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Biomedical subjects

M Morelli

Publications and source records attributed to M Morelli.

At least 145 records · Page 8Linked to original sources
PubMed1982

[Levels of xenobiotic metabolizing enzyme activities of xenobiotic tissue in different animal species].

Aminopyrine-N-demethylase, p-nitroanisole-O-demethylase and lipid peroxidation were determined in liver postmitochondrial fractions (S-9) of mice in the basal state and after induction with beta-naphtoflavone, sodium phenobarbital, or both the inducers. The two activities were similar in their response to all inductions: meanly, 1,2 times with beta-NF, 2,0 times with Na-PB, 5,8 times with Na-PB+ beta-NF. Lipid peroxidation was sensibly more active in basal animals with respect to that with induction. The results are discussed in a partial review of the sector literature, which deserves still much work to be completed.

Aminopyrine N-Demethylase↗
PubMed1982

The effect of GABA on in vitro binding of two novel non-benzodiazepines, PK 8165 and CGS 8216, to benzodiazepine receptors in the rat brain.

The effect of gamma-aminobutyric acid (GABA) on the binding of PK 8165, a quinoline derivative, and CGS 8216, a pyrazoloquinoline, was assessed in two different regions of the rat brain. PK 8165, a compound with reported anxiolytic properties, inhibited [3H]-propyl beta-carboline-3-carboxylate labeled receptors in the cerebellum with an IC50 of 844 nM and 370 nM in the absence and presence of micro M GABA, respectively. GABA (100 micro M) was less effective in the cerebral cortex, decreasing the IC50 value from 280 to 197 nM. In saturation isotherm studies with [3H]-CGS 8216, a benzodiazepine receptor antagonist, GABA (100 micro M) induced a small but significant reduction in the apparent affinity of [3H]-CGS 8216 for benzodiazepine receptors in the cerebral cortex but the Bmax was unchanged.

Animals↗
PubMed1982

A re-evaluation of the role of superior colliculus in turning behaviour.

There is much debate on the role of the superior colliculus (SC) in turning behaviour. In order to clarify this issue, unilateral kainate lesions were made by infusing 0.25 microgram of kainate at two different anterior planes (0.8 mm apart), in the lateral or in the medial aspects of the deep collicular layers (DLSC), in the dorsal mesencephalic reticular formation (MRF), or in the lateral periaqueductal grey (PAG), both in normal rats and in rats made unilaterally supersensitive to DA-receptor agonists by unilateral infusion of 6-OHDA in the rostral substantia nigra. The effect of kainate lesions on spontaneous and apomorphine-induced motor behaviour was studied. In normal rats, unilateral kainate lesions of lateral DLSC or dorsal MRF resulted in short-lasting, spontaneous ipsiversive turning and persistent ipsiversive circling after peripheral administration of apomorphine. In 6-OHDA rats, kainate lesions of lateral DLSC or of dorsal MRF ipsilateral to 6-OHDA denervation reduced or even reversed the contralateral circling normally elicited in these rats by peripheral administration of apomorphine. Lesions of dorsal MRF, when compared with lesions of lateral DLSC, were more effective in producing these changes. Kainate lesions restricted to medial DLSC or to the PAG failed to elicit motor asymmetries in normal rats or to significantly modify the intensity of contralateral turning in 6-OHDA rats. These results clearly indicate that the SC plays an important role in turning behaviour. Failure of previous studies to research this conclusion probably derives from inadequate localization of collicular lesions and from the use of bilateral lesions.

Animals↗
PubMed1982

[3H]CL 218,872, a novel triazolopyridazine which labels the benzodiazepine receptors in rat brain.

We examined the specific binding of [3H]CL 218,872, a novel triazolopyridazine to benzodiazepine receptors in the rat cerebral cortex. Two binding sites with KD values of about 10-30 nM and 200-600 nM were demonstrated. A number of benzodiazepine anxiolytics inhibited [3H]CL 218,872 binding in a manner which correlates with the potency of these drugs for inhibiting [3H]benzodiazepine binding. Our initial studies show that [3H]CL 218,872 can label the benzodiazepine receptors and may prove to be a useful probe for studying benzodiazepine heterogeneity and regulation.

Animals↗
PubMed1981

Role of substantia nigra pars reticulata neurons in the expression of neuroleptic-induced catalepsy.

Bilateral kainate-induced lesions of the substantia nigra prevented or dramatically reduced the catalepsy produced by haloperidol. In contrast, infusion of 1 or 4 micrograms 6-OHDA in the medial forebrain bundle, which decreased striatal DA by 30% and 80% respectively, failed to affect or actually potentiated haloperidol catalepsy. Since intranigral kainate, in contrast to 6-OHDA, destroys pars reticulata neurons it appears that these neurons are essential for the expression of haloperidol-catalepsy.

Animals↗
PubMed1981

Role of dorsal mesencephalic reticular formation and deep layers of superior colliculus as out-put stations for turning behaviour elicited from the substantia nigra pars reticulata.

In order to investigate the role of dorsal mesencephalic reticular formation (MRF) and deep layers of superior colliculus (DLSC) as out-put areas for non-dopamine mediated behavioural functions arising in the substantia nigra, discrete unilateral kainate-lesions as well as sham-lesions were placed in the MRF and DLSC. Ten days later kainate (0.75 microgram) was microinjected into the substantia nigra pars reticulata. Lesions of MRF as well as lesions of DLSC reduced the contralateral turning induced by kainate lesions of pars reticulata ipsilateral to the MRF or DLSC lesions. The lesions of MRF were more effective than lesions of DLSC. Lesions of MRF or DLSC on the side contralateral to intranigral kainate were ineffective. The results indicate that the MRF-DLSC complex is an essential area for the expression of motor behaviour elicited from the substantia nigra.

Animals↗
PubMed1981

Role of dorsal mesencephalic reticular formation and deep layers of superior colliculus in turning behaviour elicited from the striatum.

Kainate or electrolytic lesions were placed unilaterally in the dorsal mesencephalic reticular formation (MRF) or in the deep layers of the superior colliculus (DLSC) on the same side of a unilateral lesion of the medial forebrain bundle with 6-OHDA. Before the lesions the rats turned contralaterally when challenged with 0.25 mg/kg of apomorphine. After lesions of the MRF most rats turned ipsilaterally in response to the same dose of apomorphine. After lesions of the DLSC apomorphine-induced contralateral turning was significantly reduced but not abolished. The results indicate that the MRF and DLSC play a primary role in the expression of turning originated from the striatum.

Animals↗
PubMed1981

Benzodiazepines prevent kainate-induced loss of GABAergic and cholinergic neurons in the chick retina.

Kainic acid (50 nmol), applied intravitreally to the eyes of chicks, produces within 6 h a loss of more than 50% of biochemical markers for cholinergic and GABAergic neurons in the retina. Repeated peripheral administration of benzodiazepines, such as diazepam and clonazepam, protects from the kainate-induced loss of cholinergic and GABAergic markers in the retina. Histologically diazepam reduces the nuclear pyknosis induced by kainate particularly at the level of the amacrine cell-layer.

Animals↗
PubMed1981

Benzodiazepine receptor binding in young, mature and senescent rat brain and kidney.

Clinical reports have described age-altered pharmacological effects of anxiolytic drugs especially an increased susceptibility to their sedative actions. In order to test whether such changes may be due to age-related alterations in central benzodiazepine receptors, 3H-flunitrazepam binding was assayed in the frontal cortex and cerebellum of young, mature and senescent rats. The numbers of 3H-flunitrazepam binding sites and their affinity was determined by Scatchard analysis of saturation isotherms and the relative abundance of type I and type II benzodiazepine receptors was assessed by drug-inhibition studies using diazepam and the triazolopyridazine, CL 218,872. In addition, age related changes in the kidney and hippocampus of the Ro5-4864-sensitive benzodiazepine receptor were studied using 3H-Ro5-4864. No age-related alterations were noted in the binding characteristics of 3H-flunitrazepam. Furthermore, drug-inhibition of 3H-flunitrazepam binding by diazepam and CL 218,872 was nearly identical in young, mature and senescent rats, indicating that also the ratio of type I and type II receptors does not change with age. Binding of 3H-Ro5-4864 to membranes from rat hippocampus was not age-related. However, a significant decrease in 3H-Ro5-4864 binding to kidney membranes was demonstrated. Hence, central benzodiazepine receptors appear unaltered in the senescent rat model of aging. The clinical findings of an increased susceptibility to the sedative effects of benzodiazepines in the elderly may therefore be attributed to pharmacokinetic variables, or to events occurring secondarily to receptor activation.

Age Factors↗