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R A Rius

Publications and source records attributed to R A Rius.

28 records · Page 2Linked to original sources
PubMed1985

Age-related reduced affinity in [3H]nitrendipine labeling of brain voltage-dependent calcium channels.

Literature data indicate a reduced calcium uptake in synaptosomes prepared from old rat brains. On this line, the present paper investigates the binding of ([3H]NDP) to brain synaptic membranes prepared from rats at different ages from birth up to 24 months of age. The binding is undetectable at birth but reaches within 9-18 day the values observed in adults [3H]NDP binding affinity and sensitivity to calcium were decreased in old rats (24 months). Tritiated dihydropyridines are believed to label voltage-dependent calcium channels (VDC). The observed age-related reduction in binding suggests that the characteristics of VDC in the aged brain may change.

Age Factors↗
PubMed1985

Differential sensitivity of [3H]nitrendipine binding to cations of toxicological interest in various rat brain areas.

[3H]Nitrendipine ([3H]NTP) is a radiolabelled calcium antagonist which can be used to study neuronal calcium (Ca2+) channels. The interaction of Mn2+, Zn2+, Pb2+ and La3+ on [3H]NTP binding was studied in 3 brain areas particularly rich in [3H]NTP binding sites. Differences were observed in the brain regional distribution of [3H]NTP binding as well as in their sensitivity to the metal ions Pb, Mn and Zn. The binding data suggest that neuronal Ca2+ channels in different brain areas display distinct sensitivity to selected divalent cations.

Animals↗
PubMed1984

In vivo chronic lead exposure alters [3H]nitrendipine binding in rat striatum.

The effect of lead as a neurotoxic agent has been associated with alterations in calcium metabolism. On this line, the present study shows that lead alters the characteristics of [3H]nitrendipine ([ 3H]NDP) binding to rat striatal membranes. In vitro, lead shares the action of calcium in enhancing [3H]NDP binding although it is more potent on a molar basis. In vivo, lead exposure through drinking water enhances [3H]NDP binding to crude synaptosomal membrane preparations. This effect is lost when membranes are washed with EDTA-EGTA, indicating that the increased binding is due to the persistence of lead in the brain of treated rats.

Animals↗
PubMed1984

Chronic ethanol changes opiate receptor function in rat striatum.

Ethanol produces supersensitivity of striatal delta-opiate receptor sites labeled by [3H]DADLE and [3H]etorphine. The impairment may be ascribed to the diminished enkephalin release detected in rat striatum after chronic ethanol consumption. On the contrary, a lower affinity of striatal mu-opiate receptors results after same ethanol exposure. In fact, the Kd values of [3H]Met-enkephalin and [3H]DHM are enhanced when measured in striata of ethanol-dependent rats. The diverse sensitivity of the various classes of opiate receptors to ethanol may be ascribed to different ethanol effects on enkephalinergic transmission.

Animals↗
PubMed1984

Chronic dihydroergotoxine treatment affects the number of dopamine recognition sites in rat striatum.

Ergot derivatives have been proposed to have ameliorative effects in various pathological conditions where dopaminergic transmission is believed to be impaired, namely Parkinson's disease, amenorrhea-galactorrhea syndrome, and in the treatment of behavioural disturbances of the elderly. To get more insight into a possible involvement of a direct action of ergot derivatives on dopamine receptors we studied the effect of acute and chronic dihydroergotoxine (DHT) treatment on 3H-Spiroperidol and 3H-N-Propylnorapomorphine (3H-NPA) binding to rat striatal membrane preparations. The results are in favor of an interaction of ergot derivatives with dopamine recognition sites both after acute and chronic treatment.

Animals↗
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

Altered calcium signal transduction after chronic ethanol consumption.

Calcium and calcium-calmodulin dependent phosphorylation of several protein bands was found altered in synaptosomal membranes prepared from ethanol treated rats. The ethanol induced effect on Ca++ and Ca++-calmodulin phosphorylation presented regional differences. In particular 32P incorporation was lower in the striatum and cerebellum, higher in the hippocampus and unmodified in the cortex. Part of the phosphorylated bands had an apparent molecular weight similar to that of the phosphoproteins involved in neurotransmission. These results extend previous observations indicating that calcium movement control is modified during chronic ethanol consumption and suggest that ethanol may interfere at various steps in the calcium-promoted events.

Alcoholism↗
PubMedDate not supplied

Acute ethanol and acetaldehyde administration produce similar effects on L-type calcium channels in rat brain.

The present study investigates the effect of acute ethanol and acetaldehyde administration on neuronal L-type calcium channels by measuring the binding of 3H-nitrendipine (3H-NTP). Acute ethanol (3 g/kg orally) transiently increases (+40% at 40 min) 3H-NTP binding. Acetaldehyde has a similar effect, but the onset of action is shorter; in fact the binding increase peaks 15 min following administration and is completely reversible within 2 hours. Disulfiram pretreatment does not modify the effect produced by acute ethanol on 3H-NTP binding. The results indicate that acetaldehyde may participate in mediating the action of ethanol on voltage sensitive L-type calcium channels with consequent alterations of neuronal excitability.

Acetaldehyde↗