PubMed Health⌕ Search

Biomedical subjects

D Rotiroti

Publications and source records attributed to D Rotiroti.

At least 73 records · Page 4Linked to original sources
PubMed1979

Light-evoked changes in chick optic lobe adenylate-cyclase.

The effects of exposure to 48 h darkness and to stroboscope stimulation on chick optic lobe adenylate-cyclase activity were studied. A significant decrease in adenylate-cyclase after 48 h exposure to darkness occurred with return to normal values after re-exposure to light. Stroboscope stimulation for 3 min produced instead a marked increase in optic lobe adenylate-cyclase. Present experiments suggest that cAMP may serve as inhibitory messenger in synaptic transmission along central visual pathways.

Adenylyl Cyclases↗
PubMed1979

Light-evoked changes in chick optic lobe GABA system.

In young chicks the effects of 3 min stroboscope stimulation on GABA and free glutamic acid content and on GAD and GABA-T activity in optic lobes were studied. A significant depletion in GABA and glutamic acid levels was found to occur. In addition a sustained increase in GABA-T and GAD activity was observed. In conclusion present experiments are in favour of an inhibitory role played by GABA in chick optic tectum during stroboscope stimulation.

4-Aminobutyrate Transaminase↗
PubMed1979

Effects of intraventricular beta-endorphin on GABA system in some areas of chick brain.

In chicks with cannulae chronically implanted into the III cerebral ventricle, the effects of a single dose (10 micrograms) of beta-endorphin on GABA and free glutamic acid content, GAD and GABA-T activities in the diencephalon, brain-stem and brain hemispheres were studied at the time of maximal behavioural stuporous state and analgesia. A significant decrease in GABA concentration both in the diencephalon and brain-stem, accompanied by a significant increase in GABA-T activity in the same areas, was shown to occur. No changes were observed in GAD activity and in glutamic acid content in the studied areas of the brain. In conclusion, present experiments suggest that some central effects of a beta-endorphin may be due to an interference with GABA-ergic transmission.

4-Aminobutyrate Transaminase↗
PubMed1979

Effects of intraventricular and intra-aquaductal 6-hydroxydopamine on monoamine containing neurons of the fowl paleostriatum, diencephalon and mesencephalon.

The effects of a single intraventricular or intra-aquaductal infusion of 6-hydroxydopamine (6-OHDA) on monoamine fluorescence in the paleostriatum augmentatum, diencephalon and mesencephalon were studied. Present experiments have enable us to better characterize the distribution of catecholaminegic axons in the paleostriatum augmentatum, preoptic area, hypothalamus, median eminence, periventricular areas as well as of cell-bodies and axons exbiting green fluorescence in the n. mesencephalicus properties and other mesencephalic nuclei.

Animals↗
PubMed1978

Effects of althesin and ketamine on resting and stress stimulated adrenocortical activity in rats.

The effects were studied of two i.v. anaesthetics (Althesin and ketamine) on resting and activated adrenocortical function in the rat. Small doses of Althesin and ketamine comparable to those required to produce induction of anaesthesia in man evoked adrenocortical stimulation, but the stressing effects of ketamine were more prolonged. During deep anaesthesia with either anaesthetic there was an inhibition of pituitary adrenal activation induced by handling and surgery. However, during recovery, ketamine was associated with intense and prolonged adrenocortical stimulation. The stress of laparotomy in control rats and in rats pretreated with the anaesthetics caused a depletion of noradrenaline in the hypothalamus; this suggests that both anaesthetics inhibit adrenocortical activation by mechanisms different from adrenergic inhibition.

Adrenal Cortex↗
PubMed1978

Central cardiovascular effects of clonidine and another imidazoline derivative ST [600] in adult fowls.

In adult fowls (Gallus domesticus) with cannulae stereotaxically implanted into the III cerebral ventricle and into the hypothalamus, the effects of clonidine and another imidazoline derivative (St 600) were studied on arterial blood pressure and heart rate. It has been shown that clonidine and St 600 administration into the III ventricle or into the hypothalamus produced an immediate profound and long lasting decrease in blood pressure and heart rate. Contrary to the intravenous administration, this response was not preceded by an initial rise in blood pressure. On an equimolar basis St 600 appeared to be at least one-tenth as potent as clonidine. Prior intraventricular administration of alpha-adrenoceptor blocking agents, phentolamine and phenoxybenzamine, prevented changes in cardiovascular effects following intrahypothalamic infusion of clonidine and St 600. In conclusion, present experiments indicate that in fowls the hypothalamus represents the site or sites through which hypotension and bradycardia evoked by clonidine and related compounds are mediated.

Animals↗
PubMed1976

Acute central effects of 5,6-dihydroxytryptamine in fowl.

In adult hens (Gallus domesticus) infusion into the IIIrd cerebral ventricle of 5,6-DHT (50, 75 and 100 mug) produced, after 5-10 min behavioural and electrocortical sedation and sleep lasting about 6-8 hr,and a monophasic or biphasic increase in body temperature for about 8 hr, Two and a half hr after 5,6-DHT administration, the histochemical picture showed a sustained decrease in yellow and green fluorescence in areas adjacent to the IIIrd ventricle, in the anterior hypothalamus and in the preoptic area, whereas no significant changes were detected in fluorescence of the tegmental cell-bodies. The present experiments suggest that behavioural and electrocortical effects evoked by 5,6-DHT seem to be due to a synergistic action of 5-HT and catecholamines displaced and released by this compound, whereas hyperthermic effects seem to be due to a more sustained release of 5-HT and/or to a direct action on 5-HT receptors and/or inhibition of 5-HT reuptake.

5,6-Dihydroxytryptamine↗
PubMedDate not supplied

Evidence that behavioural and electrocortical sleep induced by guanfacine is due to stimulation of alpha 2-adrenoceptors.

The effects of guanfacine and other drugs acting at alpha 1- and alpha 2-adrenoceptors on behaviour, electrocortical activity and ECoG spectrum power were studied in chicks and rats. Guanfacine, given systematically in chicks, produced behavioural and electrocortical slow-wave sleep lasting 100-200 min, depending on the dose; these effects were prevented by yohimbine, a selective antagonist, at alpha 2-adrenoceptors and potentiated by prazosin, a selective antagonist, at alpha 1-adrenoceptors. Similar behavioural and electrocortical effects were obtained after systemic or intraventricular infusion of guanfacine in rats. In addition, a significant increase in total and in lower frequency band (0-4; 4-8 Hz) voltage power was observed. Behavioural and ECoG effects of guanfacine were prevented by phentolamine or yohimbine, whereas prazosin and propranolol were ineffective. Yohimbine itself, given systemically in chicks, produced behavioural stimulation, vocalization, increase in locomotor activity and ECoG desynchronization, with a significant fall in total and 0-3, 3-6, 6-9 and 9-12 Hz voltage power lasting approx. 3 h. Desipramine, an inhibitor of noradrenaline reuptake, produced in chicks behavioural and ECoG arousal, vocalization, pecking, escape responses and aggressive behaviour. In conclusion, the present experiments show that guanfacine sedative effects seem to be mediated predominantly via an activation of presynaptic alpha 2-adrenoceptors and suggest that arousal is due to stimulation of post-synaptic alpha 1-adrenoceptors.

Animals↗