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Biomedical subjects

G Nisticò

Publications and source records attributed to G Nisticò.

At least 145 records · Page 8Linked to original sources

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↗

Effect of central nervous system-acting drugs after selective destruction by neurotoxins of 5-hydroxytryptamine fibers in the brain.

Some behavioral effects of CNS-acting drugs have been studied in two animal species after functional impairment of central serotonergic activity. In rabbits, pretreatment with p-CPA or with 5,6-DHT counteracted the hyperthermia induced by d-amphetamine or apomorphine; the same pretreatments were ineffective in modifying pyrogen-induced fever. These data indicate a modulatory role of the 5-HT system in the hyperthermic response to dopaminergic agonists, such as d-amphetamine and apomorphine, and rule out 5-HT involvement in the hyperpyrexia induced by pyrogen. A previous intraventricular injection of 5,6-DHT significantly potentiated the increase in body temperature induced by 5-HTP in combination with a MAO inhibitor. Pretreatment with p-CPA, instead, strongly inhibited the hyperthermic response to 5-HTP. In unanesthetized fowl, at the time of the most dramatic degenerative signs of indoleaminergic neurons induced by 5,6-DHT, as documented by histofluorescence pictures, intraventricular infusion of 5-HT induced more intense behavioral, electrocortical, and body temperature modifications than in control animals. These results suggest the existence of receptor supersensitivity after 5-HT nerve ending degeneration but not after brain 5-HT depletion. The hyperthermic effect of a presynaptically acting drug, fenfluramine, was counteracted in rabbits and in fowl pretreated with either p-CPA or 5,6-DHT. Since identical behavioral, electrocortical, and body temperature effects have been observed after 5-HT or 5,6-DHT infusion into the third ventricle of fowl, it may be concluded that 5,6-DHT behaves also as a central 5-HT receptor agonist.

5-Hydroxytryptophan↗

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↗

Serotoninergic involvement in the regulation of circadian rhythms of hypothalamic-pituitary adrenal and prolactin axis.

A detailed review of their own experiments and of data existing in the literature regarding the role played by 5HT in the control of circadian rhythms of HHAA and HHPA is given by the AA. In rats, a positive correlation between 5-HT content in the limbic system and plasma corticosterone circadian rhythm has been shown to exist by means of pharmacological and neurosurgical approaches. Lesions of the raphe area result in an abolition of diurnal periodicity of plasma steroids similar to that obtained after inhibition of 5-HT synthesis by means of PCPA. A modification of the amplitude of the plasma corticosterone circadian variations also occurs after more selective destruction of some nuclei (n. centralis superior and n. raphe dorsalis) which reduced 5-HT concentration both in the hypothalamus and the hippocampus. Isolation of the mediobasal hypothalamus by a frontal cut posterior to the optic chiasma abolishes the diurnal fluctuation of plasma corticosterone, indicating that the suprachiasmatic nucleus is a focal site for the 5-HT regulation of the phasic activity of the HHAA. Evidence in favour of 5-HT mechanisms in the limbic area as the biological clock regulating the circadian variations of the adrenal axis is also provided. Restoration of the diurnal rhythm of plasma corticosterone after its abolition could be explained with the existence of a small functional pool of brain 5-HT or with the development of receptor supersensitivity. Pharmacological and surgical manipulation on central 5-HT neurons suggest the existence of two distinct serotoninergic mechanisms, a limbic one and an intrahypothalamic one, which play a modulatory role in the circadian variations of plasma PRL. Also in this case, adaptive accessory brain structures can take over in restoring the circadian hormones periodicity in conditions of impairment of the main serotoninergic mechanisms.

5,6-Dihydroxytryptamine↗

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↗

Time course of 5,6-dihydroxytryptamine neurotoxic effects on fowl diencephalon and upper brain stem monoaminergic pathways.

In adult fowls the time-course of the neurotoxic effects of 5,6-DHT on indolaminergic neurons (in comparison with controls and with animals pre-treated with mebanazine, a MAO-inhibitor) was studied. It was shown that 5,6-DHT given into the third cerebral ventricle produced a rather selective degeneration of indolaminergic neurons which was most dramatic 4 and 7 days after the injection. Injured axons characterized by a pile-up of strongly yellow fluorescent material were seen in areas bordering the third ventricle, and in the posterior, medium and anterior hypothalamus, preoptic area, median eminence, n. tuberalis and paleostriatum augmentatum. A decrease in yellow fluorescence in areas distal to the injured axons was only detectable after 19 days. A certain regrowth of some terminal networks was observed 30 days after 5,6-DHT administration. Present data indicate that, in fowls, ascending indolamine neurons mainly originate in tegmental cell bodies and are organized in a large tract which runs along the medial forebrain bundle, sending terminals innervating several diencephalic and other subcortical areas.

5,6-Dihydroxytryptamine↗

Psychotropic drugs: mechanism of action at the neurotransmitter level.

Although the intimate mechanism by which psychotropic agents exert their therapeutic effects is still not completely clear, a large bulk of evidence supports the existence of a close correlation between their clinical antipsychotic acitivity and the ability to affect by different mechanisms brain monoamines and/or other real or putative neurotransmitters. Neuroleptic drugs of the phenothiazine type and related classes possess a blocking effect on dopaminergic transmission in nigro-striatal, mesolimbic and mesocortical areas; experiments supporting both a pre-and post-synaptic site of action have been described, together with the interference at the molecular level with DA-sensitive adenylate cyclase activity. In addition, anticholinergic activity and increase in GABA turnover in the striatum have been given as evidence to explain for some neuroleptics (e.g sulpiride, clozapine) lack of extrapyramidal side-effects. Anxiolytics seem to produce their therapeutic effect through a decrease in catecholaminegic and serotoninergic turnover although new avenues have been opened by some recent reports indicating a facilitation of GABAergic and glycinergic transmission in CNS.

Animals↗

Behavioural, electrocortical and body temperature effects of cholera toxin.

In young chicks intrahypothalamic infusion of cholera toxin produced a dramatic and dose-dependent increase in motor activity. Similar effects were also obtained in adult fowls after injection of cholera toxin into the third cerebral ventricle, the hypothalamus or the paleostriatum augmentatum. Electrocortical changes consisted of a slight desynchronization during the hypermotor activity and were preceded, when the highest intraventricular doses were used, by a short period of slower frequency and higher amplitude potentials. Intraventricular and intrahypothalamic but not intrastriatal injection of cholera toxin produced a typical biphasic hyperthermic response.

Animals↗

Intraventricular antipyretics and bacterial pyrogen fever.

In adult fowls with cannulae chronically implanted into the IIIrd cerebral ventricle or into the hypothalamus, the effects of various hydrosoluble antipyretics, given intraventricularly, on bacterial pyrogen fever were studied. It has been shown that fever evoked by intrahypothalamic or intraventricular infusion of O somatic antigen of Shigella Dysenteriae was reduced by intraventricular administration of acetylsalicylate-lysine, indomethacin-methylglucamine or ibuprofen-lysine given during the febrile plateau. However, a 3-day intraventricular pretreatment with acetylsalicylate or indomethacin, or a single administration 30 min before, did not prevent fever by subsequent intraventricular or intrahypothalamic injection of pyrogen. On the contrary, intraventricular infusion of indomethacin or acetylsalicylate substantially reduced pyrogen fever when given after pyrogen latency period, e.g. just at the beginning of the febrile response. A possible involvement of E prostaglandins as mediator to pyrogen fever is discussed.

Analgesics↗

Double-blind study of a total liver extract in patients with hepatic dysfunction.

Forty hospitalized male patients with hepatic functional deficit were treated i.m. for 3 weeks with a total liver extract or placebo. The study was a double-blind. Statistical analysis (Student's t test, analysis of variance. Mann-Whitney test and Fisher's probability test) showed that liver extract therapy was more effective than placebo in improving liver function as indicated by changes in clinical features(digestive disorders, constipation, hepatomegaly) and colloidal and other laboratory tests, e.g. plasma cholesterol, prothrombin time, red cell count and hemoglobin concentration. An overall clinical assessment showed that 60% of patients treated with the liver extract were improved. In addition, no local or general side effects were observed. Present results are in favour of an hepatoprotective activity of a total liver extract.

Adult↗