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L Lucchi

Publications and source records attributed to L Lucchi.

62 records · Page 4Linked to original sources
PubMed1980

Effect of chronic lead treatment on GABA-ergic receptor function in rat brain.

The effect of chronic lead treatment on brain gamma-amino-butyric acid (GABA)-ergic function has been studied in an attempt to correlate the clinical aspects of the chronic exposure to the metal with specific neurochemical alterations. [3H]GABA-specific binding and cyclic guanosine monophosphate (GMP) content have been measured in various rat brain areas and have been found to be increased in cerebellum and decreased in the striatum of rats after chronic lead treatment. The changes found in the GABA-ergic neurons were correlated with the different levels of lead exposure in rats. Our results indicated that lead selectively affects GABA-ergic function in various rat brain areas, inducing effects which are dose-dependent.

Animals↗
PubMedDate not supplied

Protein kinase C activity, translocation, and conventional isoforms in aging rat brain.

Protein kinase C was studied in various brain areas in aging Wistar rats. Histone-directed kinase activity from the cortex, hippocampus and cerebellum did not change with aging. Using purified protein B-50 as a substrate, between 3 and 8 months a decrease in in vitro phosphorylation was detected in the membrane fraction of the cortex but after this age values remained stable. In hippocampal membranes, B-50 phosphorylation was increased in aged rats. PKC translocation was impaired in aged rats in both the cortex and the hippocampus. PKC alpha and beta mRNA decreased in the cortex between 3 and 8 months with no further decline in aged animals. Hippocampal mRNA for calcium-dependent PKC isoforms was not modified during aging, as assessed by Northern and in situ hybridization. Western blot analysis revealed a change in PKC gamma protein only, which was increased in hippocampal membranes from aged rats. The data indicate that the key PKC function that is impaired in aged rats is enzyme translocation irrespective of the brain area investigated.

Aging↗
PubMedDate not supplied

Age related differences in dopamine-stimulated adenylate cyclase sensitivity to "in vivo" chronic ethanol treatment.

The effect of chronic ethanol consumption on adenylate cyclase activity was measured in striatal membranes derived from aged male rats. The results indicate that the cyclic AMP generating system of old rats has a different sensitivity to ethanol effect compared to the adult animals. In young animals the basal adenylate cyclase activity was enhanced by alcohol consumption while the DA stimulated cyclic AMP production was reduced. In contrast, in 24 months old rats ethanol reduced the basal adenylyl cyclase and enhanced the response to DA indicating a supersensitivity of adenylate cyclase linked DA receptors. This observation was further supported by 3H-Spiperone binding studies. In fact, a higher Bmax was measured in striatal membranes of aged ethanol-dependent rats in comparison to control.

Adenylyl Cyclases↗
PubMedDate not supplied

Chronic ethanol induces changes in opiate receptor function and in met-enkephalin release.

Ethanol induces supersensitivity of striatal delta-opiate receptor sites labelled by 3H-Etorphine. This effect may be ascribed to the diminished enkephalin release detected in striatal slices after chronic ethanol consumption. On the other hand, Kd values for 3H-Met-enkephalin and 3H-DHM (mu-opiate receptors) specific binding are enhanced. The different sensitivity of the two classes of opiate receptors to ethanol may be due to specific effects on enkephalinergic transmission. It has been hypothesized that the decrease of 3H-Met-enkephalin and 3H-DHM affinity for their receptors takes place because endogenous substances from ethanol metabolism (for example salsolinol) behave as mu opioid agonists. This hypothesis is confirmed by "in vitro" studies demonstrating that salsolinol displaces 3H-Met-enkephalin and 3H-DHM but not 3H-DADLE binding. On the contrary, it seems that delta-receptors become supersensitive because of the decreased endogenous peptide release.

Animals↗
PubMedDate not supplied

Chronic ethanol exposure alters dopaminergic signal transduction processes.

A number of data suggest that the chronic ethanol treatment induces derangements of cell membrane structure leading to modifications of membrane related processes. In particular, alterations have been observed in the mechanisms of neurotransmitter recognition and in the coupling of the receptor with the effector system. Phosphorylation of specific proteins by cyclic AMP stimulated protein kinases represent the final step in the biological response in several distinct functional processes. Ethanol neurotoxic action therefore may affect neurotransmitter availability and release as well as receptors effector systems and protein phosphorylation. In this line, chronic ethanol treatment in rats decreases cyclic AMP dependent protein kinase activity in rat striatal membrane fractions. When lysine rich histone type III was used as exogenous substrate, cyclic AMP stimulated 32P incorporation was still decreased in the ethanol group. These data favor the hypothesis of a decreased capability of the enzyme to phosphorylate in response to cAMP.

Alcoholism↗
PubMedDate not supplied

Acute ethanol administration during pregnancy: effects on central dopaminergic transmission in rat offspring.

The present study investigated the effect of ethanol ingestion during pregnancy on central dopaminergic function in the nervous system of the offspring. Marked changes in striatum of both binding of 3H-spiperone and the concentrations of DOPAC were found in offspring particularly when an acute dose of ethanol was administered to pregnant dams on the fourth day of pregnancy, whereas changes in the binding of 3H-5HT in cortex were not seen. Interestingly, administration of ethanol from the fourth day to the end of gestation, or only on the 13th day, caused different effects or no effect, respectively. These data suggest that alterations of dopaminergic function may be markers of teratogenic effects of ethanol, and may be related to some of the clinical symptoms appearing in children affected by Fetal Alcohol Syndrome.

3,4-Dihydroxyphenylacetic Acid↗