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Biomedical subjects

G Nisticó

Publications and source records attributed to G Nisticó.

30 records · Page 2Linked to original sources
PubMed1979

Evidence for a receptor supersensitivity following impairment of central serotoninergic activity in the rabbit.

In order to investigate whether a chronic impairment of neuronal serotoninergic transmission in the CNS could result in a receptor supersensitivity, rabbits were pretreated either with 5,6-dihydroxytryptamine (5,6-DHT) or p-chlorophenylalanine (PCPA) and then tested for their hyperthermic response to serotoninergic agonists. A previous (10 days before) intracerebroventricular injection of 5,6-DHT (75 microgram into each cerebral ventricle) significantly potentiated the increase in body temperature induced either by quipazine (1 mg/kg i.v.) or by 5-hydroxytryptophan (5-HTP 2 mg/kg i.v.) in combination with a MAO inhibitor (phenylethylhydrazine 10 mg/kg i.v. 16 h before). Pretreatment with PCPA (100 mg/kg s.c. four times on alternate days, the last dose 48 h before the experiment) also enhanced the hyperthermic effect of quipazine, whereas it inhibited the hyperthermic response to 5-HTP plus MAO inhibitor. These results suggest the existence of a receptor supersensitivity following prolonged blockade of serotoninergic neuronal transmission in the CNS.

5,6-Dihydroxytryptamine↗
PubMed1979

Crop-sac response after systemic and intraventricular administration of neuroleptic drugs.

Present experiments were aimed at studying in pigeons the effects of some neuroleptic agents given systemically or into the 3rd cerebral ventricle on PRL secretion and following morphological changes of the crop-sac mucosa both by classical histological methods and scanning electron microscopy. In addition, such changes were also evaluated on the basis of a semiquantitative method using a 1-4 rating scale. 3- or 5-day systemic treatment with reserpine, haloperidol and (ł/-)-sulpiride produced an intense crop-sac response consisting of a marked epithelial hyperplasia and presence of milk-like material. Similarly, a much lower dose of haloperidol, clozapine, and the two enantiomers of sulpiride given into the 3rd cerebral ventricle for 3 consecutive days produced a marked crop-sac response. The l-sulpiride was more active in comparison to the d-enantiomer. In conclusion, present experiments show that, similarly to mammals, in pigeons neuroleptic drugs are able to stimulate prolactin secretion and suggest that these effects are mediated through an action at the hypothalamic and/or pituitary level by removing a tonic dopaminergic inhibition.

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

Melatonin as immunomodulator in immunodeficient mice.

Melatonin, the main hormone of the pineal gland, when chronically injected into young mice or mice immunodepressed by aging or by cyclophosphamide treatment, is able to enhance the antibody response to a T-dependent antigen. The enhancement of the antibody response is associated with increased induction of T helper cell activity and IL-2 production, as evidenced in mice immunodepressed by aging or by cyclophosphamide treatment. These observations suggest that melatonin treatment may be successfully used in the therapy of immunodepressive conditions.

Adjuvants, Immunologic↗
PubMedDate not supplied

Evidence for an involvement of dopamine D1 receptors in the limbic system in the control of immune mechanisms.

Indirect evidence suggests that dopamine within the brain may participate in the regulation of immune responses both in humans and in rodents. The aim of the present study was to investigate the possible modulatory role played by specific dopamine D1 receptor subtypes within discrete sites of the brain dopaminergic pathways. Mitogen responsiveness of splenocytes and natural killer (NK) cell activity were measured in rats following microinfusion of SKF 38393, a specific dopamine D1 receptor agonist, into the ventral tegmental area, the amygdala, the nucleus accumbens and the CA1 area of the hippocampus. We report here that microinfusion of SKF 38393 (100 nmol) within the central amygdala increased the proliferative response of splenocytes to concanavalin A (ConA) while it did not modify the proliferative response of splenocytes to lipopolysaccharide (LPS) or NK cell activity. On the contrary, microinfusion of SKF 38393 into the nucleus accumbens decreased the proliferative response of splenocytes to ConA and LPS, while NK cell activity remained unchanged. Similarly, microinfusion of SKF 38393 into the CA1 area of the hippocampus decreased the proliferative response of splenocytes to LPS, but not to ConA and did not affect NK cell activity. Finally, microinfusion of SKF 38393 into the ventral tegmental area did not significantly modify the proliferative response of splenocytes to either ConA or LPS and did not affect NK cell activity. All immunological changes evoked through the different areas of the brain following microinfusion of SKF 38393 were prevented by systemic administration of SCH 23390, a specific D1 receptor antagonist.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Effects of interleukin-2 on various models of experimental epilepsy in DBA/2 mice.

The effects of interleukin-2 (IL-2) on various models of experimental epilepsy were studied after intracerebroventricular administration in DBA/2 mice, a strain genetically susceptible to sound-induced seizures. Convulsions were induced by physical stimulus (sound of 109 dB. 12-16 kHz) or by chemical compounds (bicuculline, cephazolin or kainate). The present study demonstrated that human recombinant IL-2 (hr-IL-2) and mouse recombinant IL-2 (mr-IL-2) not only did not antagonize audiogenic seizures in DBA/2 mice but increased the incidence of seizures after the highest doses studied. In addition, hr-IL-2 and mr-IL-2 dose dependently facilitated sound-induced seizures at subthreshold sound exposure (83 dB). Pretreatment with monoclonal rat-antimouse IL-2 antibodies significantly affected the changes of occurrence of audiogenic seizures in DBA/2 mice induced by mr-IL-2. In addition, pretreatment with anti-IL-2 receptor monoclonal antibodies (anti-Tac) was able to completely antagonize or reduce the effects of IL-2 on audiogenic seizures. The effects of mr-IL-2 were also studied in two different models of epilepsy: the bicuculline and cephazolin models, due to impairment of GABAergic transmission, and the kainate model, due to an increase in excitatory amino acid transmission. In all models, mr-IL-2 demonstrated to facilitate the seizures induced by these chemoconvulsants. Since the proconvulsant properties of IL-2 were antagonized by specific monoclonal antibodies, we suggest that some epileptic phenomena may be linked to stimulation of IL-2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗