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M A Sortino

Publications and source records attributed to M A Sortino.

65 records · Page 4Linked to original sources
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↗
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

[Neuroendocrine modulation of haloperidol-induced catalepsy].

Evidence has been accumulated implicating sex hormones as possible modulators of extrapyramidal motor function. In the present study we have investigated the effects of estrogens, progesterone, testosterone, prolactin and calcitonin on behavioral parameters related to nigro-striatal dopaminergic system, such as haloperidol-induced catalepsy in male rats. It was found that 7-days estradiol benzoate treatment (5 micrograms/rat/day) significantly increases haloperidol-induced catalepsy, suggesting a possible antidopaminergic activity of estrogens. On the other hand, prolactin facilitates nigro-striatal dopaminergic transmission. Interestingly, 7 day treatment with medroxy-acetate progesterone (MAP, 5 mg/Kg, i.p.) brings about a trend to a decrease in haloperidol-induced catalepsy, while no significantly effect was observed following acute MAP administration at the same dose. So, it is tempting to speculate that chronic progestinic treatment may result in an increase in dopaminergic tonus. Testosterone, acutely administered (5mg/kg.s.c.) induces changes similar to those observed following progesterone administration. Finally, also calcitonin is able to influence haloperidol-induced catalepsy by markedly increasing it.

Androgens↗
PubMedDate not supplied

Comparative effects of estradiol benzoate, the antiestrogen clomiphene citrate, and the progestin medroxyprogesterone acetate on kainic acid-induced seizures in male and female rats.

We have investigated the comparative effects of estradiol benzoate (EB), the antiestrogen clomiphene citrate (CC), and the progestin medroxyprogesterone acetate (MPA) on seizures induced by systemic injection of kainic acid (15 mg/kg i.p.) in male and female rats. Subcutaneous administration for 10 days of EB (10 micrograms/kg) or high doses of CC (50 mg/kg) significantly potentiated kainate-induced seizures, with this effect being more pronounced in male animals. Doses of 2.5 mg/kg of CC potentiated kainate-induced seizures in male rats but were ineffective in female rats. Low doses of CC (0.5 mg/kg) exhibited a mild anticonvulsant effect in both sexes. Repeated administration of MPA (2.5 mg/kg) partially protected female animals against kainate-induced seizures; in male animals, MPA induced a 30% increase in the seizure severity score, although the difference from the score of control male rats was not significant. These data suggest that sex steroids influence kainate-induced seizures in a sex-dependent manner and that the effects of the antiestrogen CC are dose dependent. This should be taken into account in view of a possible use of CC and MPA in hormonal therapy for seizure disorders.

Animals↗
PubMedDate not supplied

Effects of CDP-choline administration on receptor-stimulated inositol phospholipid hydrolysis in brain slices and neuronal cultures.

Repeated addition of CDP-choline (100 microM, once a day since the 2nd day of maturation in culture) to corticostriatal neurons led to an increased basal hydrolysis of inositol phospholipids, as revealed by an enhanced formation of [3H]inositolmonophosphate ([3H]InsP) in the presence of 10 mM Li+. This increase was prevented by the muscarinic receptor antagonist, atropine, or by tetrodotoxin, but not by other receptor antagonists, such as L-2-amino-4-phosphonobutanoate (L-AP4), prazosin or ketanserin. The increase in inositol phospholipid hydrolysis induced by repeated addition of CDP-choline was obliterated when cultures were incubated in the presence of the muscarinic receptor agonist, carbamylcholine. CDP-choline had no effect on inositol phospholipid hydrolysis in cultured cerebellar neurons, which are devoid of cholinergic cells. The basal hydrolysis of inositol phospholipids was also increased in hippocampal slices prepared from rats repeatedly injected with CDP-choline (200 mg/kg, i.p. for 15 days). As observed in cultured cortico-striatal neurons, this increase was prevented by atropine and was masked in the presence of carabamylcholine. Taken collectively, these data indicate that repeated exposure to exogenous CDP-choline increases polyphosphoinositide turnover, an effect that results from an increased availability of acetylcholine acting on muscarinic receptors.

Acetylcholine↗
PubMedDate not supplied

Inositol hexakisphosphate stimulates 45Ca2+ influx in purified mitochondria from rat liver.

Inositol hexakisphosphate (InsP6) stimulates 45Ca2+ influx in purified mitochondria from rat liver. The action of InsP6 is concentration-dependent, with an apparent EC50 value of 50 microM. Stimulation of 45Ca2+ influx may follow the interaction between InsP6 and specific membrane receptors. Accordingly, [3H]InsP6 binds to specific and saturable recognition sites in purified mitochondria. These results support the view that InsP6 acts as a signal molecule to regulate the intracellular homeostasis of Ca2+.

Animals↗
PubMedDate not supplied

Dihydroergocryptine protects from acute experimental allergic encephalomyelitis in the rat.

The effect of dihydroergocryptine, a natural alkaloid derivative which exhibits D2 dopaminomimetic properties, has been studied in Lewis female rats with experimentally induced allergic encephalomyelitis. A chronic treatment with dihydroergocryptine started two days before immunization, induced a dramatic reduction of prolactin levels accompanied by a marked amelioration of neurological signs. In addition, the proliferative activity of splenic lymphocytes induced by the mitogen Concanavalin-A (Con-A) was reduced in dihydroergocryptine-treated animals. It is suggested that this effect is related to the ability of dihydroergocryptine to lower prolactin concentrations or also, partially, to a neuroprotective action of this drug.

Animals↗
PubMedDate not supplied

Antidegenerative effects of Mg(2+)-valproate in cultured cerebellar neurons.

We have investigated in the present study the effect of Mg(2+)-valproate on necrotic degeneration induced by an excitotoxic insult in primary culture of cerebellar neurons, that is an homogeneous population of glutamatergic neurons. Mg(2+)-valproate protected cultures against glutamate-induced neurotoxicity, acting as an indirect N-methyl-D-aspartate (NMDA) receptor antagonist, thus reducing free radical formation and affecting the biochemical parameters (i.e. 45Ca(2+)-influx, cyclic GMP formation, inositol phospholipid hydrolysis and protein kinase C translocation) that undergo modifications following NMDA receptor activation in cerebellar granule cells.

Animals↗