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Biomedical subjects

D R Haubrich

Publications and source records attributed to D R Haubrich.

48 records · Page 3Linked to original sources
PubMed1973

Prostaglandin E1 causes sedation and increases 5-hydroxytryptamine turnover in rat brain.

1. Administration of prostaglandin E(1) (1 mg/kg, i.p.) to rats induced sedation and a decrease in muscular tone. Prostaglandin E(1)-induced sedation was accompanied by the low voltage-high frequency E.E.G. pattern characteristic of the waking animal.2. Administration of prostaglandin E(1) also increased the turnover rate of 5-hydroxytryptamine and raised the concentration of acetylcholine in brain.3. The behavioural effects of prostaglandin were blocked by prior administration of p-chlorophenylalanine or pargyline, drugs which lowered the brain concentration of 5-hydroxyindoleacetic acid (5-HIAA), and was potentiated by pretreatment with probenecid, which elevated the 5-HIAA concentration. Pretreatment with atropine sulphate failed to alter prostaglandin E(1)-induced sedation.4. The results are compatible with the possibility that prostaglandin E(1) induces a state resembling paradoxical sleep through an action on 5-hydroxytryptamine metabolism in brain.

Acetylcholine↗
PubMedDate not supplied

Increased susceptibility to seizures and decreased catecholamine turnover in spontaneously hypertensive rats.

Spontaneously hypertensive rats (SHR) were compared with normotensive Wistar rats for their sensitivity to tonic extensor seizures. SHR were more sensitive to seizures and did not respond to the anticonvulsant effects of L-DOPA. SHR had a slower turnover rate of norepinephrine in brain stem and cortex and of dopamine in striatum. Steady-state levels of catecholamines were similar in both groups. These findings are consistent with earlier ones that reported an inverse relationship between central catecholamine activity and sensitivity to electroconvulsive seizures.

Animals↗