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Biomedical subjects

A Niijima

Publications and source records attributed to A Niijima.

At least 91 records · Page 5Linked to original sources
PubMed1987

Inhibition of renal sympathetic nerve activity by electrical stimulation of the hypothalamic paraventricular nucleus in anesthetized rats.

In an attempt to obtain direct evidence for involvement of sympathetic outflow in paraventricular nucleus (PVN)-induced depressor response, effects of electrical stimulation of the PVN on renal sympathetic nerve activity were examined in urethane-chloralose anesthetized rats. Low intensity stimulation of the PVN inhibited renal sympathetic nerve activity, whereas the high intensity stimulation evoked an excitation followed by long-lasting inhibition in renal sympathetic nerve activity. Latencies of the inhibitory and the excitatory responses were about 200 ms and 50-100 ms, respectively. The result suggests that a decrease in blood pressure induced by low intensity stimulation of the PVN is due to inhibiting the sympathetic outflow.

Animals↗
PubMed1987

Role of the hepatic branch of the vagus nerve in liver regeneration in rats.

The role of the vagus nerve in liver regeneration after partial hepatectomy was examined by comparing the effects of hepatic vagotomy (sectioning of the hepatic branch of the vagus nerve) with those of subdiaphragmatic vagotomy in rats. Hepatic vagotomy delayed but did not suppress the increase in the rate of hepatic DNA synthesis and the activity of thymidine kinase after partial hepatectomy. On the other hand, subdiaphragmatic vagotomy delayed and suppressed these indices. The time courses of restoration of liver DNA content after partial hepatectomy were not affected by hepatic vagotomy. However, this index was both delayed and suppressed in subdiaphragmatic vagotomized rats. Hepatic vagotomy did not affect the daily food intake or the body weight increase after partial hepatectomy. However, subdiaphragmatic vagotomy caused considerably more loss of food intake and body weight. There were no differences in the plasma insulin levels after partial hepatectomy among three groups. We concluded that a vagal specific effect is evident in the delay but fails to suppress liver regeneration.

Animals↗
PubMed1987

Pancreatic vagal nerve is receptive to somatostatin in rats.

To investigate whether somatostatin, one of the pancreatic islet hormones, influences the afferent firing activity of the vagus innervating the pancreas and whether there is any relevant morphological basis for the electrophysiological event, cyclic somatostatin-14 was injected into the rat pancreatic artery. The somatostatin injection at a physiological (0.61 pmol) or a pharmacological (3.05 pmol) dose significantly increased the afferent firing discharge rate of the pancreatic vagus in rats anesthetized with urethan and chloralose. The present histological examination disclosed a glomuslike neurovascular body in the rat peripancreatic sinusoidal vein. The body included many small corpuscles, and the corpuscle contained a structure like the afferent nerve ending. The immunohistochemical study revealed that the structure preferentially bound exogenous somatostatin. These electrophysiological and histological findings suggest that the vagal pancreatic nerve is receptive to somatostatin and that there exists a local neural monitoring system for somatostatin secreted from the islets.

Afferent Pathways↗
PubMed1987

Effects of hypothalamic stimulation and lesion on adrenal nerve activity.

Activity changes of efferent adrenal sympathetic nerves in response to bilateral manipulations of the hypothalamus, partly after intra-third cerebroventricular injection of 2-deoxy-D-glucose (2-DG) were investigated in anesthetized rats. Stimulation of the middle part of the lateral hypothalamic area (LHAm) increased adrenal nerve activity, whereas lesion caused rapid and remarkable decrease. Stimulation of the anterior part of the LHA (LHAa) tended to decrease the activity, and lesion produced either rapid decrease or late moderate increase. Stimulation of the ventromedial hypothalamic nucleus (VMH) did not affect the nerve activity, but lesion increased it gradually and then remarkably. Cerebroventricular infusion of 2-DG caused remarkable increase in activity that was suppressed by LHAm lesion. Subsequent infusion of 2-DG during the period of suppressed activity was no longer effective. The increased firing rate after 2-DG was suppressed by stimulation of the VMH, whereas lesion caused no change. These findings indicate that the central regulation of adrenal nerve activity is connected with individual hypothalamic regions and consequently depends on the degree and mode of activation of the sympathoadrenal system.

Action Potentials↗
PubMed1986

Arginine sensors in the hepato-portal system and their reflex effects on pancreatic efferents in the rat.

To investigate the possible existence of arginine sensors in the liver and their reflex effects, afferent discharges from the hepatic branch of the vagus nerve and efferent discharges from the pancreatic branches of the splanchnic and vagus nerves were recorded. Intraportal injection of arginine increased afferent discharge rate of the hepatic branch of the vagus nerve, slightly depressed the efferent discharge rate of the pancreatic vagal branch, and increased the efferent discharge rate of the pancreatic splanchnic branch. The results suggest the existence of arginine sensors in the hepato-portal system that exert reflex regulation of the pancreatic neuroendocrine system.

Animals↗
PubMed1986

Effects of taste stimuli on the efferent activity of the gastric vagus nerve in rats.

The effect of taste stimuli on the efferent discharges in the gastric branch of the vagus nerve was studied in rats anesthetized with urethane-chloralose. An increase in discharge rate following taste stimulation with 5% NaCl over the tongue for 5 min, and a decrease of it following an application of 10% sucrose for the same duration were observed in normal as well as in decerebrated rats. The results indicate the existence of a pathway from the taste receptors to the gastric vagus nerve via the brainstem. The reflex effects of taste stimuli on gastric vagal outflow may be related to gastric acid output.

Animals↗
PubMed1986

Somatostatin-sensitive neural system in the liver.

An intraportal bolus injection of cyclic somatostatin in a dose of 3.05 pmol significantly increased the vagal afferent discharge rate in the rat. The results indicate that somatostatin facilitates the vagal sensory nerve activity in the portal venous area. The present immunohistochemical examination of the rat hepatic neural system further disclosed the encapsulated corpuscles which showed intense staining for exogenous somatostatin. They were located beneath the endothelium of the large branches of the portal vein, protruded into the lumen and contained terminal nerve arborizations in the core.

Animals↗
PubMed1986

Effect of glucose and other hexoses on efferent discharges of brown adipose tissue nerves.

The activity of sympathetic nerves innervating interscapular brown adipose tissue of the rat was recorded. Intravenous administrations of glucose (100-300 mg/kg) enhanced the nerve activity. However, mannose, fructose, or galactose (300 mg/kg) showed no effect, suggesting the response is related to diet-induced thermogenesis in the brown adipose tissue.

Adipose Tissue, Brown↗
PubMed1986

Neural control of blood glucose level.

All of the experimental results described above can be categorized as follows: the relationship between glucose levels and pancreatic and adrenal nerve activities; innervations of the liver and their role in the regulation of blood glucose level; central integration of blood glucose level; glucose-sensitive afferent nerve fibers in the liver and regulation of blood glucose; oral and intestinal inputs involved in reflex control of blood glucose level. We showed that an increase in blood glucose content produced an increase in the activity of the pancreatic branch of the vagus nerve, whereas it induced a decrease in the activity of the adrenal nerve. It was also shown that a decrease in blood glucose activated the sympatho-adrenal system and suppressed the vago-pancreatic system. It seems rational that these responses are involved in the maintenance of blood glucose level. Studies on the innervation of the liver led us to a conclusion that sympathetic innervation of the liver might play a role in eliciting a prompt hyperglycemic response through liberation of norepinephrine from the nerve terminals, and that the vagal innervation synergically worked with the humoral factor (insulin) for glycogen synthesis in the hyperglycemic condition. The glucose-sensitive afferents from the liver seem to initiate a reflex control of blood glucose level. The gustatory information on EIR response, reported by STEFFENS, is supported by the electrophysiological observations. MEI's reports also indicated the importance of information from the intestinal glucoreceptors in the reflex control of insulin secretion. The role of integrative functions of the hypothalamus and brainstem through neuronal networks on neural control of blood glucose levels is also evident. A schematic diagram of the nervous networks involved in the regulation of the blood glucose levels is shown in Fig. 3.

Adrenal Glands↗
PubMed1985

Lesions of the ventromedial hypothalamic nucleus enhance sympatho-adrenal function.

The effects of lesions of the ventromedial hypothalamic nucleus (VMH) on the sympatho-adrenal function were investigated in anesthetized rats using electrophysiological and biochemical techniques. Lesions of this nucleus produced a gradual but strong increase in the efferent activity of the adrenal sympathetic nerves. Catecholamine secretion from the adrenal medulla was also facilitated by VMH lesions. The results indicate that the catecholamines from the adrenal medulla might be involved in the development of metabolic disorders seen during VMH syndrome.

Adrenal Glands↗
PubMed1985

Blood glucose levels modulate efferent activity in the vagal supply to the rat liver.

Efferent discharges were recorded from nerve filaments dissected from the hepatic branch of the vagus nerve in the rat. Intravenous administration of D-glucose enhanced efferent activity in the hepatic branch of the vagus nerve, whereas 2-deoxyglucose and insulin suppressed this activity. The rate at which these fibres fire was found to be related to the concentration of glucose in the blood. Vagal hepatic nerve activity was effectively blocked by section of the left cervical vagus indicating that this nerve is the main pathway of vagal efferent fibres innervating the liver. It is concluded that changes in the rate of hepatic glycogenesis, which occur in response to changes in blood glucose concentration, are mediated in part by the vagal efferent innervation of the liver.

Action Potentials↗
PubMed1984

Effects of hypothalamic lesion on pancreatic autonomic nerve activity in the rat.

The effects of hypothalamic lesions and intravenous glucose infusion on the efferent activity of vagal and splanchnic nerves to the pancreas were studied in anesthetized rats. Lesions of the ventromedial hypothalamic (VMH), the dorsomedial hypothalamic (DMH) and the paraventricular (PVN) nuclei increased vagal and reduced splanchnic nerve activity. Lesion of the lateral hypothalamic area (LHA) decreased pancreatic vagal nerve activity, and produced either increased or decreased activity of pancreatic splanchnic nerve. Intravenous glucose infusion increased activity of the vagal nerve and reduced that of the splanchnic nerve. These glucose responses were influenced by hypothalamic lesions only slightly or not at all. The findings suggest that hypothalamic modulation of pancreatic hormone secretion involves both the parasympathetic and sympathetic nervous systems, and provide evidence that not only the VMH and the LHA but also the DMH and the PVN are involved in this mechanism.

Animals↗
PubMed1984

Effects of D-glucose anomers on sweetness, taste and gastric acid secretion in man.

Gastric acid outputs were examined in human subjects after lingual applications of d-glucose and its anomers. A dose-dependent increase in the acid output was noted following the application of equilibrated D-glucose consisting of 36% alpha- and 64% beta-anomer. The response was not reproduced after administration of atropin. The magnitude of acid output produced by alpha-anomer was different from that induced by beta-anomer in men who could not differentiate between sweetness of the two anomers. Results indicate that recognition of sweetness in the cortex is unrelated to the gastric response, and suggest that a subcortical mechanism may detect qualitative differences in taste and produce the oral phase of gastric acid secretion via vagus action in humans.

Adult↗