Biochemical and behavioural effects of isamoltane, a beta-adrenoceptor antagonist with affinity for the 5-HT1B receptor of rat brain.

The biochemical and behavioural effects of isamoltane, a beta-adrenoceptor and 5-HT1B receptor antagonist that has higher affinity for 5-HT1B receptors than for 5-HT1A receptors, on 5-HT neurotransmission in the rat brain were examined. In binding experiments isamoltane was found to be about five times more potent as a ligand for the 5-HT1B receptor than for the 5-HT1A receptor (Ki values 21 and 112 nmol/l, respectively). Isamoltane increased the K(+)-evoked overflow of 3H from 3H-5-HT loaded slices of rat occipital cortex at 0.

Postmortem- and cryostability of the potassium-evoked release of [3H]5-hydroxytryptamine from rat cerebral cortical miniprisms.

A prerequisite for the study of neurotransmitter release from human brain autopsy samples with histories of different diseases is that the cryo- and postmortem stability of the release process is good. In the present study, the effect of post-mortem delay and of storage at -70 degrees C by the "slow freeze--fast thaw" method of Hardy et al. [J Neurochem (1983) 40: 608-614] (which allows for the retention of metabolic activity of the tissue after the storage and thawing) of rat cerebral cortex samples upon the release of [3H]5-hydroxytryptamine ([3H]5-HT) from prelabelled miniprisms has been investigated.

Norepinephrine-stimulated inositol phospholipid breakdown in the rat cerebral cortex following serotoninergic lesion.

Norepinephrine (NE)-stimulated inositol phospholipid hydrolysis ("PI breakdown") in rat cerebral cortical miniprisms was used as a measure of alpha 1-adrenoceptor function following serotonin and/or NE depletion. The use of ascorbic acid to prevent autooxidation of the NE during the PI breakdown assay was found to be warranted. Treatment of rats with 5,7-dihydroxytryptamine and DSP4 produced selective depletions of serotonin (79-95%) and NE (69-85%), respectively, in cortical and hippocampal brain regions.

Investigation into the effects in-vitro of the 5-hydroxytryptamine reuptake inhibitor, alaproclate, on carbachol-stimulated inositol phospholipid breakdown in the rat cerebral cortex.

The effect of alaproclate in carbachol-stimulated inositol phospholipid (PI) breakdown in rat cerebral cortical miniprisms has been investigated. Carbachol-stimulated PI breakdown was greatly enhanced by increasing the assay potassium concentration from 5.88 to 18.

Antagonist effects of the enantiomers of 3-PPP towards alpha 1-adrenoceptors coupled to inositol phospholipid breakdown in the rat cerebral cortex.

The effects of the two enantiomers of 3-PPP upon alpha 1-adrenergic and muscarinic receptors coupled to the inositol phospholipid (PI) breakdown response have been investigated. 3-PPP(-) and 3-PPP(+) were found to antagonize the noradrenaline (10 microM)-stimulated PI breakdown in rat cerebral cortical miniprisms with IC50 values of 18 and 61 microM, respectively. The dopamine receptor antagonists haloperidol and raclopride were also antagonists, with IC50 values of 0.