Noradrenaline-containing Terminals Research Articles

Central noradrenergic neurones concentrate 3H-oestradiol.

Central catecholamines play an important part in the regulation of hormone secretion from the pituitary gland and in the mediation of male and female sexual behaviour. Noradrenaline has been shown to stimulate the release of luteinizing hormone (LH) probably by influencing the secretion of LH-releasing hormone (LHRH). The medial preoptic and hypothalamic areas, including the median eminence, contain noradrenaline-containing terminals which originate from discrete noradrenaline-containing cell groups in the lower brain stem. These cell groups have been identified in the pons and the medulla oblongata by histochemical methods and pharmacological experiments. Recent studies with antiserum to dopamine-beta-hydroxylase (DBH), the enzyme that converts dopamine to noradrenaline, provided evidence for the existence of noradrenergic cells. These include the locus coeruleus (group A6), a ventrally located more diffuse but continuous subcoeruleus group (group A5), a cell group located dorsal to the nucleus (n.) dorsalis motorius nervi vagi (group A2) and a cell group in or near the nucleus reticularis lateralis (group A1). Using the thaw-mount autoradiographic technique, oestradiol-concentrating neurones have been localized in many areas of the lower brain stem, including the locus coeruleus, n. tractus solitarii, n. dorsalis motorius nervi vagi, and reticular formation where catecholamine-containing neurones exist. We report here the simultaneous localization, in the same histological section, of 3H-oestradiol and the enzyme dopamine-beta-hydroxylase in neurones of the rat lower brain stem with a combined technique of thaw-mount autoradiography and immunohistochemistry, demonstrating that noradrenaline- or adrenaline-containing neurones are oestradiol target cells.

Fine structure of rat cerebellar noradrenaline terminals as visualized by potassium permanganate ‘ in situ perfusion’ fixation method

The fine structure of noradrenaline-containing nerve terminals in the rat cerebellum was investigated by means of modified potassium permanganate fixation, which revealed a number of small cored vesicles in the terminals. In the molecular layer, noradrenaline-containing terminals mainly made a synaptic like contact with tertiary or secondary Purkinje cell dendrites, while in the Purkinje cell layer no direct contact between noradrenaline-containing terminals and Purkinje cell soma was demonstrated in this study. In the granular layer, noradrenaline-containing nerve terminals were found in its superficial part, particularly around the glomeruli. Noradrenaline-containing nerve terminals in the granular layer mostly make a close contact with the dendrites of the granule cells. As well as confirming the noradrenergic input to Purkinje cells, the results show that noradrenaline might directly influence the granule cells.

Noradrenaline and acetylcholine responses of supraoptic neurosecretory cells.

1. Neurones in the supraoptic nucleus were examined for their responsiveness to microiontophoretically applied monoamines and cholinomimetic agents. One hundred and sixty-one of the 749 neurones recorded were antidromically identified as neurosecretory cells.2. The monoamines, dopamine, noradrenaline and serotonin, reduced the activity of all cells which responded.3. Reduction in activity following noradrenaline administration was antagonized by the beta-adrenergic blocking agent MJ-1999 and potentiated by desmethylimipramine.4. Acetylcholine produced either a decrease or an increase in activity of responsive cells with depression the predominant result. Both the depressant and the excitatory response to acetylcholine were seen in individual neurosecretory cells which were depressed by noradrenaline.5. Application of acetyl-beta-methylcholine and carbaminoylcholine consistently resulted in depression of all responsive cells, while nicotine excited the majority of responsive cells. Both types of response were observed on the same neurosecretory cell.6. The depressant response was antagonized by the muscarinic blocking agent atropine while the excitatory response was antagonized by the nicotinic blocking agent dihydro-beta-erythroidine. Responses to acetylcholine were potentiated by the acetylcholinesterase inhibitor physostigmine.7. The data indicate that noradrenaline-containing terminals on these neurosecretory cells are likely to inhibit their discharge rate, while the presumed cholinergic terminals might function as either excitatory or inhibitory, depending on the receptor activated.8. These results support the hypothesis that ADH release is related to the neuronal activity of the supraoptic neurosecretory cell.