35 research outputs found
Bound and Free Light Chains in Subacute Sclerosing Panencephalitis and Multiple Sclerosis Serum and Cerebrospinal Fluid
Peer Reviewe
Oligoclonal Immunoglobutins, Light Chain Ratios and Free Light Chains in Cerebrospinal Fluid and Serum from Patients Affected with Various Neurological Diseases
Peer Reviewe
Measles Antibodies, Anti-Proteinase and Plasminogen Distribution in Serum and Plasma from Patients Affected with Multiple Sclerosis and Patients Affected with Non-Neurological Diseases
Peer Reviewe
Amino acid sequence of the Homo sapiens brain 21-23-kDa protein (Neuropolypeptide h3), comparison with its counterparts from Rattus norvegicus and Bos taurus species, and expression of its mRNA in different tissues
Bound and Free Light Chains in Serum from Patients Affected with Various Neurological Diseases
Peer Reviewe
Bound and Free Light Chains in Serum from Patients Affected with Various Neurological Diseases
Modulating effect of the nootropic drug, piracetam on stress- and subsequent morphine-induced prolactin secretion in male rats.
1. The effect of the nootropic drug, piracetam on stress- and subsequent morphine-induced prolactin (PRL) secretion was investigated in vivo in male rats, by use of a stress-free blood sampling and drug administration method by means of a permanent indwelling catheter in the right jugular vein. 2. Four doses of piracetam were tested (20, 100, 200 and 400 mg kg-1), being given intraperitoneally 1 h before blood sampling; control rats received saline instead. After a first blood sample, rats were subjected to immobilization stress and received morphine, 6 mg kg-1, 90 min later. 3. Piracetam had no effect on basal plasma PRL concentration. 4. While in the non-piracetam-treated rats, stress produced a significant rise in plasma PRL concentration, in the piracetam-pretreated rats PRL peaks were attenuated, especially in the group given 100 mg kg-1 piracetam, where plasma PRL concentration was not significantly different from basal values. The dose-response relationship showed a U-shaped curve; the smallest dose had a minor inhibitory effect and the highest dose had no further effect on the PRL rise. 5. In unrestrained rats, morphine led to a significant elevation of plasma PRL concentration. After the application of immobilization stress it lost its ability to raise plasma PRL concentration in the control rats, but not in the piracetam-treated rats. This tolerance was overcome by piracetam in a significant manner but with a reversed dose-response curve; i.e. the smaller the dose of piracetam, the higher the subsequent morphine-induced PRL peak. 6. There is no simple explanation for the mechanism by which piracetam induces these contradictory effects. Interference with the excitatory amino acid system, which is also involved in opiate action, is proposed speculatively as a possible mediator of the effects of piracetam