PubMed Health⌕ Search

Biomedical subjects

F Nicoletti

Publications and source records attributed to F Nicoletti.

At least 271 records · Page 15Linked to original sources
PubMed1984

[Effects of systemic administration of kainic acid on GABAergic and glutaminergic transmission in various areas of the brain].

In the present study that Authors have investigated the effects of systemic injection of kainic acid on aminoacidergic transmission of different rat brain regions. Kainic acid has been used to produce an experimental model of limbic epilepsy characterized by two different phases (KA1 and KA2). Results obtained show a significant decrease of glutamic and aspartic acids (excitatory aminoacids) and glicine and taurine (inhibitory aminoacids) in both phases at hippocampal level. On the contrary GABA concentration seems to be increased.

Animals↗
PubMed1984

Altered time course of changes in the hippocampal concentration of excitatory and inhibitory amino acids during kainate-induced epilepsy.

The temporal sequence of electrophysiological and biochemical correlates of epilepsy induced by systemic injection of kainic acid (15 mg/kg i.p.) was investigated in male rats. A significant decrease in the hippocampal concentration of glutamate and aspartate was observed 20 min after the injection. These decreases preceded both electrographic and behavioral manifestations of epilepsy, thus suggesting a causal relationship between acidic amino acid changes and the genesis of kainate-induced hyperactivity. About 30-45 min after kainate injection, a decrease in glutamate, aspartate, glycine and taurine and no change in GABA concentration were observed. Bioelectrical activity, recorded in the regio inferior (CA3) of the hippocampus or in the fascia dentata revealed the presence of high frequency bursts separated by a long-lasting depression of discharge. About 55-75 min after the injection, the number of spikes in each burst increased and the duration and frequency of interictal pauses decreased. This stage was characterized by a decrease in glutamate and aspartate, restoration to normal of glutamine, glycine and taurine and a decrease in GABA.

Amino Acids↗
PubMed1984

Hyperalgesic activity of parathyroid hormone and its fragments in male rats.

Results presented in this paper indicate that intracerebroventricular injection of parathyroid hormone reduces pain threshold in male rats. This effect is induced by whole molecule (84 amino acids) or by fragments 1-34 and 44-68 of PTH. The fragment 65-84 of PTH does not induce any change in pain threshold.

Animals↗
PubMed1984

Fastigial influences on postural tonus as studied by kainate lesions and by local infusion of GABAergic drugs in the rat.

Localized lesions with kainic acid (KA) and local infusion of GABAergic drugs were used to study the role of the nucleus fastigii (NF) in postural tonus. Unilateral axon-sparing KA lesions of NF resulted in ipsilateral limb extensor atonia and contralateral limb extensor hypertonus and abduction. This effect lasted for 3-8 days depending on the dose of KA. Lesions of sites adjacent to the NF failed to produce postural asymmetries. Local infusion of the GABA agonist muscimol (10-50 ng) in the NF produced a reversible postural asymmetry fenomenologically similar to that produced by KA lesions of NF. Infusion of agents blocking GABAergic transmission in the NF (bicuculline, picrotoxin) resulted in a postural asymmetry of inverted laterality in respect to that produced by muscimol. Bilateral KA lesions of NF or bilateral infusion of muscimol resulted in bilateral hyperextension-abduction of the limbs. Infusion of GABAergic drugs in areas adjacent to the NF failed to produce postural changes. The results are interpreted to indicate that the NF exerts a crossed inhibitory and a direct excitatory influence on limb postural tonus.

Animals↗
PubMed1983

Influence of sex steroids and prolactin on haloperidol-induced catalepsy.

The effects of sex steroids and prolactin on haloperidol-induced catalepsy were investigated in male rats. Repeated administration with estradiol benzoate (5 micrograms/rat, twice daily for 10 days) significantly potentiated catalepsy induced by 0.25 or 0.5 mg/kg haloperidol, but no effect was observed 10 min or 1 h after a single injection of estradiol benzoate (5 or 50 micrograms/rat). Conversely, a single administration with the catecholestrogen 2-hydroxyestradiol (50 micrograms/rat) significantly increased haloperidol-induced catalepsy, suggesting that catecholestrogens may directly interfere with nigrostriatal dopaminergic transmission. Haloperidol-induced catalepsy has been found to be attenuated in conditions of hyperprolactinaemia resulting from anterior pituitary isograft underneath the kidney capsule. This is consistent with the hypothesis that prolactin may stimulate nigro-striatal dopaminergic function. Results obtained also indicate that medroxy-acetate progesterone, a progesterone derivative, may influence haloperidol-induced catalepsy. Specifically, a single administration with medroxy-acetate progesterone (5 mg/kg, i.p.) enhanced catalepsy but opposite effects were observed after repeated administration of medroxy-acetate progesterone (5 mg/kg, i.p., once a day for 7 days).

Animals↗
PubMed1983

[Role of the amygdala in the sedation induced by low doses of apomorphine].

In the present study the role of amygdala in the antidepressant action of imipramine is discussed. An animal model of depression is induced, in rats, by systemic injection of low doses of apomorphine. Systemic administration of imipramine prevents, as already reported, apomorphine-induced sedation. The same effect is observed following intra-amygdaloid imipramine administration. On the contrary, local injection of imipramine in frontal cortex or caudate nucleus does not affect apomorphine-induced sedation.

Amygdala↗
PubMed1983

Antidyskinetic properties of estrogens.

There is mounting evidence that several gonadal hormones may influence central nervous system. In particular, it has been found that estrogens display an antidopaminergic activity at the level of the extrapyramidal motor system. In this line we have investigated behavioral and biochemical parameters related to nigrostriatal DAergic function. Results obtained further indicate that estrogens display an antidopaminergic activity, by acting on nigrostriatal postsynaptic DAergic receptors. These results may suggest an antidyskinetic activity of estrogens.

Animals↗
PubMed1983

Effects of calcitonin on the brain of aged rats.

We have recently demonstrated that calcitonin, a putative neuromodulator, may influence extrapyramidal motor system by decreasing nigro-striatal dopaminergic function. Since calcitonin is extensively used in aged patients, we have investigated whether calcitonin might influence extrapyramidal motor behavior (haloperidol-induced catalepsy and apomorphine-induced hyperactivity) in rats of different ages. Intracerebroventricular injection of salmon calcitonin (1 micrograms/kg) prevented apomorphine-induced hyperactivity in 2, 7, 18 or 21 month old rats, but potentiated haloperidol-induced catalepsy only in 2 or 7 month old rats. In addition, in all the animals salmon calcitonin significantly decreased the secretion of prolactin, an anterior pituitary hormone that may act at central level enhancing nigro-striatal dopaminergic activity.

Age Factors↗
PubMed1983

Hypoprolactinemic action of calcitonin and the tuberoinfundibular dopaminergic system.

The effects of calcitonin on neurochemical parameters related to the tuberoinfundibular dopaminergic system have been investigated in an attempt to elucidate how calcitonin decreases serum prolactin levels. Intracerebroventricular human or salmon calcitonin injection decreases serum prolactin, medial basal hypothalamic dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) and hypophysial DA and increases hypophysial DOPAC. Results suggest that calcitonin may decrease prolactin secretion via the tuberoinfundibular dopaminergic system.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Effects of dopaminergic drugs on cerebellar prostaglandin concentrations.

Previous data indicate that the injection of dopaminergic drugs induces changes in cerebellar 3',5'-guanosine monophosphate (cGMP) content. Accordingly, we have investigated the effects of haloperidol, sulpiride, or apomorphine on cerebellar prostaglandin (PG) concentration, a parameter related to cGMP content. Results obtained show that dopamine receptor blocking agents, such as haloperidol and sulpiride, significantly decrease cerebellar PGE2 and PGF2 alpha concentrations, while opposite changes are induced by apomorphine, a dopamine receptor agonist.

Animals↗
PubMed1983

Effects of hyper- and hypoprolactinemia on glutamate decarboxylase activity in medial basal hypothalamus of male rat.

Haloperidol, sulpiride, domperidone and apomorphine, drugs which influence dopamine (DA) receptors and in turn prolactin (PRL) secretion have been shown to induce parallel changes in medial basal hypothalamic (MBH) glutamate decarboxylase (GAD) activity and serum PRL levels. The possibility that PRL may be involved in the effects of the drugs on MBH GAD activity is suggested in view of the evidence that hypophysectomy completely prevents drug-induced MBH GAD activity changes and that hyperprolactinemia by anterior pituitary homograft results in a significant, although small, change in the enzymatic activity.

Animals↗
PubMed1983

Role of prolactin-opiate interactions in the central regulation of pain threshold.

Endogenous hyperprolactinaemia induced by anterior pituitary transplantation under the kidney capsule has been found to reduce the behavioural responsiveness to electrical footshock and to increase morphine-induced analgesia. The apparent analgesic effect of prolactin has been related to the stimulation of nigro-striatal dopaminergic transmission, as suggested by the increase in striatal dopamine turnover observed in hyperprolactinaemic rats. It seems likely that central opiate system is involved in the behavioural effects of prolactin. Thus, naloxone prevents the effects of hyperprolactinaemia on footshock responsiveness and heroin self-administration is decreased in hyperprolactinaemic rats.

Animals↗