PubMed HealthSearch

PubMed · 40501

Biochemical and behavioural studies on the interference between catecholaminergic and serotonergic central systems.

Abstract

L-DOPA, apomorphine and amphetamine increase emotional reactivity and aggressiveness, and/or evoke spontaneous attack behaviour in male rats. At the same time these compounds accelerate the turnover of endogenous serotonin (5-HT), increasing the brain concentration of 5-HIAA. L-DOPA, amphetamine and apomorphine antagonize the depressive effects of 6-tryptophan on behaviour. After the injection of L-tryptophan these dopaminomimetics facilitate the turnover of 5-HT in the brain. On the other hand, the tranquillizing effect of L-tryptophan correlates not only to the increased level of 5-HT but also to an accelerated catabolism of dopamine. After the simultaneous injection of L-DOPA and L-tryptophan, cross-influence on the turnover of 5-HT and dopamine is noted, while in behaviour the effects of L-DOPA prevail over those of L-tryptophan. PCPA blocks the behavioural effects of dopaminomimetics.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

L H Allikmets, A M Zharkovsky. 1978. Biochemical and behavioural studies on the interference between catecholaminergic and serotonergic central systems.. https://pubmed.ncbi.nlm.nih.gov/40501/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

[Beta-blocking agents alone or combined with diuretics or alpha-adrenolytics in the treatment of essential arterial hypertension].

The Authors examine the antihypertensive effectiveness of the beta-adrenergic receptor blocking agents, according to their personal experience and a review of the bibliography. It is not cleared yet how these drugs reach their hypotensive effect. It is reasonable to assume however that several factors are involved: cardiac output, intravascular volume changes, plasma renin activity and peripheral resistance. Thirty patients suffering from essential hypertension not complicated by cardiac or renale failure were treated. Patients were allocated at random into one of three subsets of ten. In group A oxprenolol was given for 8 weeks and the dose was gradually increased up to 300 mgs daily. Oxprenolol was administered in combination with clortalidone in group B and with phentolamine in group C. A clinically satisfactory reduction in blood pressure was attained in no subset, despite the significant decrease of mean blood pressure. The blockade of beta-adrenergic receptors alone has proved to be less effective than the combined administration of oxprenolol and clortalidone or of oxprenolol and phentolamine. No differences were observed between the two combinations.

Adrenergic alpha-Agonists

Presynaptic noradrenergic alpha-receptors and modulation of 3H-noradrenaline release from rat brain synaptosomes.

The depolarization (15 mM K+)-induced release of 3H-NA from superfused rat brain synaptosomes and the effects of alpha-noradrenergic drugs thereon were studied. Noradrenaline (NA; in the presence of the uptake inhibitor desipramine) reduced synaptosomal 3H-NA release. Reduction of the concentration of calcium ions in the medium during K+ stimulation greatly enhanced the sensitivity of 3H-NA release to alpha-receptor-mediated inhibition. Under these conditions NA dose-dependently inhibited 3H-NA release from synaptosomes obtained from cortex or hypothalamus, but did not affect 3H-NA release from striatal (i.e dopaminergic) synaptosomes. Adrenaline, clonidine and oxymetazoline potently inhibited 3H-NA release from cortex synaptosomes at concentrations in the nanomolar range. Phentolamine by itself did not affect synaptosomal 3H-NA release, but antagonized the inhibitory effects of both noradrenaline and adrenaline. The data obtained further substantiate the hypothesis that the alpha-receptors mediating a local negative feedback control of NA release are localized on the varicosities of central noradrenergic neurons, Furthermore, noradrenergic nerve terminals in the hypothalamus appear to be less senstive to alpha-receptor-mediated presynaptic inhibition than those in the cortex.

Adrenergic alpha-Agonists

Inhibition by alpha-adrenoceptor agonists of renin release in vitro.

A variety of alpha-adrenergic agonists encompassing a broad range of concentrations were used to investigate the existence and nature of a putative alpha-adrenergic mechanism inhibitory to renin release, which may operate at the level of the juxtaglomerular apparatus. For this purpose rat renal cortical tissue incubated in vitro was used. Concentrations of noradrenaline, adrenaline and methoxamine of 10(-6), 10(-5), 10(-4) and 10(-3) M caused significant dose-related inhibition of renin release. The inhibition of release by these doses was reversed completely by 10(-4) M phentolamine. In contrast, phenylephrine, oxymetazoline and clonidine did not inhibit renin release. The results support the concept of an alpha-adrenergic mechanism inhibitory to renin release and show that high concentrations of alpha-adrenergic agonist are required for its operation in vitro. The manner in which this inhibitory mechanism affects renin release under physiological circumstances remains to be demonstrated.

Adrenergic alpha-Agonists