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Biomedical subjects

L Rampello

Publications and source records attributed to L Rampello.

10 recordsLinked to original sources
PubMed1992

Behavioral effects of L-alpha-glycerylphosphorylcholine: influence on cognitive mechanisms in the rat.

The phosphorylcholine precursor, L-alpha-glycerylphosphorylcholine (alpha-GPC), was injected at the dose of 100 mg/kg/day for 20 days to aged male rats of the Sprague-Dawley strain, 24 months old, showing a deficit of learning and memory capacity. The drug was also administered to rats with amnesia induced pharmacologically with bilateral injections of kainic acid into the nucleus basalis magnocellularis (NBM). Learning and memory capacity of the animals, studied with tests of active and passive avoidance behavior, was improved after treatment with alpha-GPC in all experimental groups. These results indicate that this drug affects cognitive mechanisms in the rat through an involvement of central neurotransmission.

Animals↗
PubMed1992

Effects of TRH-T on spinal motoneurones in man.

The effect of thyrotropin-releasing hormone tartrate (TRH-T) on the decrease in H Max/M Max ratio, an index of the spinal motoneurone pool, induced by haloperidol, was studied in 15 healthy volunteers. In all subjects, the H response was examined by an electromyographic apparatus. The values were expressed as H Max/M Max ratio, that gives an index of excitability of the spinal motoneurone pool. It was found that the mean H Max/M Max ratio value significantly decreased after haloperidol administration, but this effect was completely reversed by the injection of TRH-T. This finding suggests that the peptide may modulate motoneurone functions.

Adult↗
PubMed1992

Trophic action of acetyl-L-carnitine in neuronal cultures.

Daily addition of acetyl-L-carnitine (100 microM) to cultured cerebellar granule cells since the first day of maturation led to an increased rate of expression of D-[3H]aspartate uptake (an established marker of maturation of glutamatergic neurons) and of N-methyl-D-aspartate (NMDA) receptors linked to large conductance ion channels permeable to Ca2+. Acetyl-L-carnitine treatment also increased neuronal survival, as reflected by a greater percentage of cultures retaining functional NMDA receptors after 15 days of maturation. These results support the view that acetyl-L-carnitine exerts neuronotrophic activity and prevents age-dependent neuronal degeneration.

Acetylcarnitine↗
PubMed1991

Adenosine deaminase increases release of excitatory amino acids through a mechanism independent of adenosine depletion.

Addition of adenosine deaminase to cultured cerebellar neurones, led to large increases in the influx of 45Ca2+ and hydrolysis of polyphosphoinositide. These effects were inhibited or attenuated by glutamate receptor antagonists (AP5 or MK-801) and were not observed in cells stimulated by maximum concentrations of glutamate or quisqualate. Stimulation of the influx of 45Ca2+ and hydrolysis of phosphoinositide by adenosine deaminase may be secondary to an enhanced release of endogenous glutamate that in turn activates specific excitatory amino acid receptors. Accordingly, adenosine deaminase potently increased release of D-[3H]aspartate, an effect that requires the presence of extracellular Na+ and is insensitive to inhibition by MK-801. None of the effects of adenosine deaminase may be simply related to a fall in endogenous adenosine. In fact, the action of adenosine deaminase was neither reversed by agonists (L-PIA or NECA), nor mimicked by antagonists (IBMX or theophylline) of adenosine receptors. It is speculated that adenosine deaminase stimulates release of neurotransmitter through a mechanism independent of depletion of adenosine. A possible direct action of adenosine deaminase should be taken into account when the enzyme is used to unmask the effects of endogenous adenosine.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Dopaminergic hypothesis for retarded depression: a symptom profile for predicting therapeutical responses.

We assessed the therapeutical efficacy of various antidepressants (amineptine, minaprine and clomipramine) in patients affected by retarded depression. All patients exhibited symptoms of retardation, including hypokinesia, anergia, reduction of speech, increased salivation, hypersomnia, Parinaud's syndrome, reduced sexual activity, slowness, hypomimia, orthostatic hypotension, dysphagia and drowsiness. Antidepressant drugs were administered for a 6-week period in a randomized double-blind vs placebo design. The rank order of clinical effectiveness (amineptine much greater than minaprine greater than clomipramine greater than placebo) paralleled the specificity of antidepressants as dopaminomimetic agents. These results support the view that a reduced dopaminergic transmission contributes to the pathophysiology of retarded depression.

Adult↗
PubMed1989

L-acetylcarnitine attenuates the age-dependent decrease of NMDA-sensitive glutamate receptors in rat hippocampus.

NMDA-sensitive glutamate receptors are involved in the regulation of neuronal plasticity, and contribute to the synaptic mechanisms underlying the learning process. Aging is associated with a reduction in the maximal density of NMDA-sensitive glutamate binding sites in rat hippocampus. This reduction is attenuated after long-term administration with L-acetylcarnitine (10 mg/Kg i.p. once a day for 4 months). These results support a neuroprotective and neurotrophic role for L-acetylcarnitine during aging.

Acetylcarnitine↗
PubMedDate not supplied

Homologous and heterologous adenylate cyclase system desensitization in glial cells.

In the present research the desensitization of adenylate cyclase system induced by isoproterenol (IPR), a beta-adrenergic agonist, in primary glial cell cultures and the effects of an exposure to 3-isobutyl-1-methylxanthine (IBMX) on the response to a subsequent stimulation with IPR have been investigated. A pretreatment with the phosphodiesterase inhibitor IBMX induced refractoriness to a subsequent IPR challenge suggesting a possible involvement of cAMP in heterologous desensitization. Moreover the present results show that IPR desensitized cells in confluent cultures retained a normal response to cholera toxin, while IBMX treated cells exhibited a reduced response to the toxin. So IPR induces a rather specific desensitization while IBMX induced refractoriness seems to be non specific.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

[The H2-antagonist therapy withdrawal syndrome: the possible role of hyperprolactinemia].

Patients previously treated with H2-receptor blocking agents (cimetidine or ranitidine) exhibited a complex neurobehavioral and gastroenteric syndrome, including anxiety, insomnia, anorexia, growing thin, irritability, tachycardia, diarrhoea, nausea, vomiting, abdominal pain, headache, vertigo. These symptoms were dramatically reduced by administration of cimetidine or ranitidine, and reappeared with a new suspension of the therapy. The withdrawal syndrome from H2-receptor antagonists was reversed by treatment with domperidone (10 mg three times per day), a potent hyperprolactinaemic drug which does not cross the blood brain barrier. These results suggest that the drop in prolactin levels that occurs when cimetidine or ranitidine are suspended may contribute to the development of the withdrawal syndrome.

Adult↗
PubMedDate not supplied

[Tardive dyskinesia. A possible complication of chronic treatment with neuroleptics].

Tardive dyskinesia consists of abnormal involuntary movements at the oro-facial area (mouth, tongue, maxillary) or generalized choreoathetotic disorders of the limbs and trunk occurring in at least 10-20% of chronically neuropsychiatric patients exposed to neuroleptics. Age (over 50), gender (female), affective disorders, individual predisposition, type of drug, dosage and duration of neuroleptic exposure (over 3 months), anticholinergics, appear to be risk factors. In this brief review some current pathophysiological mechanisms and clinical therapeutical trials are also discussed.

Antipsychotic Agents↗