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Biomedical subjects

G Nisticò

Publications and source records attributed to G Nisticò.

At least 163 records · Page 9Linked to original sources
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.

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PubMedDate not supplied

Tetanus toxin as a neurobiological tool to study mechanisms of neuronal cell death in the mammalian brain.

Tetanus toxin is a potent clostridial neurotoxin responsible for causing spastic paralysis in humans, often accompanied by seizures and death. The tetanic syndrome is believed to originate from a disinhibitory action of the toxin in the CNS. To produce its effects, tetanus toxin undergoes retrograde, intra-axonal transport to the CNS, where it blocks preferentially the release of gamma-aminobutyric acid and glycine, two inhibitory neurotransmitters. These effects stem from the cleavage of synaptobrevin, a constitutive small-vesicle protein, by tetanus toxin, whose zinc-dependent metalloprotease characteristics recently have been recognized. Blockade of inhibitory transmission produces a predominance of excitatory amino acid neurotransmission, which is responsible for the neurodegenerative effect caused by tetanus toxin after intrahippocampal injection in rats. In fact, hippocampal damage can effectively be prevented by reduction of glutamate-mediated excitatory transmission, thus suggesting that unopposed excitation may be the underlying mechanism for neuronal cell death.

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PubMedDate not supplied

Corticotropin-releasing factor microinfused into the locus coeruleus produces electrocortical desynchronization and immunosuppression.

In freely moving rats with cannulae chronically implanted into the locus coeruleus (LC), the effects of corticotropin-releasing factor (CRF) on electrocortical (ECoG) spectrum power activity and on immune mechanisms (splenocyte mitotic response to concanavalin A, Con A, and lipopolysaccharide, LPS, natural killer cell, NK, activity) were assessed. CRF (100-300 ng) microinfused into the LC produced marked ECoG desynchronization characterized by a significant decrease in total voltage power as well as in power of frequency bands of 0.25-3 and 3-6 Hz. These effects lasted 30-60 min according to the dose. A prior administration of alpha-helical CRF(9-41) (200 ng into the LC 15 min before) prevented ECoG desynchronization induced by CRF (100 ng). In addition, CRF (100 ng) given into the LC produced a significant decrease 45 min later in the splenocyte proliferative response to Con A and LPS and a significant fall of NK activity. These effects were prevented by prior microinfusion into the same site of alpha-helical CRF (200 ng). In conclusion, the present experiments show that CRF given into the LC produces an intense state of ECoG desynchronization accompanied by marked immunodepression and suggest that LC is an important site in the brain through which CRF exerts its immunosuppressive activity.

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A reappraisal of the role of the various opioid receptor subtypes in cell-mediated immunity.

Opioid peptides have been shown by several studies to modulate various parameters of the immune response, but scant experimental findings exist on the role played by specific opioid receptor subtypes in the control of immune mechanisms. This study focuses on the in vitro influences of [Trp4,Asn7]dermorphin, a mu-selective agonist, [D-Ala2]deltorphin I, a delta-selective agonist and U50,488, a kappa-selective agonist, on the proliferative response of splenocytes to concanavalin A (Con A). [Trp4,Asn7]dermorphin at low concentrations (10(-11P) and 10(-12) M) enhanced the proliferative response to Con A, whereas higher concentrations (10(-6) to 10(-7) M) inhibited it. Both effects were antagonized by naloxone. [D-Ala2]deltorphin I at very low concentrations (10(-12) to 10(-13) M) also produced a significant increase in the proliferative response of splenocytes to Con A. This effect was significantly antagonized by natrindole, a specific delta-receptor antagonist. Finally U50,488 at concentrations ranging from 10(-8) to 10(-9) M inhibited the proliferative response to Con A. The effects of U50,488 were mediated by the stimulation of the kappa-opioid receptors, since a preincubation of splenocytes with the selective antagonist norbinaltorphimine significantly reduced or abolished the U50,488-induced suppression of the mitotic response. In conclusion, our results clearly indicate that the different opioid receptor subtypes play a different role in the control of immune mechanisms and suggest that immunoenhancing effects of opioid peptides are very likely due to the stimulation of mu- and delta-receptors, whereas the immunosuppressive effects are mediated through the stimulation of kappa-opioid receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMedDate not supplied

Electrocortical power spectrum changes induced by microinfusion of corticotropin-releasing factor into the locus coeruleus in rats.

Rat corticotropin-releasing factor (CRF) microinfused unilaterally or bilaterally into the locus coeruleus (LC) of awake, chronically cannulated rats produced a dose-dependent ECoG desynchronization and behavioral activation. ECoG spectra analysis revealed a significant decrease of total voltage power and of 0.25-3 and 3-6 Hz frequency bands. These effects were prevented by a pretreatment into the same site with alpha-hCRF, a selective antagonist at CRF receptors and by alprazolam, a benzodiazepine derivative. In conclusion, the present results indicate that CRF produces its behavioral and ECoG activating effects by interaction with specific receptors located on LC neurons.

Alprazolam↗
PubMedDate not supplied

Delta opioid receptors mediate seizures produced by intrahippocampal injection of ala-deltorphin in rats.

The effects of the selective delta opioid receptor agonist, ala-deltorphin, microinfused into the dorsal hippocampus or into the locus coeruleus, on the electrocorticographic (ECoG) activity continuously quantified in its spectrum were studied in rats. The microinjection into the dorsal hippocampus of ala-deltorphin (0.03, 0.3 and 1.0 nmol) produced dose-dependent motor and ECoG epileptogenic disorders. The microinfusion of similar doses of ala-deltorphin into the locus coeruleus did not evoke motor and ECoG changes. Intrahippocampal injection of naltrindole (10 and 20 pmol) antagonized the epileptogenic effects induced by ala-deltorphin; also naloxone (20 and 50 pmol) was able to prevent the effects induced by ala-deltorphin, although with a minor potency. In conclusion, the present experiments show that ala-deltorphin is a useful tool to characterize central opioid effects mediated by delta receptors in the brain and suggest that the stimulation of this subtype of receptors in the hippocampus is responsible for epileptogenic effects of opiates.

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PubMedDate not supplied

Rubidium shows effects different from lithium on phosphatidylinositol metabolism in a cell line of human neuroblastoma.

In a SK-N-BE human neuroblastoma cell line the incubation of rubidium (1 and 10 mM) for 24 h significantly increased IP2 formation, whereas it apparently did not affect other inositol phosphates. In comparison to lithium (10 mM), which significantly enhanced inositolmonophosphate and IP2 accumulation following carbamoylcholine (1 mM) stimulation, rubidium at the same concentration, was unable to affect inositol phosphate accumulation. In conclusion, the present experiments show that rubidium, compared with lithium, shows a different profile on phosphoinositide metabolism since its main action is an increase in phosphatidylinositol turnover. These results may have some relevance to the use of rubidium as antidepressant in man.

Cell Line↗
PubMedDate not supplied

Distribution of paraquat into the brain after its systemic injection in rats.

Paraquat concentrations were determined in specific brain areas of rats systemically treated with different doses of the herbicide and sacrificed at different time periods following the acute administration. The systemic treatment with paraquat gave rise to a regional differential distribution of the herbicide into the rat brain, the highest levels being detected in the prefrontal cortex and hypothalamus. The rate of paraquat elimination showed time-dependency in the prefrontal cortex and hypothalamus; by contrast, in the other regions studied the initial drop observed at 3 h was followed by a second phase of significant accumulation. The concentrations detected into the cortex may account for the neuronal cell death reported in rats following systemic injection of this herbicide.

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PubMedDate not supplied

N omega-nitro-L-arginine-methyl ester inhibits electrocortical recovery subsequent to transient global brain ischemia in Mongolian gerbil.

Electrocorticographic (ECoG) activity remains isoelectric for about 15 min after transient (10 min) bilateral carotid arteries occlusion in mongolian gerbils. In this model of global forebrain ischemia N omega-Nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, significantly delays the recovery of ECoG amplitude. Thus, the present experiments suggest that NO is involved in the cerebrovascular physiological response to brain ischemia.

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PubMedDate not supplied

Inhibition by intraventricular microinfusion of ketanserin of the cardiovascular responses to peripheral administration of methoxamine in rats.

The cardiovascular responses induced by intracerebroventricular or intravenous administration of ketanserin in normotensive rats were evaluated. Ketanserin, which is an antagonist at 5-HT2 receptors, when microinfused into the third cerebral ventricle, did not induce significant cardiovascular effects, except for a slight and transitory hypotensive response after the microinfusion of the highest dose (200 micrograms). However, at doses which were unable to affect directly blood pressure or heart rate, ketanserin, microinfused into the same site, antagonized the pressor response induced by peripheral administration of methoxamine, an alpha 1-adrenoceptor agonist. Furthermore, peripheral administration of ketanserin produced dose-dependent hypotension and bradycardia and antagonized the pressor effect of an intravenous bolus injection of methoxamine. In conclusion, the present experiments confirmed the ability of ketanserin to produce cardiovascular effects when administered peripherally and provides evidence for an involvement of ketanserin-sensitive receptors in the brain in the regulation of phasic responses during experimentally induced hypertension.

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