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Biomedical subjects

E Costa

Publications and source records attributed to E Costa.

At least 505 records · Page 28Linked to original sources
PubMed1978

[Met5]Enkephalin content in brain regions of rats treated with lithium.

In rats, chronic treatment with lithium elicits a dose-dependent increase in the [Met5]enkephalin content of nucleus caudatus and globus pallidus. A single injection of lithium fails to change the striatal [Met5]enkephalin content. The increase in [Met5]enkephalin caused by chronic lithium is proportional to the serum lithium level. The extent of the increase in striatal [Met5]enkephalin content levels off at a value of about 250% that of untreated rats. This increase has a time latency of 2--3 days and reaches a plateau at 5 days. The increase that was present at 5 days was no longer evident if the treatment was continued for 2 weeks. Lithium also increases striatal [Leu5]enkephalin content by an extent equal to the increase of [Met 5]enkephalin. Based on the characteristics of the lithium-induced increase in [Met6]enkephalin content, it is proposed that lithium may reduce the rate of release of [Met5]enkephalin from the small enkephalinergic neurons that are intrinsic to the striatum; this action may be related to a change in the regulation of striatal neurons.

Amygdala↗
PubMed1978

Purification of an endogenous protein inhibitor of the high affinity binding of gamma-aminobutyric acid to synaptic membranes of rat brain.

In a medium without Na+, gamma-aminobutyric acid (GABA) binds at 0 degrees to freshly prepared crude synaptic membranes from rat cerebral cortex with an apparent dissociation constant of 218 nM. An endogenous inhibitor of the Na+-independent GABA binding was removed from these membranes by freezing and thawing and by repeated washing with Tris citrate buffer (50 mM, pH 7.1) containing 0.01% Triton X-100. As a result, the crude synaptic membranes bind GABA at 0 degrees with two dissociation constants, 20 nM and 111 nM. The endogenous inhibitor is a thermostable (95 degrees for 15 min) acidic protein of approximately 1.5 X 10(4) daltons. It was purified (about 500-fold) with a series of procedures including gel chromatography on Sephadex G-100 and ion exchange chromatography on Dowex 50W-X8 (H+). Recombination of the purified endogenous inhibitor with crude synaptic membrane preparations deprived of the endogenous inhibitor showed that the purified inhibitor blocked noncompetitively the sites for high-affinity GABA binding. A role of this endogenous regulator in the functional of GABA-ergic synapses is discussed.

Animals↗
PubMed1978

Molecular mechanisms mediating the action of diazepam on GABA receptors.

Two types of crude synaptic membranes have been prepared which differ in their kinetic properties to bind 3H-GABA in a Na+-free medium. One type (B) has one type of receptor (affinity or KD about 0.2 micrometer), the other type (A) has two populations of receptors which have a high (0.16 micrometer) and a low ((.02 micrometer) KD for GABA binding. This difference is due to the presence of a selective endogenous inhibitor of the high affinity receptor for GABA, a thermostable protein of about 15,000 molecular weight. Inhibitor action is counteracted by diazepam (7 X 10(-7) M), competitively. Clonazepam is more active but chlordiazepoxide is less active than diazepam. Two enantiomers of a benzodiazepine were studied. One of them is endowed with anxiolytic activity and nullifies the action of the endogenous inhibitor on high affinity GABA binding, the other is devoid of anxiolytic activity and is inactive against the inhibitor. The endogenous protein inhibitor also competitively blocks the high affinity binding of 3H-diazepam to Type A membranes. It is concluded that the endogenous inhibitor and diazepam act on the same receptor; and suggested that the endogenous inhibitor may be the natural ligand for the brain receptors that bind benzodiazepines with high affinity.

Animals↗
PubMed1978

Opiate receptor agonists as modulators of gamma-aminobutyric acid turnover in the nucleus caudatus, globus pallidus and substantia nigra of the rat.

The injection of various doses of morphine, subcutaneously, or of beta-endorphin, intraventricularly, changes the turnover rate of gamma-aminobutyric acid (TRGABA) in the substantia nigra, globus pallidus and nucleus caudatus. The TRGABA decreases in N. caudatus but increases in globus pallidus and substantia nigra. These changes are dose related and can be inhibited by naltrexone. The increased TRGABA in globus pallidus elicited by these opioid receptor agonists may be associated with catalepsy since muscimol, a specific GABA receptor agonist, injected into the globus pallidus causes a dose-related catalepsy. Since this GABA receptor agonist injected into the substantia nigra fails to cause catalepsy, one can exclude that the increase in the TRGABA of substantia nigra elicited by opiate receptor agonists is operative in mediating the catalepsy elicited by opioids.

Animals↗