Biomedical subjects
Publications and source records attributed to F Patti.
In the present study the Authors have investigated the effects of chronic pretreatment with injections of Zn++ sulphate solution on kainic acid induced epilepsy, to verify wether or not Zn++ is able to change the epileptiform pattern induced by kainic acid infection. Results obtained show that Zn++ do not produce any significant change in the experimental parameters by us study.
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.
Zinc has been analysed in bone samples taken from ribs and from vertebrae collected in the Paris region. X-ray fluorescence, with a detection limit of 30 ppm, has been applied to the bone ash. In the ash, the individual average concentration is 234 +/- 125 micrograms g-1 and is quite independent of age (p = 0.95 for one analysis). The vertebrae contain 14% more zinc than the ribs; the difference is significant at the 0.01 level. No difference between the sexes has been observed. An adult ingests on the average 20 mg Zn daily with his food intake. The inhaled amount is much less, approximately 9 micrograms. A skeleton contains on the average 520 mg Zn.
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).
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.
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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.
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.
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.
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.
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.
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The effects of i.v.c. injection of human and salmon calcitonin on biochemical and behavioral parameters related to the extrapyramidal motor system, were investigated in male rats. Calcitonin injection resulted in a potentiation of haloperidol-induced catalepsy and a partial prevention of apomorphine-induced hyperactivity. Moreover calcitonin induced a significant decrease in nigral GAD activity but no change in striatal DA and DOPAC concentration or GAD activity. The results are discussed in view of a primary action of calcitonin on the striatonigral GABAergic pathway mediating the DA-related behavioral messages of striatal origin.
We have investigated the effects of estrogens and prolactin on nigro-striatal dopaminergic function. In this regard, apomorphine-induced hyperactivity has been evaluated in hyperprolactinemic rats. Results obtained suggest the possibility that hyperprolactinemia potentiates nigro-striatal dopaminergic transmission inducing, in chronic, charges in dopamine receptor sensitivity. As a neurochemical parameter of the extrapyramidal motor system, we have investigated the activity of the GABA-synthesizing enzyme glutamate decarboxylase (GAD, EC 4.1.1.15) in corpus striatum and substantia nigra. Hyperprolactinemia induced by anterior pituitary homograft under the kidney capsule or systemic sulpiride injection significantly increases GAD activity. In contrast, estrogen treatment decreases nigral GAD activity even though increases plasma prolactin levels. From a clinical point of view, preliminary data indicating a good therapeutical efficacy of estrogens and progesterone in psychiatric patients are reported.
The comparative effects of a 10 day estrogen treatment and estrogen independent hyperprolactinemia on nigral and striatal glutamic acid decarboxylase (GAD, EC 4.1.1.15) activity were investigated in male rats. Data obtained show that estrogen treatment decreases GAD activity in substantia nigra, while an increase was observed in conditions of hyperprolactinemia induced by adenohypophysis homograft or acute and chronic sulpiride injection. The possibility of an opposite modulation of strio-nigral GABAergic system by estrogens and prolactin is suggested.
Sulpiride, a benzamide derivative neuroleptic, was shown to significantly increase glutamic acid decarboxylase activity in substantia nigra and corpus striatum in either acutely or chronically injected male rats. Hypophysectomy completely prevented this effect suggesting an involvement of an anterior pituitary factor in the central action of sulpiride. Prolactin might possibly mediate the effects of sulpiride since it is known to increase prolactin secretion by an action at the level of the anterior pituitary. Consistent with this hypothesis was the finding of a similar increase in nigral and striatal glutamic acid decarboxylase activity in hyperprolactinemic animals in which an anterior pituitary had been implanted under the kidney capsule.