Secretory Nerve Research Articles

Effects of secretory nerve stimulation on acid phosphatase and peroxidase in submandibular saliva and acini in cats.

The effects of parasympathetic or sympathetic nerve stimulation either alone, or in combination, on the acid phosphatase-containing central acinar cells and the peroxidase-containing demilunar cells of the cat submandibular salivary gland have been investigated by histochemical and cytochemical techniques. The results obtained with these techniques were correlated with biochemical assays for both enzymes in the saliva secreted. The results indicate that, although both sets of nerves probably affect both sets of cells, the predominant secretory effect of parasympathetic stimulation is on the central cells and, conversely, the predominant secretory effect of sympathetic stimulation is on the demilunes. Sympathetic stimulation appeared also to have initiated synthesis of peroxidase in the demilunar cells, especially when it was superimposed upon parasympathetic stimulation.

Responses of the submandibular secretory nerve to taste stimuli

Responses of the submandibular secretory nerve to taste stimuli

Choline acetyltransferase activity in parotid glands of rats after prolonged treatment with pilocarpine.

The enzyme activity, expressed as total activity and concentration, was found to be decreased in the cholinergic neurones of the glands after treatment with pilocarpine for 10 days. The secretion of saliva evoked by the parasympathomimetic drug is thought to have reduced the reflex stimulation of the glands via the cholinergic secretory nerves and thereby lowered the enzyme activity in the nerves.

Morphological and morphometric studies on the ultrastructural changes during the active release of neurosecretory substance from the neurohypophyseal nerve terminals in dehydrated rats.

Secretory nerve terminals in the posterior pituitaries of normal rats and animals dehydrated for 1, 3, 5, 7, and 9 days were observed with the transmission electron microscope. Neurosecretory granules were markedly decreased after dehydration and received the minimum number at 5 days. Small vesicles in the terminals may be classified into two types: one in aggregated vesicles about 53 nm in diameter and the other is dispersed vesicles 66 nm in diameter. The former vesicles are seen in the normal terminals and slightly decreased in number after dehydration, while the latter are hardly seen in normal pituitaries, but increase enormously due to dehydration at 3 days and thereafter. It may be conjectured that the former are the real synaptic vesicles probably containing acetylcholine, while the latter are the fragments of limiting membranes of the neurosecretory granules. Inversely to the slight decrease of dispersed vesicles at 7 and 9 days of dehydration, reticular tubules in the nerve terminals were strikingly increased in volume. Such a terminal reticulum may be formed by fusion of vesicles derived from fragmentation of the envelopes of neurosecretory granules. Finally the reticulum as well as dispersed vesicles may be destroyed by lysosomes.

Localization of monoamine nerve fibres by formaldehyde fluorescence histochemistry in the posterior salivary duct and gland of Octopus vulgaris

A bright yellow-green specific fluorescence is induced by formaldehyde histochemistry for monoamines in the secretory nerve trunks of the Octopus vulgaris posterior salivary duct, and in their ramifications in the gland tubules. In contrast, the motor nerve trunks of the duct contain few fluorescent elements. The muscular and connective coat of the duct is provided with fluorescent globular and varicose structures, of various sizes and colours, which become numerous in the duct branches. At least some of these peripheral structures belong to varicose monoamine nerve fibres. In the gland, on the contrary, the muscle cells surrounding the tubules are not supplied with fluorescent nerve fibres.

An electron microscopic radioautographic study of the uptake of tritiated serotonin by nerve fibres in the posterior salivary duct and gland of cephalopods.

In the posterior salivary duct and gland of Octopus vulgaris and of Eledone cirrhosa, the duct secretory nerve trunks and their ramifications in the gland tubules include many fibres that incorporate labelled serotonin. However, there are also unlabelled secretory fibres, which cannot be discriminated from incorporating fibres on morphological grounds. Neuroglandular junctions are not apparently established by incorporating fibres. In the duct, the motor nerve trunks contain a small number of labelled fibres, and nerve bundles supplying the duct muscle contain, in variable proportions, serotonin incorporating fibres. Both labelled and unlabelled nerve fibres reach the duct muscle fibres, but neuromuscular junctions involve only unlabelled presynaptic fibres. The nerve fibres which join the gland muscle are usually unlabelled, and the small quota of incorporating fibres in the motor trunks apparently supply only duct tissues. Both secretory and motor trunks, originating from different ganglia, can be considered to contain heterogeneous fibres, releasing different neurotransmitters at the terminals. Certain of these fibres could be serotoninergic.

The control of adaptive hypertrophy in the salt glands of geese and ducks.

1. Factors controlling adaptive hypertrophy, which occurs when marine, or potentially marine, birds drink salt water, have been investigated in geese and ducks using changes in salt-weight weight, RNA and DNA contents as indices of this process. 2. Unilateral post-ganglionic denervation in geese prevented the changes in [RNA] and [RNA]:[DNA] that occurred in the intact gland of birds given salt water for 24 hr; denervation had no significant effect in birds on fresh water throughout. 3. Atropine treatment also prevented the adaptive changes in geese given salt water. 4. In ducks give 0.3 M-NaCl for 48 hr salt-gland weight, [RNA] and [RNA]:[DNA] increase markedly. Treatment of ducks drinking fresh water with large doses of corticosterone and mammalian ACTH for 48 hr had no significant effects on salt-gland weight, RNA or DNA; mammalian prolactin treatment for 48 hr significantly raised [RNA]. 5. No changes in the total amount of DNA in the glands were observed in these experiments, thus indicating that hyperplasia does not occur within 48 hr of a bird first drinking salt water. 6. It is concluded that adaptive hypertrophy is controlled by secretory nerves, and that hormones, if they play any part in this process, have a permissive or secondary role. It is suggested that hypertrophy and the maintenance of the secretory cells in the fully-adapted state may be obligatorily related to secretory activity induced by cholinergic secretory nerves.

The parasympathetic secretory nerves of the nose of the cat.

1. A flow of watery nasal secretion can be induced in the anaesthetized cat either by electrical stimulation of the brain stem or by the simpler procedure of stimulating the cut peripheral end of the Vidian nerve. In both instances the rate of flow of secretion was dependent on the stimulation frequency. Because brain stem stimulation caused an increase in arterial blood pressure, nasal secretion was evoked in subsequent experiments by Vidian nerve stimulation.2. The application of nicotine to the sphenopalatine ganglion shows that the secretory fibres in the Vidian nerve relay in this ganglion and reach the nasal mucosa by way of the posterior nasal nerve.3. Inhibition by atropine of the secretion induced by Vidian nerve stimulation indicates that the secretory fibres are cholinergic.4. It is suggested that the induction of nasal secretion by Vidian nerve stimulation may be useful in assessing the effects of drugs on this secretion.

Choline acetyltransferase in the normal and parasympathetically denervated parotid gland of the dog.

AbstractThe reduction of the activity of the acetylcholine‐synthetizing enzyme, choline acetyltransferase, has been used as an indicator of the effectiveness of the denervation obtained by various operative procedures in the parotid gland of the dog. After division of the auriculo‐temporal nerve about 30 % of the normal enzyme activity still remained in the gland A reduction of the activity to about 10 % was obtained when both this nerve and the recently described secretory nerves on the internal maxillary artery had been cut. When in addition to these two sets of nerves, the facial nerve was severed as well, the choline acetyltransferase activity was not measurable. Electrical stimulation of the facial nerve was found to provoke a slight secretion from the gland.

Nature and location of the receptors for salt‐gland secretion in the goose

1. The nature and location of the receptors which stimulate salt-gland secretion in the goose have been investigated.2. The rapid injection of homologous blood (sufficient to raise the blood volume by 16 and 9%) into the right atrium failed to induce secretion. In contrast, hypertonic sucrose, Na(2)SO(4) and LiCl initiated secretion.3. These results support the theory that osmoreceptors initiate secretion by detecting an increase in plasma tonicity.4. The minimal amount of hypertonic NaCl required to initiate secretion when infusions were made into a carotid artery or into various arteries and veins in the splanchnic region was not less than that required by an I.V. route.5. Cross-circulation and perfusion studies also showed that a raised [NaCl] in the blood perfusing the head was ineffective in evoking secretion and thus that plasma tonicity must be raised elsewhere in the body.6. Secretion in response to salt-loading was abolished or prevented by cutting the vagus nerves or blocking them with local anaesthetic. Stimulation of the cephalic end of the cut vagi in an isolated, perfused decerebrate head induced secretion, indicating that the afferent fibres from the receptors to the C.N.S. lie in the vagus nerves. Cutting the vagi below the heart, however, had no effect on the secretory response.7. Blocking nerves in the crop with local anaesthetic had no effect on secretion induced by salt-loading but when local anaesthetic was injected into the pericardial sac, secretion decreased immediately, stopped, and recovered with a time course similar to that seen after blocking the vagus nerves.8. Section of the vagi in the neck abolished the tachycardia observed in response to the injection of hypertonic NaCl into the right atrium.9. As in other species, stimulation of the ;secretory nerve' induced secretion in anaesthetized or decerebrate geese.10. Hexamethonium given I.V. or applied topically to the ;secretory nerve ganglion' blocked secretion in response to salt-loading or to secretory nerve stimulation.11. It appears that the receptors for salt-gland secretion are located in or near the heart and that afferent fibres from these receptors travel in the vagus nerves to the C.N.S.12. A possible scheme of the secretory reflex which initiates and maintains salt-gland activity is proposed.

Pre- and postganglionic secretory pathways for the parotid gland of the dog.

AbstractRecently earlier unknown secretory nerve fibres to the parotid of the dog have been traced outside the auriculo‐temporal nerve, on the internal maxillary artery and in the facial nerve. In the present experiments it was investigated whether they conveyed impulses from the “classical” preganglionic nerve, the tympani one, or from secretory nerves outside this nerve, the existence of which has been suggested by previous workers. The parotid secretory response to electrical stimulation of the tympanic nerve was found to be successively reduced when the auriculo‐temporal nerve, the internal maxillary artery and the facial nerve were divided. Some additional evidence is presented for the conception, that most of the impulses travel in the tympanic nerve and are conveyed to the gland via the auriculo‐temporal nerve and the adventitia of the internal maxillary artery. Uncharted secretory pathways outside the tympanic nerve were found to contribute very little to the reflexly induced secretory response, because after division of the tympanic nerve this response was abolished in 5 glands out of 10, whereas only a slight secretion was obtained in the others.

Ultrastructure of the pituitary complex in the genus Raia (elasmobranchii). I. The pars neurointermedia.

A single secretory cell type is predominant in the neurointermediate lobes of Raia clavata, R. batis and R. radiata; a few glia cells are also present. Nerve bundles entering the lobe between the cell cords contain two secretory nerve types, and possibly a third type devoid of secretory granules. Type A axons containing granules of mean diameter 2000 A are presumed peptidergic, and type B axons with 1000 A granules, aminergic. Both axon types make numerous synaptoid contacts with the secretory cells, and also make contact with the basement membrane of the capillary walls. A few neuroglial contacts were also noted. The implications of this innervation pattern with respect to the control of MSH secretion are discussed. A colloid-filled cavity present in the lobes of two juvenile fish is interpreted as a remnant of Rathke's pouch. It is lined with a layer of interdigitating undifferentiated cells bearing microvilli, interspersed by a few ciliated cells.

Effect of corticosteroid on hyperactive carotid body and carotid sinus in asthmatics.

Steroids usually eliminate the hyperactivity of carotid body and carotid sinus in asthmatics. They also either weaken or eliminate pulmonary vagotonia that most asthmatics have even during asthmatic attack-free period. However, if patients discontinue their use, the hyperactivity of both the carotid body and the carotid sinus, as well as the intensity and stability of pulmonary vagotonia, usually returns to the original state, sooner or later. When the pulmonary vagotonia is eliminated by steroid, the vagotonia in other organs is frequently heightened. Indeed, in the initial stage of the treatment with this type of drugs, the irritability of the bronchial vagi of all functions is usually completely eliminated by steroids. But, after their long-term use, the effect often becomes only partial. That is, the irritability of the vagal bronchoconstrictor nerve is eliminated by steroids by varying degrees, whereas that of the vagal vasodilator and secretory nerves of the bronchial walls is heightened. Thus, the mucous and secretory symptoms that appear more strongly than the bronchospasm often become so severe as to be nearly uncontrollable by steroids or other drugs.

The secretory nerves of the parotid gland of the dog.

1. Secretory nerve fibres to the parotid gland of the dog have been found in the adventitia of the internal maxillary artery. In dogs under chloralose anaesthesia the course of these fibres from the mandibular nerve to the gland was determined by electrical stimulation at different sites. Secretion induced by these nerves was abolished by atropine but not by hexamethonium.2. In dogs in light barbiturate anaesthesia parotid secretion was evoked reflexly by pouring citric acid on the tongues. After division of the auriculo-temporal nerve and the nerves on the artery this secretion disappeared in about half the experiments and was greatly reduced in the others.3. The maximal secretory rate which could be obtained reflexly from the normally innervated parotid gland was first estimated in light barbiturate anaesthesia. Chloralose was then given and the auriculo-temporal nerve and the nerves on the artery were electrically stimulated together; in about half the experiments this could produce secretion at a rate as high as that obtained reflexly.4. By separate and simultaneous stimulation of different sets of nerve fibres convergence of the secretory fibres to the glandular cells could be demonstrated.5. It is concluded that a large number of post-ganglionic, cholinergic secretory fibres to the canine parotid gland run on the internal maxillary artery. In some dogs a small number of fibres seem to have escaped detection. Possibly they may reach the gland by way of the facial nerve.

Salivary secretion in the rat in a hot environment.

AbstractConscious rats were found to secrete saliva from the submaxillary gland when exposed to heat. In rats with sympathetically denervated glands the secretory rate was a little lower and in parasympathetically denervated glands the secretion was almost abolished. The salivary flow appeared to increase with increasing ambient temperature and the secretion started earlier at higher temperatures. The secretion elicited by heat stress was compared to the secretion evoked by electrical stimulation of the parasympathetic nerve to the gland. It is concluded that the salivary secretion evoked by heat stress is mainly mediated by the parasympathetic secretory nerves, although the sympathetic fibres also take part.

The parasympathetic secretory nerves of the lacrimal gland of the cat.

1. Electrical stimulation of the brain stem of the anaesthetized cat induces a secretion from the lacrimal gland.2. The secretion is abolished either by Vidian nerve section or by the application of nicotine to the sphenopalatine ganglion.3. In contrast to stimulation of the peripheral end of the cut Vidian nerve, stimulation of the central end induces lacrimal secretion.4. A new pathway is proposed in the light of the experimental findings.

Role of sympathectomy for hyperhidrosis.

Sweat glands are of two main types, eccrine and apocrine. Apocrine glands develop in association with hair follicles and play no part in thermor?gulation. They are distributed in the axilla, perineum, and mammary areola and secrete a milky odourless fluid, are probably under the control of circulating adrenaline, and do not appeau to be supplied by secretory nerves.1 On the other hand, eccrine glands are found throughout most of the skin?very dense on the palms and soles but less so in the head and neck, trunk, and upper arms and legs. They are situated deep in the dermis and secrete a dilute solution containing urea and lactic acid. The sodium chloride concentration varies according to the level of adrenocortical activity.2 Eccrine glands are important in ther mor?gulation, are supplied by cholinergic fibres present in sympathetic nerves, and are inhibited by atropine.

Spinal root pathway of the adrenal medullary secretory nerve fibers in the dog.

In dogs anesthetized with sodium pentobarbital, adrenal venous blood was collected and analyzed for adrenaline and noradrenaline fluorometrically. Electrical stimulation of the ventral spinal root from the fifth thoracic (T5) to the first lumbar (L1) segments produced a significant increase in adrenal medullary secretion. On the contrary, stimulation of the dorsal spinal root had no effect on adrenal medullary secretion. Unilateral section of the ventral spinal roots from T5 to L1 abolished an increased adrenal medullary secretion of the ipsilateral adrenal gland in response to insulin-induced hypoglycemia. Section of the dorsal spinal roots had no effect. It is concluded that the adrenal medullary secretory nerve fibers in dogs pass through the ventral spinal roots at the levels of T5-L1.

The secretory and vascular response to nervous and hormonal stimulation in the pancreas of the pig.

1. The atropine-resistant action of the vagus nerves on the flow of pancreatic juice in the pig has been examined and related to certain properties of the pancreas in this species.2. The pancreas was more sensitive to secretin in the pig than in the dog, although similar maximal rates of secretion were observed in both species.3. The potentiation by secretin of the effects of parasympathetic stimulation on the flow of juice was conspicuous in the pig because of the heightened sensitivity to secretin and the resistance to atropine of this action of the secretory nerves.4. Stimulation of the vagus nerves increased the output of amylase in pancreatic juice more readily than injections of pancreozymin in the pig. In the dog pancreozymin was more effective than stimulation and could alone raise the amylase output to values comparable with those attained by stimulation in the pig. In both species atropine reduced the response to pancreozymin by only 20-25%, compared with 70-95% for vagal stimulation.5. Stimulation of the vagus nerves caused an intense, well maintained vasodilatation in the pancreas, which appeared after a shorter latent period than the secretion and was not diminished by atropine. Pancreozymin caused a smaller, and secretin only a slight, increase in pancreatic blood flow, which was also resistant to atropine, but appeared at the same time as the enhanced flow of juice. Injections of acetylcholine caused a vasodilatation which preceded the secretion but was abolished by atropine. The possibility that the pancreas receives an atropine-resistant parasympathetic vasodilator nerve supply is discussed.6. The results provide no evidence that a substance with specific secretin-like properties might be released within the pancreas to act as a secondary transmitter for the effect of stimulation of the vagus nerves on the flow of pancreatic juice.7. The experiments indicate that differences in the parasympathetic innervation of the exocrine cells of the pancreas between the pig and dog may underlie the observed differences in the secretory responses of the gland in these species.

An investigation of the nerve supply to thealt gland of the duck.

Secretion can be produced from the salt gland of the duck by electrical stimulation of nerves reaching the gland and by the administration of parasympathomimetic drugs; the latency of this response is similar to that of the secretory response produced by intravenous salt loading and is similarly inhibited by atropine. The salt gland contains both acetyl‐ and butyrylcholinesterase; the former appears to be associated with nerve fibres which originate in cells occurring along the gland's secretory nerve and in its ganglion. There is no obvious difference in cholinesterase content of secreting and resting glands. Denervation of the salt gland, by an operation which includes removal of the ganglionic portion of the secretory nerve, abolishes secretory response to salt load and leads to disappearance of cholinesterase. Such denervated glands may be caused to secrete by administration of carbachol; this response is potentiated by concurrent salt loading. Section of the secretory nerve central to its ganglionic region, however, fails to abolish secretion in response to salt loading and does not alter cholinesterase content. Hexamethonium in large doses fails to influence the establishment or course of a secretory response to salt loading. These findings, coupled with the demonstration that cholinesterase staining in the secretory nerve is only seen in and distal to its ganglion cells, suggests that the cholinergic nerve supply to the gland is unusual. The findings support the concept that a cholinergic secretomotor mechanism can produce salt gland secretion. They also imply that any associated hormonal control of secretion cannot operate in the absence of intact peripheral nerve supply. The possibility is discussed that the ganglion cells of the secretory nerve may have an osmoreceptive function.