Search PubMed⌕ Search

Biomedical subjects

M Trabucchi

Publications and source records attributed to M Trabucchi.

At least 217 records · Page 12Linked to original sources
PubMed1991

The aging brain: protein phosphorylation as a target of changes in neuronal function.

There is evidence that senescence affects neurotransmission at different levels. In particular, this review summarizes the studies on age-dependent modifications in protein phosphorylation, which represents the final pathway in the action of transmitters and hormones at neuronal level. Cyclic AMP-dependent protein kinase and protein kinase C have been reported to be modified during aging in various cerebral areas; the changes may involve either enzyme activity or substrate availability. These findings can be related to the alterations in neurotransmitter function and synaptic efficiency observed in the senescent brain. The activity of the other types of protein kinases (tyrosine-, cGMP-, calcium/calmodulin-dependent) during aging needs to be explored. An emerging point is the role of protein phosphorylation in the transfer of membrane signals to the nucleus, for the activation or disactivation of specific genes responsible for long-term neuronal events. Along this view, alterations in protein kinase pathway during senescence would ultimately affect gene expression, resulting in long term modifications of cell function. The reviewed literature opens the perspective of restoring some of the deficits associated with senescence by modulating protein phosphorylation pathway.

Aging↗
PubMed1991

Effect of a new cognition enhancer, alpha-glycerylphosphorylcholine, on scopolamine-induced amnesia and brain acetylcholine.

The present study investigates the effect of the administration of alpha-glycerylphosphorylcholine (alpha-GPC) on scopolamine-induced amnesia and on brain acetylcholine (ACh) levels and release in rats. The results indicate that alpha-GPC, when administered orally, reverses the amnesia caused by scopolamine in passive avoidance. The peak effect is observed using 600 mg/kg IG, 5 h before training. The effect of the drug is long lasting (up 30 h) in accordance with its pharmacokinetic characteristics. Since, alpha-GPC administered IG is cleaved within the gut mucosal cells to glycerophosphate and free choline, it is tempting to speculate that this drug acts by increasing the ACh precursor pool. This view is supported also by the observation that alpha-GPC partially counteracts the decrease of brain ACh levels elicited by scopolamine administration. The effect is observed in the hippocampus and cortex, but not in the striatum. Moreover, in ex vivo experiments, alpha-GPC is able to increase the amount of ACh released by rat hippocampus slices following potassium stimulation.

Acetylcholine↗
PubMed1991

Evaluation of beta-endorphin/beta-lipotropin immunoreactivity content in the CSF of patients affected by deafferentation pain syndromes.

Beta-endorphin/beta-lipotropin immunoreactivity (BE/BLPH-IR) content was evaluated in the CSF of patients suffering by deafferentation pain syndromes. BE/BLPH-IR CSF concentrations of these patients were compared with those obtained in a group of patients affected by low back pain and in a control group without pain problems. No statistically significant variation in BE/BLPH-IR levels were found between controls and subjects with different types of chronic pain.

Adult↗
PubMed1991

The value of memory.

Explore the source record for details and available documents.

Activities of Daily Living↗
PubMed1990

Calcium antagonists inhibit met-enkephalin immunoreactive material release: in vitro and ex vivo experiments.

Depolarizing stimuli increase the release of neurotransmitter met-enkephalin from rat striatal slices. Bay K8644, a calcium agonist, significantly enhances the submaximal release of this peptide. Several organic calcium antagonists, including nimodipine, nifedipine, nicardipine, gallopamil and flunarizine, are able to inhibit the potassium-evoked met-enkephalin release both in vitro and ex vivo. The data suggest that the release of this neuropeptide is modulated by calcium antagonist-sensitive calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Characterization of peripheral benzodiazepine receptors in human blood mononuclear cells.

In the present study, peripheral-type benzodiazepine receptors in human circulating mononuclear cells were characterized, using [3H]PK 11195 as specific ligand. The specific binding was saturable, with a Bmax of 14 pmol/mg protein and a Kd of 7 nM. The pharmacological characterization, using different displacing drugs, indicated a mitochondrial type of peripheral benzodiazepine receptor since it was not coupled to the GABA receptor and was displaced by protoporphyrin IX. These data indicate that human circulating mononuclear cells possess benzodiazepine recognition sites, similar to non-neuronal receptors. The role of these receptors and possible modifications in different diseases need to be investigated.

Adult↗
PubMed1990

Nutritional intake, socioeconomic conditions, and health status in a large elderly population.

The nutritional intake of a large population of noninstitutionalized older people living in an urban area was studied in relation to socioeconomic conditions (living environment, income, and education) and health status (affective, functional, and physical health) to identify the subgroups at risk for malnutrition. Twenty-four-hour dietary recall was used to determine the percentage of older subjects with dietary intake of specific nutrients below two thirds of the 1980 Recommended Dietary Allowances. Ninety percent of the older people examined showed inadequate intake of thiamine and vitamin B6, and 30% to 40% demonstrated deficiencies of vitamin A, vitamin C, niacin, vitamin B12, calcium, and iron; only 10% of subjects had inadequate intake of protein. Poor nutritional intake was correlated more strongly with socioeconomic conditions, functional level, and affective status than with physical health status.

Activities of Daily Living↗
PubMed1990

Decreased density of benzodiazepine receptors in lymphocytes of anxious patients: reversal after chronic diazepam treatment.

Peripheral-type benzodiazepine receptors were measured in human circulating lymphocytes using 3H-PK 11195 as specific ligand. In a group of outpatients with anxiety disorders a significant decrease of receptor density (-37%) was found compared with age-matched controls. In these patients long-term diazepam treatment restored binding density to normal levels: the effect persisted after drug withdrawal. Acute i.v. diazepam administration did not change receptor density. The observed receptor changes could reflect a down-regulation phenomenon and indicate that lymphocyte function reflect central nervous events.

Anxiety Disorders↗
PubMed1990

Modulation of dihydropyridine-sensitive calcium channels: a role for G proteins.

The present study investigates the effect of G protein activation on dihydropyridine recognition sites in PC12 cell membranes. The addition of a stable analogue of GTP, GMP-PNP, increases the displacement of tritiated PN 200-110 produced by Bay K 8644 without modifying the one produced by nitrendipine. This effect is prevented by Pertussis toxin treatment. Functional studies based on the measurement of intracellular calcium concentrations by means of the fura 2 technique show that Pertussis toxin reduces the ability of Bay K8644 to potentiate the increase of cytosolic calcium elicited by 80 mM K+. The results support the hypothesis that a G protein may modulate the activity of voltage-dependent, dihydropyridine-sensitive calcium channels.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Decrease in phorbol ester receptors in human brain tumors.

We have characterized the specific binding of [3H]-phorbol-12,13-dibutyrate in the white and gray matter of normal human brain and in cerebral tumors as an index of the availability of protein kinase C enzyme molecules. White matter has less than 50% phorbol-ester-binding capacity in comparison to gray matter. The binding is lower in tumors of glial origin when compared with normal white matter. Tumors of nonglial origin such as neurinoma and meningioma have a lower binding capacity than glial tumors. Metastatic tissues have the lowest binding capacity. The analysis of binding parameters in tumors and in the corresponding normal peritumoral tissues confirms the decreased binding capacity of neoplastic tissues in comparison to tissues not undergoing malignant transformation. These data suggest that brain glial tumors have a low availability of protein kinase C enzyme molecules and point to the potential involvement of this system in malignant transformation of human brain cells.

Adult↗
PubMed1988

Lead neurotoxicity: a role for dopamine receptors.

Chronic lead exposure differentially affects dopamine receptor subtypes (D1 and D2). In particular dopamine D2 recognition sites in striatum are up-regulated while in nucleus accumbens they are down-regulated. These changes may be correlated to the observed alterations of dopamine terminal activity. Consistent with these biochemical changes behavioral studies indicate that lead-treated rats show more pronounced basal activity, attenuation of apomorphine (63 micrograms/kg s.c.) induced hypomotility and tendency to increased stereotyped response to apomorphine (300 micrograms/kg s.c.). On the contrary, both behavioral and biochemical markers of D1 receptors are unmodified by lead treatment. In fact, SKF 38393-induced grooming behavior, [3H]SCH 23390 binding and the dopamine stimulated adenylate cyclase activity are comparable in controls and lead-exposed rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1988

Direct coupling of a G-protein to dihydropyridine binding sites.

Electrophysiological data support the existence of GTP-binding proteins interacting with voltage dependent calcium channels. Along this line the present study investigates the effect of GMP-PNP, a stable GTP analogue, on the displacement of [3H]-PN 200-110 binding by agonist and antagonist dihydropyridines in synaptic membranes prepared from rat cortex. The results show that GMP-PNP increases the ability of the agonist dihydropyridine BAY K 8644 to displace [3H]-PN 200-110 binding. The in vivo treatment with Pertussis Toxin abolishes the effect produced by the non-hydrolysable GTP analogue.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Mechanisms of the effect of lead on brain neurotransmission: a calcium mediated action.

Data on the effect of chronic lead ingestion on brain neurochemistry in laboratory rodents show the involvement of several neurotransmitters including catecholamines. In the case of dopamine (DA), the action of lead is not uniform in all the DA-innervated areas. The reason for the regional susceptibility to the effect of lead is at present unknown, but points to the existence of specific neuronal mechanisms. Results obtained from animals exposed from birth to lead show that calcium channels are differentially modified in various brain areas. In particular, calcium antagonists display regional sensitivity both after in vivo lead treatment and after in vitro lead addition. These data support the concept that the area selective effects of the metal on neurotransmission may depend on the mechanisms controlling nerve terminal activity in different neuronal populations.

Animals↗
PubMed1988

Effect of chronic ethanol treatment on dopamine receptor subtypes in rat striatum.

Chronic exposure to ethanol (6% in the drinking water, 25 days) reduces the responsiveness of both the dopamine-stimulated and of the dopamine-inhibited adenylate cyclase in rat striatum. The changes in the adenylate cyclase activity are paralleled by alterations in dopamine recognition sites, in fact binding studies using selective ligands indicate that the number of both D1- and D2-receptors is reduced in striatal membranes of treated rats.

Adenylyl Cyclases↗