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The distribution of monoamine transmitters in the area near the ventral surface of the rat medulla oblongata was studied using the Falck-Hillarp histofluorescence method. Histological examination and scanning electron microscopy of these regions were also performed. It was found that there is a wide area dense with catecholamine terminals in the external layer of the ventral medulla oblongata. 5-Hydroxytryptamine-containing terminals and nerve cell bodies on and near the surface were also found. Due to their superficial localization these monoamines may influence the content of cerebrospinal fluid and in this way have effects on cardiovascular and other physiological functions.
Clorgyline (0.3-10 mg/kg, i.p.) inhibited type A monamine oxidase (5-hydroxytryptamine as substrate) but not type B monoamine oxidase (phenylethylamine as substrate) in homogenates of rat striatum and olfactory tubercle; deprenyl (0.3-3 mg/kg, i.p.) inhibited type B but not type A monoamine oxidase in these homogenates. The same doses of clorgyline increased concentrations of dopamine in striatum, and dopamine and norepinephrine in the olfactory tubercle, median eminence and posterior pituitary; they also reduced the concentrations of dihydroxyphenylacetic acid and the rate of synthesis of dopamine (DOPA accumulation after a decarboxylase inhibitor) in the same brain regions. On the other hand, the administration of deprenyl at doses that markedly inhibited type B monoamine oxidase did not alter the concentrations of dopamine, norepinephrine and dihydroxyphenylacetic acid or the rate of accumulation of DOPA in these brain regions. In addition, only clorgyline significantly lowered serum concentrations of prolactin. These results that type A monoamine oxidase catalyzes the intraneuronal deamination of dopamine within terminals of nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophyseal dopamine neurons.
Bromocriptine (BRC) produced neither locomotor stimulation nor stereotyped behavior in mice and rats pretreated with reserpine plus alpha-methyl-p-tyrosine (AMPT). However, the blockade of locomotor stimulation in mice by AMPT could be reversed by their prior treatment with a low, behaviorally inactive dose of L-DOPA. BRC potentiated the stereotypy (rats) and locomotor stimulation (mice) produced by apomorphine in animals pretreated with reserpine plus AMPT. Moreover, BRC potentiated the stimulant effect of d-amphetamine in reserpinized mice, while nomifensine, but not fluoxetine or desipramine, potentiated the stimulant effect of BRC in mice. After direct application to the nucleus accumbens or caudate nucleus of rats, BRC was inactive. However, when BRC and DA were applied together to the nucleus accumbens, BRC enhanced the stimulant effect of DA. These data show that BRC by itself does not cause behavioral stimulation in rodents. Despite having affinity for the DAD 2-receptor, BRC is incapable of causing excitation in rats and mice unless another DA-receptor agonist such as apomorphine or DA is present. The data are discussed in relation to the published literature and the hypothesis presented that BRC affects the signal transmitted by DA-receptor agonists such as apomorphine at or beyond the postsynaptic DA-receptor.
The effect of transplantable tumours (Yoshida Sarcoma) on pineal melatonin content was studied in Wistar rats. A negative correlation between pineal melatonin content and size of growing tumours was observed. Effects of chronic treatment with drugs interfering with n=melatonin or serotonin biosynthesis on tumour growth as well as the influence of tumour growth on pineal melatonin content were investigated. Tumour growth enhancement observed after administration of some substances producing a decrease of pineal melatonin is discussed. Pinealectomy stimulates malignant growth. This may be caused by lack of endogenous melatonin.
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The rate of accumulation of DOPA after the administration of decarboxylase inhibitor (NSD 1015) was determined in the striatum, olfactory tubercle, median eminence and posterior pituitary of the rat brain in order to obtain an index of the rate of synthesis of dopamine (DA) in the terminals of nigrostriatal, mesolimbic, tuberoinfundibular and tuberohypophyseal neurons, respectively. In all brain regions an increase in the concentration of DA by the administration of a monoamine oxidase inhibitor decreased DOPA accumulation while a decrease in the concnetration of DA by the administration of reserpine increased DOPA accumulation. These results indicate that end product inhibition plays a role in regulating DA synthesis in all four neuronal systems. Injections of DA agonists decreased and DA antagonists increased the accumulation of DOPA instriatum, olfactory tubercle and posterior pituitary, but not in median eminence. The administration of gamma-butyrolactone (GBL) and baclofen increased the concentration of DA and the accumulation of DOPA in the striatum, olfactory tubercle and posterior pituitary, and these effects were reversed by the administration of apomorphine. On the other hand, GBL and baclofen had no effect on the concentration of DA or the accumulation of DOPA in the median eminence. These two drugs did, however, reduce the alpha-methyltyrosine-induced decline of DA in the median eminence suggesting that they inhibit the activity of tuberoinfundibular nerves just as they do DA nerves in other systems. These results suggest that the regulation of DA synthesis in terminals of nigrostriatal, mesolimbic and tuberohypophyseal nerves is different from that in tuberoinfundibular nerves in that the latter nerves appear to lack an autoreceptor regulatory mechanism.
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Experiments involving combined injections of a drogue (Ro4-4602 or nialmide) and precursor (3H-5-HTP) allowed to determine the best conditions for performing an experimental study of serotonin (5-HT) synthesis and metabolism in the embryonic pineal organ of Lacerta vivipara. Inhibition of 5-HT synthesis at the decarboxylation step using Ro4-4602 significantly reduces the tritiated indolamine rates in the pineal sensory epithelium of embryos of the stages 37-40. In contrast with the embryos of stages 36 to 40 which received injections of 3H-5-HTP only, the secretory rudimentary photoreceptor cells (SRP) of embryos of the same stages which were pretreated with Ro4-4602 do not show a selective radioautographic labeling. After inhibition of the monoamine oxidases with nialomide, the tritiated indolamine rates are significantly increased in the SRP of embryos of stages 35 to 40. Our radioautographic studies show indirectly the early presence of 5-HTPD and MAO in the SRP (stage 35) during the pineal embryogenesis of Lacerta. In the distal part of the pineal, monoamine oxidase activity is histochemically demonstrated at stage 34. During ontogenesis, the reaction becomes increasingly intensive in the apical part of the epithelial cells while it extends to the epithelium of the proximal part of the pineal organ.
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In the ganglion paracervicale uteri of the rat, there are principle neurons which are able to take up offered catecholamines. Normally there is an inverse relationship between their size and their mean catecholamine-fluorescence. A comparison with the catecholamine-fluorescence of depleted and repleted adrenergic perikarya in the ganglion cervicale superius is made.