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D F Condorelli

Publications and source records attributed to D F Condorelli.

At least 91 records · Page 5Linked to original sources
PubMed1983

Effects of dopaminergic drugs on cerebellar prostaglandin concentrations.

Previous data indicate that the injection of dopaminergic drugs induces changes in cerebellar 3',5'-guanosine monophosphate (cGMP) content. Accordingly, we have investigated the effects of haloperidol, sulpiride, or apomorphine on cerebellar prostaglandin (PG) concentration, a parameter related to cGMP content. Results obtained show that dopamine receptor blocking agents, such as haloperidol and sulpiride, significantly decrease cerebellar PGE2 and PGF2 alpha concentrations, while opposite changes are induced by apomorphine, a dopamine receptor agonist.

Animals↗
PubMed1982

Comparative effects of estrogens and prolactin on nigral and striatal GAD activity.

The comparative effects of a 10 day estrogen treatment and estrogen independent hyperprolactinemia on nigral and striatal glutamic acid decarboxylase (GAD, EC 4.1.1.15) activity were investigated in male rats. Data obtained show that estrogen treatment decreases GAD activity in substantia nigra, while an increase was observed in conditions of hyperprolactinemia induced by adenohypophysis homograft or acute and chronic sulpiride injection. The possibility of an opposite modulation of strio-nigral GABAergic system by estrogens and prolactin is suggested.

Animals↗
PubMed1982

Sulpiride effects on nigral and striatal glutamic acid decarboxylase activity: a possible involvement of prolactin.

Sulpiride, a benzamide derivative neuroleptic, was shown to significantly increase glutamic acid decarboxylase activity in substantia nigra and corpus striatum in either acutely or chronically injected male rats. Hypophysectomy completely prevented this effect suggesting an involvement of an anterior pituitary factor in the central action of sulpiride. Prolactin might possibly mediate the effects of sulpiride since it is known to increase prolactin secretion by an action at the level of the anterior pituitary. Consistent with this hypothesis was the finding of a similar increase in nigral and striatal glutamic acid decarboxylase activity in hyperprolactinemic animals in which an anterior pituitary had been implanted under the kidney capsule.

Animals↗
PubMed1982

Effects of some typical and atypical antidepressants on GAD activity in various brain regions.

The AA. have investigated the effects of acute or chronic injection of typical and atypical antidepressants on the activity of the GABA--synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) in discrete brain regions. Very significant changes in GAD activity were only observed with sulpiride and nomifensine, two atypical antidepressants that selectively influence dopaminergic transmission and, in turn, prolactin secretion.

Animals↗
PubMed1981

[Effects of different doses of apomorphine on the glutamate decarboxylase activity of the substantia nigra and the medial basal hypothalamus].

The activity of gamma-aminobutyric acid (GABA) synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) was assayed in the rat substantia nigra (SN) and medial basal hypothalamus (MBH) following systemic injection of different doses of the dopamine receptor agonist apomorphine. In SN, the highest dose of apomorphine (1000 micrograms/kg) causes an increase of the GAD activity whilst an opposite effect is observed with the lowest dose (35 micrograms/kg). Results obtained in SN are in accordance with previous neurochemical and behavioural data suggesting an opposite action of high (500 micrograms/kg) and low doses (100 micrograms/kg) of apomorphine in nigro-striatal system, probably due to the existence of two classes of dopamine receptors, i.e. classical postsynaptic dopamine receptors and presynaptic inhibitory dopamine autoreceptors. In MBH, the evidence for similar effects of low and high doses of apomorphine (the decrease of GAD activity) may suggest that, as already reported, at this level only one class of dopamine receptors is present.

Animals↗
PubMed1981

[Hyperprolactinemia and catalepsy induced by haloperidol].

The effect of endogenous hyperprolactinemia induced by pituitary transplantation under the kidney capsule on haloperidol induced catalepsy was evaluated in male Wistar rats treated with two doses of the drug (500 gamma/kg; 2 mg/kg i.p.). Rats of 220 +/- 30 g received intraperitoneal injection of haloperidol. Every five minutes following drug administration the rats were assessed for catalepsy by placing the forepaw on a horizontal bar, and observed for two minutes. Data obtained show that hyperprolactinemia potentiates the cataleptic score in rats treated with dose of 500 gamma/kg i.p., while no significant difference was observed between hyperprolactinemic rats and control rats, at the dose of 2 mg/kg i.p. of haloperidol.

Animals↗
PubMed1981

Effects of chronic haloperidol and sulpiride treatment on rat nigral GABA content.

The effects of chronic haloperidol and sulpiride treatment on nigral GABA content were investigated in rats. Chronic sulpiride treatment is capable of inducing an increase in nigral GABA content whilst no significant effect is observed following chronic haloperidol treatment at the doses used. The different effects of haloperidol and sulpiride on nigral GABA content were related to the different neuropharmacological spectrum of the two drugs.

Animals↗
PubMed1981

Possible role of prolactin in the modification of medial basal hypothalamic glutamic acid decarboxylase activity.

The effects of acute and chronic injections of haloperidol, sulpiride and apomorphine on serum prolactin (PRL) levels and medial basal hypothalamus (MBH) glutamic acid decarboxylase (GAD) activity were investigated in male rats. Parallel changes in PRL and GAD activity were observed in acutely treated animals. Conversely, a return to normal of the GAD activity associated with high plasma PRL levels was induced by chronic haloperidol and sulpiride treatment. Results are discussed in the light of the possible existence of a hypothetical PRL-gamma-aminobutyric acid (GABA) subsidiary feedback loop.

Animals↗
PubMed1981

Effects of different doses of apomorphine on GAD activity in rat substantia nigra.

The effects of different doses of the dopamine (DA) receptor agonist apomorphine on the activity of the gamma-aminobutyric acid (GABA)-synthesizing enzyme glutamic acid decarboxylase (GAD, EC 4.1.1.15) were investigated in rat substantia nigra in comparison with haloperidol and sulpiride, two DA receptor blocking agents. Results obtained show that low doses (10,35 microgram/kg, s.c.) of apomorphine induce a decrease in nigral GAD activity whilst an opposite effect is observed with the highest dose (1000 microgram/kg, s.c.). No significant change is observed following injection of the intermediate doses (100 and 500 microgram/kg, s.c.). Moreover, sulpiride at the dose used (2 mg/kg, i.p.) induces an increase in GAD activity whilst no effect follows systemic injection of the same dose of haloperidol. The results are discussed in light of recent neurochemical and behavioral data.

Animals↗
PubMed1981

Comparative effects of chronic haloperidol and sulpiride treatment on nigral and striatal GABA content.

Nigral and striatal GABA contents were assayed in male rats treated chronically with haloperidol or sulpiride, two dopamine-receptor blocking agents that have different neuropharmacological spectra in regard to their biochemical, behavioural, and clinical properties. No great difference was observed between the chronic effects of haloperidol and sulpiride on nigral and striatal GABA content. However, low doses (30 micrograms/kg, intraperitoneally) of the dopamine-receptor agonist apomorphine, injected 12 h after the discontinuation of chronic haloperidol or chronic sulpiride treatment, induced opposite changes in nigral GABA levels suggesting the existence of a different "status" of the dopamine receptors during the 12 h-period following the withdrawal of haloperidol or sulpiride.

Animals↗
PubMed1981

Influence of hyperprolactinemia induced by adenopituitary transplantation under the kidney capsule on the glutamic acid decarboxylase activity in various brain regions.

Glutamic acid decarboxylase activity was assayed in rat substantia nigra, corpus striatum, medial basal hypothalamus and cerebellum under conditions of hyperprolactinemia induced by transplantation of adenopituitary under the kidney capsule. The results indicate that hyperprolactinemia induces a slight increase in the glutamic acid decarboxylase activity of substantia nigra and medial basal hypothalamus and a more evident increase at striatal level. No change was observed in the cerebellum.

Animals↗