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Biomedical subjects

G Nisticò

Publications and source records attributed to G Nisticò.

At least 91 records · Page 5Linked to original sources
PubMed1989

Age-related alterations in cardiovascular responsiveness to clonidine infused into the nucleus tractus solitarii in rats.

The cardiovascular response to the unilateral injection of clonidine into the nucleus tractus solitarii in old compared to young rats was evaluated. In 3-month old rats clonidine (0.25, 0.5 and 1 microgram) injected into the nucleus tractus solitarii in anaesthetized rats produced a significant fall in blood pressure (BP) and a significant decrease in heart rate (HR). In contrast, in 12 month old rats the maximum fall in blood pressure and heart rate was significantly less than in young animals. In addition, in older rats (24 month old) clonidine, at the same or larger doses given into the nucleus tractus solitarii did not produce any significant change in the cardiovascular parameters studied. In conclusion, the present experiments provide evidence that during ageing there is a progressive decrease in the cardiovascular response to alpha 2-adrenoceptor stimulation in the nucleus tractus solitarii. In addition, it is conceivable that such a decrease and subsequently the lack in response may be related to a progressive decrease in the number and/or affinity of the specific alpha 2-adrenoceptor binding sites at this level.

Aging↗
PubMed1989

Inhibition by pertussis toxin of the soporific effects induced by stimulation of dopamine D2 autoreceptors in the ventral tegmental area in rats.

The behavioural and ECoG spectrum power effects of agonists at dopamine D2 autoreceptors, both after systemic or intracerebral administration, were studied in rats. It was shown that the bilateral injection of apomorphine or (+) 3PPP (0.1, 0.5 and 1.0 nmol for each compound) into the ventral tegmental area produced behavioural and ECoG sleep, accompanied by a statistically-significant increase in ECoG total spectrum power. These effects were completely antagonized by a pretreatment (24, 48 or 72 hr before) with pertussis toxin (0.34 and 3.4 micrograms), given into the same site. Similarly, behavioural sleep and an increase in ECoG total voltage power, produced by systemic administration of apomorphine (263 nmol/kg i.p.), were abolished by pertussis toxin (3.4 micrograms) injected bilaterally into the ventral tegmental area 24, 48 or 72 hr before. In conclusion, the present results suggest that behavioural and ECoG spectrum power effects, triggered by stimulation of dopamine D2 autoreceptors in the ventral tegmental area of rats, seem to be linked to the inhibition of adenylate cyclase activity through a Gi protein and or to other biochemical events linked to Gi proteins.

Adenylate Cyclase Toxin↗
PubMed1989

Age-dependent ECoG spectrum power alterations are reduced by phosphatidylserine in rats.

The present experiments were carried out in order to characterize the changes in ECoG spectrum power occurring in old compared with young rats. In addition, it was planned to ascertain whether chronic treatment with phosphatidylserine affected possible ECoG changes occurring in aged animals. In comparison to 3 months-old rats, the ECoG activity of 13-15 months-old rats showed spontaneous single or bursts of monophasic and biphasic spikes. In addition, spectrum analysis revealed a significant increase in the power of the lowest frequency band (0.25-3 Hz), accompanied by a decrease in 6-9, 9-12 and 12-16 Hz power. Chronic oral or parenteral treatment with phosphatidylserine gradually reversed the changes in ECoG spectrum power occurring in old rats and produced, at the ECoG level, a distribution pattern of single frequency, bands similar to that observed in young animals.

Age Factors↗
PubMed1989

Behavioural and electrocortical effects after injection of two ornithine decarboxylase inhibitors into several areas of the brain in the rat.

The behavioural and electrocortical effects of alpha-methylornithine and alpha-difluoromethylornithine, two ornithine decarboxylase inhibitors, were evaluated after their infusion into several areas of the brain in the rat. Both compounds induced, in dose-dependent manner, similar epileptogenic effects, stereotyped behaviour and postural asymmetry, depending upon the site of injection. Unilateral injection of DFMO into the entopeduncular nucleus or the substantia nigra pars reticulata, caused an increase in locomotor activity. Unilateral injection of DFMO into the caudate nucleus or the substantia nigra pars compacta had no effect on locomotor activity. Among the areas of the brain studied, the most sensitive site from which electrocortical epileptogenic disorders were evoked, was the hippocampus. The GABA agonist muscimol, infused prior to DFMO, resulted in an anticonvulsant action, while DFMO, infused prior to putrescine, increased the convulsant properties of putrescine. In conclusion, these results indicate that DFMO and alpha-methylornithine produced epileptogenic effects after their intracerebral infusion and suggest that may act as analogues of putrescine.

Amygdala↗
PubMed1989

Pinealectomy inhibits interleukin-2 production and natural killer activity in mice.

Four--five-week-old C57BL/6 mice were surgically pinealectomized. At different time intervals after surgery their spleens were removed and assayed for interleukin-2 (IL-2) production and natural killer (NK) cell activity. Non-operated and sham-operated mice were used as controls. The present results indicate that pinealectomy significantly reduced IL-2 production and NK cell activity, in comparison to sham-operated mice. These effects seem to be related to the lack of melatonin. In fact the subcutaneous injection of this hormone (50 or 100 mg/kg at 5 p.m.) in pinealectomized mice was able to restore IL-2 production and NK cell activity. However, chronic treatment with melatonin (10, 20 and 50 mg/kg for 9 consecutive days) failed to reverse the impairment of the immune responses.

Animals↗
PubMed1989

Effects of pertussis toxin on the behavioural and ECoG spectrum changes induced by clonidine and yohimbine after their microinfusion into the locus coeruleus.

1. Pertussis toxin, a substance which interferes selectively with receptor-mediated signal transduction mechanisms, was injected into the locus coeruleus of rats 1, 2, 3, 6 or 10 days before the microinjection of clonidine or yohimbine into the same site. 2. Clonidine produced in control rats typical behavioural sedation and/or sleep and ECoG synchronization while yohimbine produced behavioural arousal and ECoG desynchronization. 3. The behavioural and ECoG effects of both compounds were blocked in animals pretreated with pertussis toxin. This activity was more marked from 2 to 6 days after pertussis toxin pretreatment and was restored 10 days after toxin administration. In addition, the behavioural and ECoG slow-wave sleep observed after intraperitoneal administration of clonidine (0.2 mumol kg-1) was significantly reduced by prior (3 days) microinfusion of pertussis toxin into the locus coeruleus. 4. These results are consistent with the hypothesis that the behavioural and ECoG effects of clonidine and yohimbine are mediated via a guanine regulatory protein which is affected by pertussis toxin.

Animals↗
PubMed1988

Behavioural and electrocortical changes induced by paraquat after injection in specific areas of the brain of the rat.

The behavioural and electrocortical effects of paraquat were studied after its administration into the substantia nigra, pars compacta, an area where dopamine-(DA) containing cell bodies are present, into the caudate nucleus, where DA-containing nerve endings of the DA nigro-striatal system project, into the locus coeruleus, an area containing noradrenaline cell-bodies and into the n. raphe dorsalis or into the n. raphe medianus, two nuclei containing serotonin (5-HT) cell bodies. The intraventricular administration of paraquat (10 and 50 micrograms) produced an intense pattern of behavioural stimulation and an increase in locomotor activity, circling and the wet-dog syndrome. This symptomatology was accompanied by desynchronization of the electrocorticogram (ECoG) and the appearance of bilateral high voltage epileptogenic spikes, culminating in clonic convulsions. The infusion of paraquat into the s. nigra produced contralateral head and neck deviation, behavioural and motor stimulation, these effects being observed also with smaller doses (1 and 5 micrograms), than those used intraventricularly. The ECoG activity was desynchronized and characterized by high voltage spike discharges. A similar behavioural, postural and ECoG pattern was also observed after infusion of paraquat into the caudate nucleus (10, 25 and 50 micrograms). In addition, paraquat, infused into the locus coeruleus or into the raphe nuclei (5 and 10 micrograms), produced circling, escape responses, jumping and clonic convulsions accompanied by ECoG desynchronization and epileptic phenomena. In conclusion, the present experiments showed that paraquat was able to produce central neurotoxicological effects which did not seem to be specific, at least for the doses used, for the DA nigro-striatal system.

Animals↗
PubMed1988

Ventral tegmental area: site through which dopamine D2-receptor agonists evoke behavioural and electrocortical sleep in rats.

1. In freely moving rats the effects on behaviour and electrocortical (ECoG) spectrum power of some dopamine agonists, i.e. apomorphine and (+)-3PPP, given directly into different areas of the rat brain were studied. In particular, dopamine agonists were microinfused in the ventral tegmental area (VTA) and substantia nigra (SN) or into the caudate nucleus, n. accumbens and prefrontal cortex. The ECoG spectrum power effects were continuously analysed by means of a computerized Berg-Fourier analyser as total spectrum power and power in preselected frequency bands. 2. Apomorphine and (+)-3PPP (0.01, 0.1 and 1.0 nmol) given bilaterally into the VTA produced behavioural and ECoG sleep in a dose-dependent fashion. A statistically significant (P less than 0.01) increase in ECoG total spectrum power with a predominant increase in the lower frequency bands (0.25-3, 3-6 and 6-9 Hz) occurred. No behavioural and ECoG changes were evoked by the same doses of apomorphine bilaterally microinfused into the SN or into the caudate nucleus or by (+)-3PPP (1.0 nml) microinjected into the n. accumbens or applied onto the prefrontal cortex. 3. Behavioural and ECoG sleep was also induced in rats after systemic administration of apomorphine (263 nmol kg-1, i.p.). 4. The behavioural and ECoG spectrum power effects of apomorphine (1.0 nmol) bilaterally micro-infused into the VTA were prevented by a previous microinjection into the same site of (-)-sulpiride (9.8 nmol). Similarly, behavioural and ECoG effects evoked by (+)-3PPP (0.1 nmol) given bilaterally into the VTA, were completely antagonized by a previous injection into the same site of haloperidol (16 pmol given 10 min before). In contrast, pretreatment with SCH 23390 (50 pgkg-1, s.c.), a selective antagonist at dopamine Dl-receptors, was unable to antagonize the behavioural and ECoG spectrum power effects of ( +)-3PPP. 5. Soporific effects induced by systemic administration of apomorphine were antagonized by (-)- sulpiride (9.8 nmol) given bilaterally into the VTA 10min before, whereas, yohimbine (1.3 nmol), (an antagonist at alpha 2-adrenoceptors) bilaterally microinfused into the VTA, was ineffective in this respect. 6. The present experiments provide evidence suggesting that stimulation of dopamine D2-receptors located at the cell body level and/or the dendrites of dopaminergic neurones in the VTA may represent the mechanism through which apomorphine or (+)-3PPP exert their soporific effects in rats.

Animals↗
PubMed1988

Microinfusion of clonidine and yohimbine into locus coeruleus alters EEG power spectrum: effects of aging and reversal by phosphatidylserine.

1. The behavioural and electrocortical (ECoG) power spectrum effects of clonidine, and yohimbine, an agonist and an antagonist at alpha 2-adrenoceptors, after their unilateral microinfusion into the rat locus coeruleus (LC) in young (50-70 days old) and old (13-15 months old) rats were studied. 2. Clonidine (0.09, 0.19, 0.28 and 0.56 nmol) microinfused into the LC of young rats induced dose-dependent behavioural and ECoG slow wave sleep (SWS) with a significant increase in total voltage power and power in the lower frequency bands. In contrast, yohimbine (1.3 and 2.6 nmol) infused into the LC of young rats produced ECoG desynchronization and a significant decrease in total voltage power. 3. In contrast to young rats, clonidine (0.19 and 0.28 nmol) given into the LC did not affect behaviour and the ECoG power spectrum in old rats. However, after higher doses of clonidine (0.56 and 1.2 nmol) a small and short-lasting period of behavioural and ECoG SWS was still evident. Similarly, in old rats yohimbine, at a dose (1.3 nmol) which was stimulative in young animals, did not significantly affect behaviour and ECoG power spectrum. Higher doses of yohimbine (2.6 and 5.2 nmol) were required to induce behavioural and ECoG changes similar to those observed with lower doses of yohimbine in young rats. 4. Chronic treatment with phosphatidylserine (30 mg kg-1, orally, daily for 21 and 30 days), was able gradually to restore in old rats, in comparison with a vehicle-treated group, the responsiveness of alpha 2-adrenoceptors to clonidine and yohimbine given into the LC.

Aging↗
PubMed1987

Electrocortical spectrum power effects of different classes of neuroleptics in rats.

In freely moving rats the effects on behaviour and ECoG spectrum power of different classes of neuroleptics (phenothiazines, butyrophenones and benzamides) after systemic and intraventricular administration were studied. Chlorpromazine and haloperidol given systemically or microinjected into the third cerebral ventricle produced behavioural and ECoG slow-wave sleep (SWS) accompanied by a significant increase in ECoG total voltage power as well as in the lower frequency bands; haloperidol was found to be more powerful in inducing behavioural and SWS. In contrast, equimolar doses of 1-sulpiride given systemically or higher doses microinjected into the third cerebral ventricle did not produce significant behavioural and ECoG changes. Thus, the present experiments confirm that neuroleptic drugs may possess a different ECoG profile depending on their structure and provide further evidence concerning the role played by dopaminergic mechanisms in the control of sleep-arousal.

Animals↗
PubMed1987

Behavioural and electrocortical spectrum power effects of growth hormone releasing factor in rats.

The effects on behaviour and electrocortical spectrum power of intracerebroventricular, intrahippocampal and intracaudate injections of human pancreatic growth hormone releasing Factor-40 (hpGRF) (10-100 ng) were studied in rats. The hpGRF, given into the third cerebral ventricle or into the dorsal hippocampus (50-100 ng), in freely-moving rats, produced behavioural sedation accompanied by electrocortical synchronization and an increase in the total voltage power with a predominant increase in the lower frequency bands. On the contrary, unilateral injection of hpGRF (75 ng) into the head of the caudate nucleus produced an increase in locomotor activity, marked postural changes, episodes of contralateral circling and an intense pattern of stereotyped movements. In all, these results indicate that, besides its specific endocrinological effects, hpGRF possesses, in small doses, marked behavioural and electrocortical actions, the mechanism(s) of which still remain to be elucidated.

Action Potentials↗
PubMed1987

Behavioural and electrocortical changes induced by muscimol in rats withdrawn from chronic treatment with diazepam.

In rats withdrawn from a chronic treatment with diazepam, the effects of muscimol, given into the III cerebral ventricle, on behaviour and spectrum power of activity in the electrocorticogram (ECoG) were studied. In comparison to control rats which received only muscimol, in rats pretreated with diazepam (1 mg/kg/day for 30 consecutive days) the behavioural and ECoG effects of muscimol were significantly reduced or abolished. In fact, in rats pretreated with diazepam a small dose (50 ng) of muscimol did not affect behaviour or ECoG activity, in contrast to control animals in which the same dose produced, after a period of locomotor stimulation and ECoG desynchronization, typical and long-lasting behavioural sedation or sleep accompanied by a significant increase in total voltage power and in the lower frequency bands in the ECoG. In addition, larger doses (100 and 200 ng) of muscimol, which in control rats produced a typical biphasic pattern of ECoG and behavioural changes, i.e. an initial period of ECoG desynchronization and behavioural stimulation, followed by a second period of behavioural and ECoG sleep, in animals pretreated with diazepam, produced only an increase in total voltage power and in the lower frequency bands in the ECoG resembling the effects of the smaller (50 ng) dose. The present experiments suggest that, after chronic stimulation of benzodiazepine receptors a decrease in sensitivity of receptors for gamma-aminobutyric acid (GABA) occurs, since the effects of muscimol on behaviour and spectrum power were significantly reduced or abolished.

Animals↗
PubMed1987

Behavioural and ECoG spectrum power effects after intraventricular injection of drugs altering dopaminergic transmission in rats.

In rats with cannulae permanently implanted into the third cerebral ventricle, the effects of different pharmacological manipulations affecting dopaminergic mechanisms, were studied on behaviour and electrocorticographic (ECoG) activity, continuously quantified in its spectrum power. The intraventricular injection (0.1-1 nmol) of (-)3PPP[3-(3-hydroxyphenyl) N-n-propylpiperidine], a specific agonist at dopamine (DA) autoreceptors, produced dose-dependent behavioural sedation or sleep and an increase in ECoG spectrum power, with a predominant increase in the lower frequency bands. Short episodes of stereotyped movements, wet-dog syndrome, penile grooming and erection were also observed. Similar behavioural and ECoG effects were elicited by the intraventricular injection of R-(+)-8-chloro-2,3,4,5-tetrohydro-3-methyl-5-phenyl-1H-3-benzazepi ne-7-ol (SCH 23390), a selective antagonist at D1 postsynaptic receptors, although these were preceded by a short period of behavioural and sexual stimulation. In addition, the intraventricular administration of some neuroleptics, chloropromazine and haloperidol, produced behavioural and ECoG slow wave sleep. No significant changes were observed with a neuroleptic drug, 1-sulpiride, which is reputed to act selectively as an antagonist at dopamine D2 receptors. In conclusion, the present experiments add new evidence in favour of the idea that dopaminergic mechanisms are involved in mammalian species in the control of arousal and that both post-synaptic D1 and D2 receptors may take part in such a control.

Animals↗
PubMed1987

Evidence that locus coeruleus is the site where clonidine and drugs acting at alpha 1- and alpha 2-adrenoceptors affect sleep and arousal mechanisms.

The behavioural and electrocortical (ECoG) effects of clonidine were studied after microinjection into the third cerebral ventricle, or microinfusion into some specific areas of the rat brain rich in noradrenaline-containing cell bodies (locus coeruleus) or into areas receiving noradrenergic terminals (dorsal hippocampus, amygdaloid complex, thalamus, frontal and sensimotor cortex). The ECoG effects were continuously analysed and quantified by means of a Berg-Fourier analyser as total power and as power in preselected bands of frequency. Clonidine (9.4 to 75 nmol) given into the third cerebral ventricle produced behavioural sedation and sleep and a dose-dependent increase in ECoG total voltage power as well as in the lower frequency bands. Much lower doses were required to produce similar behavioural and ECoG spectrum power effects after either unilateral or bilateral microinfusion of clonidine into the locus coeruleus. Doses of clonidine equimolar to those given into the third cerebral ventricle, were almost ineffective in inducing behavioural and ECoG sleep after their microinfusion into the dorsal hippocampus. In addition, a dose (0.56 nmol) of clonidine which, given into the locus coeruleus, produced marked behavioural sleep and ECoG synchronization, lacked effects when given into the ventral or anterior thalamus, into the amygdaloid complex or onto the frontal and sensimotor cortex. The behavioural and ECoG spectrum power effects of clonidine given into the third cerebral ventricle or into the locus coeruleus were prevented by antagonists of alpha 2-adrenoceptors but not by alpha 1-adrenoceptor antagonists. Intraventricular microinjection, or microinfusion into the locus coeruleus, of yohimbine, a selective alpha 2-adrenoceptor antagonist, produced behavioural arousal, increase in locomotor and exploratory activity, tachypnoea and ECoG desynchronization with a significant reduction in total voltage power. Similar stimulatory effects were also observed after microinjection of phentolamine into the same sites. No significant effects on behaviour and ECoG activity were evoked after intraventricular injection or microinfusion into the locus coeruleus of prazosin or methoxamine.

Adrenergic alpha-Antagonists↗
PubMed1986

Behavioral and electrocortical effects of tolonidine in rats.

The rats systemic administration of tolonidine in rats (0.05-5.0 mumol/Kg) produced behavioural and electrocortical slow-wave sleep lasting between 35 and 200 min depending on the dose. In addition, a dose-dependent fall in deep body temperature was observed. Similar effects were evoked by infusing tolonidine (5-80 nmol) into the third cerebral ventricle. Behavioural, ECoG and body temperature effects were prevented by previous intraventricular or systemic injection of phentolamine, an antagonist at alpha 1- and alpha 2-adrenoceptors, and of yohimbine, an antagonist at alpha 2-adrenoceptors, whereas prazosin, an alpha 1-adrenoceptor antagonist, was ineffective. In conclusion, the present experiments show that tolonidine possesses central effects similar to those evoked by clonidine and provide further evidence in favour of the idea that central alpha 2-adrenoceptors are involved in the control of slow-wave sleep and body temperature.

Animals↗