Biomedical subjects

D Fage

Publications and source records attributed to D Fage.

39 records · Page 3Linked to original sources

PubMed1984

Hypophysectomy fails to affect the supersensitivity of striatal dopamine target cells induced by prolonged haloperidol treatment.

The influence of hypophysectomy on biochemical indices of striatal dopamine target cell supersensitivity induced by prolonged haloperidol treatment was investigated in the rat. Hypophysectomy itself did not modify dihydroxyphenylacetic acid (DOPAC) levels but slightly enhanced acetylcholine concentrations in the striatum. Hypophysectomy failed to affect the ability of haloperidol, apomorphine and pergolide to alter these biochemical parameters after acute administration. Prolonged administration of haloperidol (by means of osmotic minipumps delivering 2.5 micrograms/h) for 14 days caused a decrease in DOPAC and an increase in acetylcholine levels in the striatum during withdrawal; these effects were of a similar magnitude in sham-operated and hypophysectomized rats. Moreover, there was a similar degree of tolerance to the elevation of DOPAC and to the diminution of acetylcholine concentrations in striatum in response to challenge with haloperidol during withdrawal in sham-operated and hypophysectomized animals. Finally, a similar supersensitive biochemical response to pergolide (decrease in DOPAC and increase in acetylcholine levels) was observed in both hypophysectomized and sham-operated animals after prolonged haloperidol treatment. These data suggest that hypophyseal factors do not affect the development of striatal dopamine target cell supersensitivity caused by prolonged haloperidol treatment.

Acetylcholine↗

PubMed1984

Effects of cyclo (Leu-Gly) on neurochemical indices of striatal dopaminergic supersensitivity induced by prolonged haloperidol treatment.

The effects of a prolonged treatment with cyclo (Leu-Gly) and/or haloperidol on biochemical parameters indicative of striatal dopamine target cell supersensitivity have been investigated in the rat. When given acutely, cyclo (Leu-Gly) (2 mg/kg sc) did not affect striatal homovanillic acid, dihydroxyphenylacetic acid and acetylcholine levels both under basal conditions or after acute haloperidol (1 mg/kg ip) treatment. When given concomitantly with haloperidol (infused by means of osmotic minipumps at a rate of 2.5 micrograms/h sc) for 14 days, cyclo (Leu-Gly)(2 mg/kg sc once daily) failed to prevent the fall of striatal dopamine metabolites observed 2 days following withdrawal and the tolerance to the elevation of dopamine metabolites which occurs in response to challenge with the neuroleptic during withdrawal. Prolonged treatment with cyclo (Leu-Gly) also failed to affect the tolerance to the decrease of striatal acetylcholine levels which occurs under chronic haloperidol treatment. These data suggest that the mechanism whereby cyclo (Leu-Gly) inhibits the development of neuroleptic-induced dopaminergic supersensitivity does not involve an action of the peptide on nigro-striatal dopaminergic and striatal cholinergic neurons and is probably exerted distally to both dopaminergic and cholinergic synapses.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1983

Influence of lithium on biochemical manifestations of striatal dopamine target cell supersensitivity induced by prolonged haloperidol treatment.

The effects of prolonged treatment with dietary lithium and/or haloperidol (infused by means of osmotic minipumps) on biochemical parameters indicative of striatal dopamine target cell supersensitivity have been investigated in the rat. When given concomitantly with haloperidol, lithium failed to prevent the fall of striatal dopamine metabolites observed 2 days following withdrawal and the tolerance to the elevation of dopamine metabolites in response to challenge with the neuroleptic during withdrawal. Prolonged treatment with lithium also failed to modify the changes in nigral dihydroxyphenylacetic acid levels and in striatal acetylcholine levels which occur under chronic neuroleptic treatment. Chronic dietary lithium alone consistently elevated substance P levels in substantia nigra. The usual decrease in nigral levels of the peptide that occurs in response to chronic treatment with haloperidol was prevented in animals treated concomitantly with lithium. These data suggest that the mechanism whereby lithium stabilizes dopaminergic supersensitivity does not seem to involve an action of the compound on the neuronal mechanisms regulating the activity of the nigro-striatal dopaminergic system or on striatal cholinergic neurons but may be related to the restoration of normal striato-nigral substance P ergic transmission.

3,4-Dihydroxyphenylacetic Acid↗