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Biomedical subjects

E Costa

Publications and source records attributed to E Costa.

At least 469 records · Page 26Linked to original sources
PubMed1979

Repeated electroconvulsive shocks and the brain content of endorphins.

Repeated electroconvulsive shocks (ECS) cause an increase of [met5]-enkephalin (ME) content in hypothalamus and some limbic areas such as n. accumbens, septum and amygdala. The temporal characteristics of this increase resemble the time course of the clinical effects of electroconvulsive therapy (ECT). Single shock failed to change the ME content in any part of the brain. After 6 daily shocks ME content increases by 60% in hypothalamus and maximal effect (100% increase) was obtained after 10 daily shocks. The increase of ME content persists 6 days after the termination of ECS. Subconvulsive shocks failed to alter the content of ME in all the brain gions determined. When the seizure induced by ECS was prevented by pretreatment with an anesthetic dose of phenobarbital, the ECS-induced increase in hypothalamic and septal ME content was also blocked. beta-Endorphin content of hypothalamus remained unchanged after repeated ECS despite a two-fold increase in the ME content in the same region. These observations indicate that the time constant for the increase in ME content induced by ECS resembles the time constant for the appearance of the clinical benefits by ECT and may give credence to the possibility that the ME increase may participate in the antidepressive action of ECS.

Amygdala↗
PubMed1979

GABA receptors in clonal cell lines: a model for study of benzodiazepine action at molecular level.

A "recptor unit" for gamma-aminobutyric acid (GABA), which includes brainlike receptor binding sites for tritium-labeled GABA and benzodiazepines (diazepam, clonazepam, and flunitrazepam) and a thermostable endogenous protein (GABA modulin) that inhibits both GABA and benzodiazepine binding, has been demonstrated in membranes prepared from NB2a neuroblastoma and C6 glioma clonal cell lines. In these cells, as in brain, diazepam (1 micromolar) prevents the effect of GABA modulin, and in turn GABA (0.oma and, to a lesser extent, the glioma cells represent a suitable model to study the interactions and the sequence of membrane and intracellular events triggered by the stimulation of benzodiazepine and GABA receptors.

Animals↗
PubMed1979

Translocation of cytosol protein kinase into nuclei and the induction of tyrosine hydroxylase in NBD-2 neuroblastoma cells.

Exposure of neuroblastoma cells (NBD-2) to 8-bromo-adenosine 3',5'-cyclic monophosphate (0.2-1.0 mM) (8-Br-cAMP) for 15 min caused a long term increase in the Vmax of tyrosine-3-monooxygenase activity (TH) beginning about 1 day after 8-Br-cAMP application. Cyclic AMP-dependent histone kinase was maximally activated in about 30 min and stayed activated above pretreatment levels for one hour. In cells exposed to 8-Br-cAMP for 15 min, separation of soluble and particle bound histone kinase showed that the total histone kinase activity in the soluble fraction decreased by 40%. This decrease was accompanied by an increase in protein kinase activity in the particulate fraction, suggesting enzyme translocation. After translocation, the enzyme appears to acquire a different substrate affinity because it prefers as a PO43- acceptor, acidic protein rather than histone. In NBD-2 cells this kinase appears to precede, and may be related to, the delayed increase in TH Vmax.

Cell Nucleus↗
PubMed1979

beta-Adrenergic receptors of frog erythrocytes. Biochemical sequelae following stimulation with isoproterenol.

Following persistent stimulation of beta-adrenergic receptors of frog erythrocytes with (-)-isoproterenol, the cyclic adenosine 3',5'-monophosphate-dependent protein kinase (cAMP-dependent protein kinase) (EC 2.7.1.37) was activated for several hours. This activation outlasted the duration of the increase of cAMP content. Following a persistant stimulation of beta-adrenergic receptors with isoproterenol, the phosphorylation of selective membrane proteins was increased. This increase in phosphorylation lasted longer than 4 hr but less than 12 hr. Between 2 and 4 hr after receptor stimulation the loss of beta-adrenergic receptor from plasma membrane was maximal, and the phosphorylation of two membrane proteins characterized by molecular weights of 60,000 and 38,000 daltons was selectively enhanced. In addition we found that isolated erythrocytes are capable of synthesizing RNA and polypeptides and that incubation with (-)-isoproterenol indices a long-term delayed increase of the synthesis of erythrocyte proteins. This increase in the synthesis of proteins appears to require new RNA synthesis. Thus the possibility can be entertained that this delayed increase in protein synthesis participates in the new synthesis of receptor and is operative in the termination of beta-adrenergic receptor subsensitivity elicited by a persistent stimulation with (-)-isoproterenol.

Alprenolol↗
PubMed1979

Molecular mechanisms regulating the interactions between the benzodazepines and GABA receptors in the central nervous system.

Using radioreceptor assay techniques to measure the kinetics of GABA and diazepam receptors, a relationship between GABA and benzodiazepine receptors has been firmly established in membranes of brain and neuroblastoma NB2a clonal cell lines. Occupancy of benzodiazepine receptors uncovers a new population of GABA receptors (GABA2 receptors) endowed with high affinity for GABA. Moreover, stimulation of GABA receptors increases the affinity of 1,4-benzodiazepine receptors for 1,4-benzodiazepines. This reciprocal interaction appears to be mediated by an endogenous regulatory protein (for details on this protein see [14 and 29]) which allosterically regulates GABA2 receptors while it competitively interacts with benzodiazepines for their specific binding sites. The rank order of potency of the various 1,4-benzodiazepines to block the action of this protein inhibitor on GABA receptors is related to their capacity to displace 3H-diazepam binding. These data suggest that the interaction between the 1,4-benzodiazepine receptors and the endogenous protein modulator of GABA2 receptors might play a role in the pharmacological action of the 1,4-benzodiazepines.

Animals↗
PubMed1979

Cortical lesions modulate turnover rates of acetylcholine and gamma-aminobutyric acid.

Interruption of the cortico-striatal glutamatergic pathway by decoratication results in significant decreases in the turnover rates of acetylcholine TRACh and gamma-aminobutyric acid TRGABA of striatum. These data support the hypothesis that the cortical input to the striatum is excitatory and acts to modulate cholinergic and GABAergic function in this nucleus. Studies of kainate-induced lesions of the striatum also indicate that most striatal cholinergic interneurons receive a glutamatergic input and that multiple injections of kainate are required to destroy this large population of interneurons.

Acetylcholine↗