Animals↗
PubMed1978

Toxicological and teratological studies of azanidazole.

A toxicological study of 4-[(E)-2-(1-methyl-5-nitro-1H-imidazol-2-yl)-ethenyl]-2-pyrimidinamine (azanidazole, Triclose), a new systemic antitrichomonas agent, was run in laboratory animals in order to evaluate its safety. Studies also covered the effects of azanidazole on reproduction in rats treated prior to mating, on fetal development in rabbits and rats, and on fetal survival and growth in rats treated with it during late pregnancy and lactation. The obtained data indicate that azanidazole was well tolerated when administered as a single dose or repeated daily doses for six months. Furthermore, no adverse reproductive effects and no evidence of teratogenic activity were observed in all of the tested animal species. Survival indices were not affected, and body weight of progeny was normal in all studies on reproduction and peri- and post-natal toxicity.

Animals↗
PubMedDate not supplied

Peripherally administered benzodiazepines increase morphine-induced analgesia in the rat. Effect of RO 15-3505 and FG 7142.

The influence of alprazolam, chlordiazepoxide and midazolam on the antinociceptive effect of subcutaneous morphine was investigated in rats, using the tail-flick test. After intraperitoneal administration, all drugs significantly enhanced the morphine-induced analgesia. Both the benzodiazepine receptor antagonist RO 15-3505 and the benzodiazepine receptor inverse agonist FG 7142 antagonized the potentiating effect of alprazolam, chlordiazepoxide and midazolam. Our results suggest that the interaction between benzodiazepines and opioids in modulating nociceptive responses involves primarily benzodiazepine receptors and that different pathways are involved in the anxiolytic and pro-analgesic actions of benzodiazepines.

Animals↗