Biomedical subjects

T Reum

Publications and source records attributed to T Reum.

20 records · Page 2Linked to original sources

PubMed1994

Fetal mesencephalic grafts influence the dopamine release in the non-lesioned striatum of 6-OHDA-lesioned rats: a behavioral and in vivo voltammetric study.

This study was performed to investigate the effect of intraventricular fetal mesencephalic grafts on the non-lesioned nigro-striatal system of rats with unilateral lesions of dopaminergic neurones in the medial forebrain bundle and to analyze the involvement of the non-lesioned side in functional recovery due to grafts in this model. Grafts placed to the lesioned striatum produced a continuous decrease of apomorphine (APO, 0.25 mg/kg intraperitoneally (i.p.)) and amphetamine (AMPH, 5 mg/kg, i.p.) induced rotations over 7 months after grafting. Using differential pulse voltammetry (DPV) in anaesthetized and pargyline (75 mg/kg, i.p.) pretreated rats we found that 8 months after grafting in the lesioned striatum AMPH (5 mg/kg, i.p.) produced a higher increase of the dopamine (DA) signal (i.e., it became measurable), whereas in the non-lesioned striatum the same treatment produced a smaller increase of the DA signal, both compared to that in sham-grafted controls. After grafting onto the non-lesioned striatum, only a slight decrease of APO-induced rotations was observed, whereas AMPH-induced rotations were increased. In these animals AMPH did not produce a measurable DA signal in the lesioned striatum. The DA signal in the non-lesioned striatum was slightly higher than that of non-grafted controls. These results show clearly that unilateral fetal mesencephalic grafts producing behavioural recovery in the unilateral 6-OHDA model of the rat produce changes at dopaminergic mechanisms in the non-lesioned striatum.

Amphetamine↗

PubMed1990

Hepatic encephalopathy influences high-affinity uptake of transmitter glutamate and aspartate into the hippocampal formation.

The present work was carried out to study the influence of ammonia and factors from sera and cerebrospinal fluid (CSF) from patients with different degrees of chronic liver diseases on [3H]D-aspartate (Asp) and [3H]L-glutamate (Glu) high-affinity uptake into the rat hippocampal formation. For comparison, high-affinity uptake of Glu and Asp was determined in human hippocampal brain tissue obtained at autopsy from cirrhotic patients dying in hepatic coma and from control brains free from neurological, psychiatric, or hepatic diseases. Sera and CSF from patients with chronic liver failure and hepatic encephalopathy (HE) were seen to reduce dramatically Glu and Asp uptake into rat hippocampal dendritic layers. A close inverse relationship was found to exist between the level of ammonia in the sera and the inhibition of uptake, both phenomena correlating highly with the extent of liver failure. The present findings, obtained after dilution of sera from patients with HE while maintaining initial ammonium levels, elucidate, however, that ammonia alone cannot account for the reduction in Glu/Asp uptake capacity. The inhibition of Asp uptake into human hippocampal formation of patients dying in hepatic coma was even more pronounced when compared to that found in rat hippocampus incubated in sera and CSF from patients. Glu/Asp uptake into brain tissue is supposed to be an important factor in the pathogenesis of HE accompanying liver dysfunctions.

Adult↗