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Biomedical subjects

G Biggio

Publications and source records attributed to G Biggio.

At least 199 records · Page 11Linked to original sources
PubMed1980

Failure of ketamine to interact with opiate receptors.

Ketamine, an anesthetic agent endowed with several morphine-like effects, failed to displace 3H-dihydromorphine or 3H-methionine-enkephalin from opiate receptors in the rat brain synaptosomal-mitochondrial membrane preparations. Furthermore, ketamine-induced analgesia in rats was not antagonized by naloxone, suggesting that this effect is not mediated by opiate receptors.

Animals↗
PubMed1979

Decrease of cyclic GMP in cerebellar cortex by intrastriatal (--)-sulpiride.

Intraperitoneal administration of (--)-sulpiride (12 to 50 mg/kg) produced a dose-related decrease in cGMP content in cerebellar cortex, while the (+)-sulpiride (10 microgram), but not after intracerebellar injection. These findings support the contention that (--)-sulpiride modifies cerebellar cGMP levels through and action on striatal dopamine receptors.

Animals↗
PubMed1979

Neuronal localisation of benzodiazepine receptors in cerebellum.

The cellular localisation of benzodiazepine receptors was studied. Kainic acid induced neuronal lesions (2 x 0.25-2 x 2 micrograms; 2-26 days in rat cerebellum decreased specific binding of [3H]flunitrazepam down to 35% of controls. Specific binding of [3H]flunitrazepam was also decreased (to 80% of controls) in the cerebllum of mutant nervous mouse (nr/nr) where Purkinje cells are degenerated but in the mutant weaver mouse where granule cells are degenerated. These results show that benzodiazepine receptors are located mainly on neurons; both on Purkinje cells and other neurons, but not to a great extent on granule cells.

Animals↗
PubMed1978

Stimulation of dopamine synthesis in caudate nucleus by intrastriatal enkephalins and antagonism by naloxone.

The intraventricular injection of methionine-enkephalin (50 to 100 micrograms) or [d-Ala2]-methionine-enkephalinamide (1.5 to 12 micrograms), a synthetic enkephalin analog resistant to enzyme degradation, caused a marked dose-dependent increase in dihydroxyphenylacetic acid and homovanillic acid concentrations in the rat striatum. The [d-Ala2] analog increased the accumulation of dopa in the striatum after aromatic amino acid decarboxylase inhibition, indicating that it increased dopamine synthesis. At the highest doses used both enkephalins failed to modify brain serotonin metabolism. The monolateral microinjection of the [d-Ala2]] analog (3 to 6 micrograms) into the caudate nucleus increased the concentration of dihydroxyphenylacetic acid in the injected side, whereas bilateral injection increased the concentration of this compound in both caudate nuclei and caused catalepsy. The stimulant effect of the [d-Ala2] analog on dopamine synthesis in the striatum persisted after destruction of striatal postsynaptic dopamine receptors with kainic acid. The biochemical and behavioral effects of enkephalins were prevented by naloxone, a specific narcotic antagonist. The results indicate that enkephalins stimulate dopamine synthesis by an action on opioid receptors localized on dopaminergic nerve terminals.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Kainic acid-induced lesion of dopaminergic target cells in the striatum: consequences on the dynamics of cerebellar cGMP.

The bilateral intrastriatal injection of kainic acid (2 microgram/caudate) caused a marked decrease in the activity of striatal dopamine-sensitive adenylate cyclase. This probable loss of target cells for dopamine was associated with a parallel decrease of the cGMP level in the cerebellar cortex, which was maximal (80% loss) by 24 h and prevented apomorphine from raising cerebellar cGMP levels. On the contrary harmaline and isoniazid both increased the levels of cerebellar cGMP in kainic-lesioned rats to the same extent as in control rats. The results indicate that dopamine mechanisms in the striatum are involved in the regulation of cerebellar cortex cGMP.

Adenylyl Cyclases↗