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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 89 (1986), S. 121-124 
    ISSN: 1432-2072
    Keywords: Antinociception ; PGD2 ; Serotonin ; Endogenous opioid peptides ; 5,6-Dihydroxytryptamine ; p-Chlorophenylalanine ; Naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intracerebroventricular administration of prostaglandin D2 (PGD2), the major PG in the rat brain, produced a dose-related anti-nociceptive effect in rats as assessed by the rat tail-hot wire, hot plate and phenylquinone-induced writhing techniques. The antinociceptive action of centrally-administered PGD2 was markedly attenuated after pretreatment of the rats with 5,6-dihydroxytryptamine, a selective neurotoxin for central serotonergic neurones, and p-chlorophenylalanine, a specific inhibitor of serotonin synthesis, indicating that the PGD2 action is serotonin-mediated. Naloxone, an antagonist of endogenous opioid receptors, also antagonised the antinociceptive action of PGD2. Earlier reports from this laboratory have shown that the antinociceptive action of centrally-administered PGE1 in rats is a serotonin-mediated effect and is also antagonised by naloxone. It was further shown that PGD2, like PGE1, augments serotonin turnover in the rat brain. The present findings support the view that PGD2 shares some of the central actions of PGEs and, like the latter, may function as a neuromodulator in the central nervous system.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-2072
    Keywords: Key words Streptozotocin ; Experimental diabetes mellitus ; Anxiety ; Diazepam ; Brain monoamines ; Tribulin ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The anxiolytic activity of diazepam (DZP) (0.25–1 mg/kg) was investigated in streptozotocin (STZ)-induced diabetic adult Charles Foster albino rats of either sex. Diabetes was induced by injecting STZ IP (50 mg/kg; in citrate buffer, pH 4.5). Experiments were performed 72 h later. The rats were subjected to various anxiety paradigms, including the open-field exploratory behaviour, elevated plus maze and elevated zero maze behaviours and the social interaction tests. In addition, rat brain tribulin activity was also assessed as a biochemical marker of anxiety. The results indicate that diabetic rats showed significantly more anxiogenic activity in comparison to non-diabetic rats on open-field, elevated plus maze, zero maze and social interaction tests. In diabetic rats, brain tribulin activity (MAO-A inhibitory component) was significantly increased. DZP dose dependently produced anxiolytic activity on the various behavioural parameters in non-diabetic rats. DZP (0.5 and 1 mg/kg) partially reversed the anxiogenic behaviour of STZ diabetic rats in elevated plus maze and zero maze tests. However, in open field behaviour and social interaction tests significant anxiolytic activity was observed only at a higher dose of DZP (1 mg/kg). The findings indicate that STZ-induced diabetic rats exhibited augmented anxiety on various experimental paradigms and that the anxiolytic effect of diazepam was less marked in diabetic rats as compared to their euglycaemic counterparts.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Psychopharmacology 59 (1978), S. 293-297 
    ISSN: 1432-2072
    Keywords: Cannabis indica ; Anticonvulsant action ; Brain monoamines
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The role of brain monoamines in the anticonvulsant action of Cannabis indica resin (CI), against maximal electroshock-induced seizures in albino rats, was investigated by using pharmacologic agents that influence brain monoamine activity. Delta-9-tetrahydrocannabinol content of cannabis resin was estimated to be 17%. The anticonvulsant action of CI (200 mg/kg, i.p.) was significantly inhibited after pretreatment with drugs that reduce brain serotonin activity but not by drugs that reduce brain catecholamine activity. Similarly, the anticonvulsant action of a subanticonvulsant dose (50 mg/kg, i.p.) of CI was potentiated by serotonin precursors but not by catecholamine precursors. Potentiation of the anticonvulsant action of CI by nialamide or by imipramine was inhibited after pretreatment with 5,6-dihydroxytrypt-amine. The results suggest that the anticonvulsant action of CI in the rat is serotonin- and not catecholamine-mediated.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2072
    Keywords: Antinociception ; PGE1 ; 5,6-Dihydroxytryptamine ; Serotonin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It is generally accepted that prostaglandins (PGs) are nociceptive substances. However, earlier studies from this laboratory indicated that morphine analgesia, in the rat, was not only serotonin mediated, but involved PGs as well. Several PG synthesis inhibitors were shown to inhibit morphine analgesia and PGE1 was shown to potentiate the antinociceptive effect of morphine. Intraperitoneal administration of PGE1, but not PGE2 and PGF2α, elicited antinociceptive effect per se, by the radiant heat method. The present study was undertaken to confirm the antinociceptive action of PGE1, after intracerebroventricular administration, against nociceptive impulses induced by radiant heat, pressure, and high frequency electric current. PGE1 produced a dose-dependent antinociceptive effect by the radiant heat and pressure methods. It potentiated the antinociceptive action of morphine by the electrical stimulation method. The antinociceptive action of PGE1 was not evident in 5,6-dihydroxytryptamine-pretreated rats, suggesting that this effect is serotonin mediated. The present study thus confirms the antinociceptive action of PGE1 and suggests that, unlike its peripheral action, the central action of PGE1 results in suppression of nociceptive responses which may be serotonin mediated.
    Type of Medium: Electronic Resource
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