Biomedical subjects

A Tihanyi

Publications and source records attributed to A Tihanyi.

3 recordsLinked to original sources

PubMed1984

Catecholamine utilization in specific rat brain nuclei after short-term hyperprolactinaemia.

Endogenous hyperprolactinaemia was induced in intact male rats by transplantation of pituitaries under the kidney capsule. Five days later the utilization of noradrenaline (NA) and dopamine (DA) in individual brain nuclei and changes of plasma prolaction (PRL) were measured. Inhibition of catecholamine synthesis by alpha-methyl-p-tyrosine (alpha-MPT) was used to measure utilization. Hyperprolactinaemia increased the utilization of NA in the locus coeruleus, the cell-body region of the dorsal noradrenergic bundle (DNB), but decreased it in some terminal projections of the same pathway (e.g. the cingulate gyrus). DA utilization was increased by hyperprolactinaemia in the eminentia mediana. In the nigrostriatal DA-ergic projection, hyperprolactinaemia decreased the utilization of DA in the cell-body region (substantia nigra) and increased it in the terminal projection (nucleus caudatus). In the ventral tegmental area (mesolimbic DA-ergic projection), hyperprolactinaemia decreased the utilization of DA. It is concluded that hyperprolactinaemia affects neurotransmission in the hypothalamus and also in specific extrahypothalamic pathways (e.g. DNB, nigrostriatal and mesolimbic DA-ergic projections) and that these changes may correlate with some behavioural effects of the pituitary hormone.

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PubMed1983

Catecholamine utilization in distinct mouse brain nuclei during acute morphine treatment, morphine tolerance and withdrawal syndrome.

The steady-state levels and utilization (alpha-MPT-induced disappearance) of noradrenaline (NA) and dopamine (DA) were measured in distinct mouse brain nuclei after acute morphine challenge, in mice rendered tolerant to morphine, and during the naloxone-precipitated morphine withdrawal syndrome. Mouse brain nuclei containing mainly the cell body areas and some terminal projections of major NA- and DA-containing pathways were selected (nucleus tractus solitarii, locus coeruleus, substantia nigra, area tegmentalis ventralis and nucleus caudatus, nucleus accumbens, gyrus dentatus hippocampi, nucleus raphe dorsalis respectively). Acute morphine treatment reduced the utilization of NA in all brain nuclei but the substantia nigra. In morphine-tolerant mice, all changes characteristic for acute morphine treatment disappeared. Instead, an increased NA utilization was observed in the nucleus tractus solitarii and the area tegmentalis ventralis in the tolerant animals. During morphine withdrawal, an abrupt decrease was observed in the utilization of NA in the nucleus tractus solitarii, whereas the NA utilization in the gyrus dentatus abruptly increased, as compared to the tolerant state. Acute morphine challenge decreased the utilization of DA in the nucleus caudatus, locus coeruleus and nucleus raphe dorsalis. In the tolerant mouse, an increased utilization of DA was observed in the nucleus tractus solitarii. During morphine withdrawal, DA utilization was decreased in the substantia nigra and the area tegmentalis ventralis, while in the nucleus accumbens withdrawal resulted in an increase of DA utilization. The data suggest that acute effects of morphine as well as morphine tolerance/dependence are accompanied by, and likely to be associated with, distinct changes in the catecholamine metabolism of specific mouse brain nuclei.

Animals↗

PubMed1983

Influence of Z-Prolyl-D-Leucine on alpha-MPT-induced catecholamine utilization in specific mouse brain nuclei.

The synethetic dipeptide Z-Prolyl-D-Leucine (Z-Pro-D-Leu) inhibits the development of tolerance to and dependence on morphine in mice. The possible mode of action of the dipeptide was studied by measuring the alpha-MPT-induced disappearance of noradrenaline (NA) and dopamine (DA) either by a spectrofluorimetric assay in major brain areas (lower brainstem, striatum) or by a radioenzymatic assay in specific brain nuclei. For the latter purpose, mouse brain nuclei containing mainly the cell body areas (nucl. tractus solitarii, locus coeruleus, substantia nigra, area tegmentalis ventralis) or some selected terminal projections (nucl. caudatus, nucl. accumbens, gyrus dentatus hippocampi, nucl. raphe dorsalis) of major NA- and DA-containing pathways were selected. In the lower brainstem studied as a whole, the dipeptide did not affect the utilization of either NA or DA. Analysis of the data on the NA utilization in specific brain nuclei, however, revealed that the dipeptide affected NA disappearance in some mesencephalic-limbic nuclei which receive noradrenergic innervation from the dorsal noradrenergic bundle (e.g., nucl. raphe dorsalis, area tegmentalis ventralis, gyrus dentatus). NA utilization in the cell body region of the same pathway (locus coeruleus), however, was not affected by the dipeptide. The dipeptide facilitated DA utilization in the main terminal area of the mesolimbic DA-ergic projection (nucl. accumbens), whereas the same treatment inhibited DA utilization in the main terminal region of the nigro-striatal DA-ergic pathway (nucl. caudatus). The data suggest that localized changes in NA and DA utilization following Z-Pro-D-Leu might be important for peptide-induced changes in morphine tolerance and dependence.

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