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L H Allikmets

Publications and source records attributed to L H Allikmets.

10 recordsLinked to original sources
PubMed1986

Benzodiazepine binding sites in mice forebrain and kidneys: evidence for similar regulation by GABA agonists.

Benzodiazepine binding sites in mice forebrain and kidney homogenate were labelled either in vivo (SC injection) or in vitro by 3H-flunitrazepam. The binding in both cases was carried out in vitro in the presence or absence of 10 microM unlabelled flunitrazepam during 60 min at 0 degrees C. When benzodiazepine binding sites were labelled in vivo pretreatment of animals with muscimol (0.75 and 1.5 mg/kg, IP) and fenibut (25 and 100 mg/kg, IP) in a dose-dependent manner facilitated 3H-flunitrazepam binding both in mice forebrain and kidneys. In vitro labelling of benzodiazepine binding sites demonstrated similar to in vivo labelling in forebrain but not in kidneys. The peripheral benzodiazepine binding sites in kidneys are therefore modulated similarly to benzodiazepine binding sites in forebrain by GABA-ergic drugs.

Animals↗
PubMed1983

The action of benzodiazepine antagonist Ro 15-1788 on the effects of GABA-ergic drugs.

The interaction of Ro 15-1788 (5 mg kg-1 i.p.) a benzodiazepine antagonist, with GABA-ergic drugs muscimol (1.4 mg kg-1 i.p.), fenibut (100 mg kg-1 i.p.) and baclofen (5 mg kg-1 i.p.) was examined in behavioural and biochemical studies in rats. All the above-mentioned GABA-ergic drugs produced motor depression and with the exception of muscimol, where anti-aggressive effect was evident, fenibut and baclofen showed only slight antiaggresive properties. Ro 15-1788 attenuated the motor depression produced by these compounds but potentiated their antiaggressive effect. Moreover, it was found that Ro 15-1788 itself possessed dose-related antiaggressive properties. Fenibut increased, whereas muscimol and Ro 15-1788 decreased, the GABA content in the rat striatum. Ro 15-1788 and all the studied GABA-ergic compounds increased the level of the dopamine metabolite 3,4-dihyroxyphenylacetic acid (DOPAC) in the striatum. In spite of this no further increase of DOPAC was observed after concomitant use of Ro 15-1788 with GABA-ergic drugs. The action of investigated GABA-ergic drugs via GABA receptors linked to benzodiazepine receptors is suggested.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1982

Intrastriatal injection of kainic acid prevents the development of postsynaptic dopamine receptor hypersensitivity after chronic haloperidol treatment.

Rats injected intrastriatally with kainic acid (KA), in contrast to sham-treated (control) animals, showed no tolerance toward catalepsy induced by chronic haloperidol treatment (28 days). After termination of chronic haloperidol treatment in control animals, apomorphine-induced stereotypy was significantly enhanced as compared to chronic saline-injected controls. Rats injected with kainic acid and treated with chronic haloperidol or saline showed no differences in apomorphine stereotypy. These results show that the development of tolerance and behavioural hypersensitivity after chronic neuroleptic treatment is mediated via striatal postsynaptic receptors sensitive to kainic acid lesions.

Animals↗
PubMed1981

Effects of piracetam on the central dopaminergic transmission.

The effects of piracetam on dopamine metabolism in rat striatal tissue and on behavioural and biochemical effects of haloperidol were studied. Piracetam in doses 600 mg/kg and 1,000 mg/kg (i.p.) increased the levels of dopamine metabolites (homovanillic acid and 3,4-dihydroxy-phenylacetic acid) but did not influence the content of dopamine in the striatum. Piracetam (1,000 mg/kg) also increased haloperidol-induced catalepsy in rats. These results are discussed in relation to the hypothesis that some behavioural effects of piracetam can be connected with its action on dopaminergic transmission.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Biochemical and behavioural studies on the interference between catecholaminergic and serotonergic central systems.

L-DOPA, apomorphine and amphetamine increase emotional reactivity and aggressiveness, and/or evoke spontaneous attack behaviour in male rats. At the same time these compounds accelerate the turnover of endogenous serotonin (5-HT), increasing the brain concentration of 5-HIAA. L-DOPA, amphetamine and apomorphine antagonize the depressive effects of 6-tryptophan on behaviour. After the injection of L-tryptophan these dopaminomimetics facilitate the turnover of 5-HT in the brain. On the other hand, the tranquillizing effect of L-tryptophan correlates not only to the increased level of 5-HT but also to an accelerated catabolism of dopamine. After the simultaneous injection of L-DOPA and L-tryptophan, cross-influence on the turnover of 5-HT and dopamine is noted, while in behaviour the effects of L-DOPA prevail over those of L-tryptophan. PCPA blocks the behavioural effects of dopaminomimetics.

Adrenergic alpha-Agonists↗