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Biomedical subjects

A Niijima

Publications and source records attributed to A Niijima.

At least 37 records · Page 2Linked to original sources
PubMed1998

An electrophysiological study on the autonomic innervation of the mesenteric lymph node in the rat.

Splanchnic innervation of the mesenteric lymph node was studied by means of electrophysiological technique in the rat. The effect of intravenous (i.v.) injection of recombinant human interleukin-1beta (rhIL-1beta) on the activity of efferent nerve fibers innervating the mesenteric lymph node was observed in the urethane anesthetized rat. An i.v. injection of 10 ng rhIL-1beta caused a gradual increase in efferent activity which lasted longer than 90 min. Dose related responses were observed at doses of 1, 10 and 100 ng. The least effective dose was about 10 ng. The conduction velocities estimated in mesenteric nerve fibers to the lymph node distributed in the range of 1.9-0.9 m/s, and the mean velocity was 1.39+/-0.34 m/s (n = 5). These observations implicate the involvement in the neural modulation of immune function of the mesenteric lymph node.

Action Potentials↗
PubMed1998

Impaired vagus nerve-mediated control of insulin secretion in Wistar fatty rats.

It has been reported that hyperglycemia in the portal venous blood suppresses afferent activity of the hepatic branch of the vagus nerve, which in turn accelerates efferent activity of the pancreatic branch of the vagus nerve to stimulate insulin secretion. The present study examined this neural control mechanism in genetically obese diabetic male Wistar fatty (fa/fa) rats. Adult (aged 12 to 14 weeks) Wistar fatty rats were obese, hyperinsulinemic, and hyperglycemic. Young (aged 5 to 6 weeks) Wistar fatty rats were slightly obese and hyperinsulinemic, but were euglycemic compared with the lean littermates. In both adult and young lean littermates, the plasma insulin response after an intragastric glucose load (1 g/kg) was diminished by intracerebroventricular (i.c.v.) atropine methylbromide (methylatropine 10 nmol) pretreatment, and a transient increase in plasma insulin was observed after selective hepatic vagotomy, as reported in normal rats. In contrast, in both adult and young Wistar fatty rats, the plasma insulin response after an intragastric glucose load was not diminished by i.c.v. methylatropine pretreatment, and plasma insulin decreased slightly after selective hepatic vagotomy. Further, afferent discharges of the hepatic vagal branch decreased and efferent discharges of the celiac/pancreatic vagal branch increased when 10 mg glucose was infused into the portal vein in the 9-week-old lean littermates, as reported in normal rats. In 7-week-old Wistar fatty rats, afferent discharges of the hepatic vagal branch decreased but efferent discharges of the celiac/pancreatic vagal branch did not increase after intraportal glucose infusion. It is concluded that the vagus nerve-mediated regulation of insulin secretion is impaired from an early stage of life in Wistar fatty rats. Efferent discharges of the vagus nerve to the pancreas seem not to be suppressed by afferent discharges from the hepatic vagus branch, which may lead to insufficient insulin secretion in response to nutrient ingestion followed by a delayed peak. These abnormalities may thus lead to the insulin resistance and fasting hyperinsulinemia that characterize the Wistar fatty rat model.

Animals↗
PubMed1998

Acidic fibroblast growth factor activates hypothalamic-pituitary-adrenocortical axis in rats.

Effects of acidic fibroblast growth factor (aFGF), an endogenous satiety substance, on the hypothalamic-pituitary-adrenocortical axis were examined under pentobarbital sodium anesthesia in rats. A guide cannula was inserted into the cerebral third ventricle and a vascular indwelling catheter was inserted into the right atrium from the jugular vein 2 wk and 3 days, respectively, before the experiment. A marked dose-dependent increase in plasma corticosterone was detected from 20 min to 2 h after intracerebroventricular administration of aFGF (1-10 ng). Significant increases in plasma adrenocorticotropic hormone (ACTH) were observed from 5 to 150 min after the intracerebroventricular administration of 10 ng aFGF. Significant dose-dependent increases in plasma corticosterone were also observed after intravenous injections of aFGF (1, 10, and 100 ng), together with increases in the plasma ACTH level. Pretreatment with antibody to corticotropin-releasing factor via the intracerebroventricular route abolished the increases in corticosterone induced by intracerebroventricularly administered aFGF, but not those induced by intravenous injection of aFGF. In adrenal glands perfused in situ with artificial medium, the corticosterone secretion rate increased slightly in response to 10(-9) M aFGF. These findings suggest that intracerebroventricular administration of aFGF activates the hypothalamic-pituitary-adrenal axis via corticotropin-releasing factor release in the brain, whereas peripheral administration of aFGF activates adrenocortical secretion mainly via a direct action on ACTH release.

Adrenal Cortex↗
PubMed1998

Acidic fibroblast growth factor activates adrenomedullary secretion and sympathetic outflow in rats.

Effects of exogenous acidic fibroblast growth factor (aFGF), which is increased in the brain by food intake, on the plasma levels of catecholamines and on sympathetic efferent outflow were examined in anesthetized rats. A guide cannula was inserted into the cerebral third ventricle, and a vascular indwelling catheter was inserted into the right atrium from the jugular vein. Plasma epinephrine (Epi) and norepinephrine (NE) increased markedly in a dose-dependent manner for up to 120 min after intracerebroventricular or intravenous administration of aFGF (6-667 fmol/rat). Concomitant increases occurred in the efferent activity in the sympathetic nerves supplying the adrenal, spleen, and interscapular brown adipose tissue after the above administrations of aFGF. Both intravenous and intracerebroventricular administration of 10 ng basic FGF (bFGF) also increased sympathetic adrenal efferent activity and plasma Epi and NE concentrations. However, the increases induced by 10 ng bFGF were smaller than those induced by 10 ng aFGF. Bilateral splanchnicotomy completely prevented the increases in Epi induced by intracerebroventricular or intravenous aFGF but had less effect on the increases in NE. Pretreatment with an antibody against corticotropin-releasing factor (CRF), given via the intracerebroventricular route, significantly attenuated the increases in Epi and NE evoked by intracerebroventricular or intravenous administration of aFGF. Hepatic vagotomy also greatly reduced the increases in both catecholamines and the increases in sympathetic efferent firing rates evoked by intravenous administration of aFGF. These findings indicate that 1) aFGF administered intracerebroventricularly activates adrenomedullary secretion and sympathetic outflow via CRF release and 2) aFGF injected intravenously also induces sympathoadrenomedullary activation via centrally released CRF. The idea is discussed that sympathetic activation induced either by endogenous aFGF after feeding or by exogenously administered aFGF may play roles both in energy expenditure after overeating and in the modulation of immune functions.

Adipose Tissue, Brown↗
PubMed1997

Melatonin suppresses hyperglycemia caused by intracerebroventricular injection of 2-deoxy-D-glucose in rats.

To elucidate the role of melatonin (MT), we examined the effects of intracranial injection of MT and an MT-antagonist (S20928) on the hyperglycemic response to intracranial injection of 2-deoxy-D-glucose (2DG) in rats. The hyperglycemic and hyperglucagonemic responses caused by intracerebroventricular injection of 2DG were inhibited by intracerebroventricular co-injection of MT, but enhanced by co-injection of the MT-antagonist. Intraperitoneal injection of MT also inhibited the hyperglycemic response, though the inhibition seemed to be less than that after intracranial injection of MT. These results suggest that MT plays an endogenously suppressive role in the hyperglycemia caused by 2DG, possibly through a brain site.

Animals↗
PubMed1997

Effect of byakko-ka-ninjin-to on the efferent activity of the autonomic nerve fibers innervating the sublingual gland of the rat.

The effect of intraduodenal infusion of Byakko-ka-ninjin-to (BN) on the efferent activity of the autonomic outflow to the sublingual gland was observed in the anesthetized rat. Intraduodenal infusion of BN (50-200 mg/kg) resulted in a dose-related increase in efferent activity. The enhancement of the nerve activity following administration of 200 mg/kg BN lasted longer than three hours. It was observed that the suppressive effect on efferent activity due to i.v. administration of hypertonic saline was antagonized by intraduodenal infusion of BN. From these observations it is suggested that Byakko-ka-ninjin-to acts as a facilitatory agent on salivary secretion.

Adrenergic alpha-Agonists↗
PubMed1997

Possible mechanisms underlying the suppression of gastric vagal afferents due to ecabapide (DQ-2511), a gastroprokinetic agent, in rats.

We examined the implication of a nitric oxide (NO)-guanosine 3',5'-cyclic monophosphate (cGMP) cascade in the suppression of gastric vagal afferents due to ecabapide in anesthetized rats using a standard extracellular method of multi-unit recording. Sodium nitroprusside (SNP, 0.5 mg/kg), an NO donor, depressed the afferent discharge rate of the vagus nerve, like ecabapide (60 micrograms/kg). On the other hand, NG-nitro-L-arginine (L-NNA, 5 mg/kg), an NO biosynthesis inhibitor, significantly elevated its discharge rate. Pretreatment with L-NNA completely blocked the action of ecabapide. Atropine (0.05 mg/kg), a competitive antagonist of muscarinic cholinoceptors, showed no effect on the afferent firing. These results suggest that ecabapide may suppress the activation of vagal afferents in gastric inhibitory vago-vagal reflex pathways through the NO-cGMP cascade.

Animals↗
PubMed1996

The afferent discharges from sensors for interleukin 1 beta in the hepatoportal system in the anesthetized rat.

The effect of intraportal administrations of interleukin 1 beta (IL-1 beta) on the afferent activity of the hepatic branch of the vagus nerve was observed in urethane anesthetized rats. An intraportal injection of IL-1 beta in doses of 10 pg and 100 pg per animal (300-400 g body wt.) resulted in dose-dependent increase in the afferent activity, which lasted about 70-100 min. Further, intraportal injection of IL-1 beta (100 pg) induced reflex activation of efferent activity of the splenic (sympathetic) nerve and vagal thymic nerve. This reflex activation was not observed in hepatic vagotomized rat and after an administration of the same dose of IL-1 beta into the systemic vein in normal rat. The results suggest the existence of sensors for IL-1 beta which send information on IL-1 beta in the portal venous blood to the central nervous system through the hepatic branch of the vagus nerve and play some role in reflex regulation of immune function.

Anesthesia↗
PubMed1996

The hepatic vagal nerve is receptive to incretin hormone glucagon-like peptide-1, but not to glucose-dependent insulinotropic polypeptide, in the portal vein.

To examine whether incretin hormones, truncated glucagon-like peptide-1 (tGLP-1) and glucose-dependent insulinotropic polypeptide (GIP), are recognized by the hepatic vagal nerve, changes of the impulse discharge rate in the afferent vagus upon their intraportal administrations were measured in situ in rats anesthetized with urethan and chloralose. One-min injection of tGLP-1 at a periphysiological dose of 0.2 pmol or a pharmacological dose of 4.0 pmol, but not of the vehicle, significantly facilitated the hepatic vagal afferents. However, the injection of GIP at either a physiological dose of 0.2 pmol, a periphysiological dose of 4.0 pmol, or an even much larger dose of 40.0 pmol did not change the afferents at all. The present results indicate that the hepatic vagus specifically recognizes an intraportal appearance of tGLP-1 in the hepatoportal area, suggesting that the vagal monitoring system for intraportal levels of the incretin hormone operates on ingestion of a mixed meal.

Afferent Pathways↗
PubMed1996

Intraportal infusion of 2,5-anhydro-D-mannitol increases afferent activity in the common hepatic vagus branch.

Peripheral administration of the fructose analogue 2,5-anhydro-D-mannitol (AM), that inhibits hepatic glucose release and ATP formation, stimulates food intake in rats. This effect is partly generated in the hepato-portal area and transmitted to the central nervous system by the common hepatic vagus branch because hepatic branch vagotomy eliminated the feeding response to AM. In the present study, we investigated if the pertinent signal to increase food intake changes the discharge rate in hepatic vagal afferents. An in vivo preparation was used to record afferent hepatic vagal activity following intraportal infusion of AM in anaesthetized rats. Fine nerve filaments were isolated from the distal cut end of the hepatic vagus branch. Nerve activity was recorded by a bipolar electrode and analyzed after conversion of raw data to standard pulses. Standard pulses were integrated into spike counts of 5 s duration and the mean number of spikes in a 50 s interval at baseline was compared to spike count 10, 30 and 50 min after infusion of AM (100 or 300 mg/kg) or saline (control). Saline infusion did not influence afferent hepatic vagal activity. Intraportal infusion of AM, however, dose-dependently increased afferent activity in the hepatic vagus branch. In conclusion, AM increased the afferent discharge rate in the common hepatic vagus branch at doses that have previously been shown to increase food intake. These findings agree with the proposed role of fuel metabolism in the hepato-portal area in the control of food intake and with the suggestion that fuel availability controls food intake by influencing the hepatic afferent discharge rate.

Animals↗
PubMed1996

Bilateral lesions of the hypothalamic suprachiasmatic nucleus eliminated sympathetic response to intracranial injection of 2-deoxy-D-glucose and VIP rescued this response.

We previously found that bilateral lesions of the suprachiasmatic nucleus abolished hyperglycemic response to intracranial injection of 2-deoxy-D-glucose in rats. Because the hyperglycemia due to 2-deoxy-D-glucose was shown to be dependent on the functions of the adrenal medulla and sympathetic nervous system, the effect of bilateral lesions of the suprachiasmatic nucleus on changes in the nervous activity of sympathetic efferents to the adrenal after intracranial injection of 2-deoxy-D-glucose was examined in rats. It was found that bilateral lesions of the nucleus eliminated the increase in neural activity of the sympathetic efferent that occurred after the injection of 2-deoxy-D-glucose. Because the suprachiasmatic nucleus possesses neurons containing a vasoactive intestinal polypeptide-like substance, the effects of vasoactive intestinal polypeptide and 2-deoxy-D-glucose, administered alone or in combination, on the sympathetic activity were examined in intact control rats and in rats with bilateral lesions of the suprachiasmatic nucleus. It was found that in the normal control rats, vasoactive intestinal polypeptide alone increased the sympathetic activity, whereas it dramatically enhanced the sympathetic response to 2-deoxy-D-glucose. However, in rats with bilateral lesions of the suprachiasmatic nucleus, vasoactive intestinal polypeptide alone elicited no increase in the nervous activity of the sympathetic efferents to the adrenal, but combined administration of vasoactive intestinal polypeptide and 2-deoxy-D-glucose caused an increase in the nervous activity of sympathetic efferents to the adrenal. These findings suggest that the suprachiasmatic nucleus is involved in the enhancement of sympathetic activity caused by intracranial injection of 2-deoxy-D-glucose, and that neurons containing a vasoactive intestinal polypeptide-like substance in the suprachiasmatic nucleus play an important role in the sympathetic enhancement that occurs after intracranial injection of 2-deoxy-D-glucose. This role might be a permissive and facilitative one.

Analysis of Variance↗
PubMed1996

Effects of DQ-2511 on neutral activity in afferent and efferent loops of gastric vago-vagal reflex pathways in the rat.

1. DQ-2511 is a new substituted benzamide compound that has gastric prokinetic properties. Actions of the drug on neural discharge in the innervation of the stomach of anaesthetized rats were studied. Standard extracellular methods of multi-unit recording were used to study rates of firing in afferent and efferent filaments teased from gastric branches of the vague nerve. 2. Decreased firing in gastric vagal efferents was associated with increased rates of discharge in the gastric afferents. 3. Intravenous application of DQ-2511 resulted in increased frequency of firing in the efferents in association with decreased rate of discharge in afferent fibres. 4. Application of cholecystokinin octapeptide (CCK8) suppressed activity in the gastric efferents which occurred coincident with the elevated discharge in the afferents. Pretreatment with DQ-2511 blocked the actions of CCK8. 5. The results suggest that the gastric prokinetic action of DQ-2511 may involve suppression of activation of afferents in the sensory component of gastric inhibitory vago-vagal reflex pathways.

Afferent Pathways↗
PubMed1996

Vagal hepatopancreatic reflex effect evoked by intraportal appearance of tGLP-1.

Among proglucagon-derived peptides, the truncated form of glucagon-like peptide-1, GLP-1(7-36)amide (tGLP-1), is known as the most likely physiological humoral incretin. To examine whether there exists any relationship between tGLP-1 levels in the portal vein and activities of the hepatic and pancreatic vagal system, changes of the impulse discharge rate in the hepatic afferent vagus and the pancreatic efferent vagus upon intraportal tGLP-1 injection were measured in situ in rats anesthetized with urethan and chloralose. First, a 1-min bolus tGLP-1 injection at a periphysiological dose of 0.2 pmol or a pharmacological dose of 4.0 pmol, but not the vehicle injection, significantly facilitated the hepatic vagal afferents for > 90 min, showing weaker facilitation at the 0.05 pmol dose. Notably, the injection of noninsulinotropic full-length GLP-1 failed to facilitate the afferents at the 4.0 or 40.0 pmol dose. Second, the intraportal tGLP-1 injections at the 0.05 and 0.2 pmol dose facilitated marginally and significantly the pancreatic vagal efferents in normal rats, respectively, but had no effect on the hepatic vagotomized rats, even at the 40.0 pmol dose. The present results indicate that an intraportal appearance of tGLP-1 is specifically recognized by the hepatic vagal nerve, and this recognition further augments the pancreatic vagal efferent activity in a reflex way, suggesting another nature of tGLP-1 as neuroincretin in the enteroinsular axis.

Afferent Pathways↗
PubMed1996

Effects of Hoelen on the efferent activity of the gastric vagus nerve in the rat.

Hoelen is used to treat gastric disease in Eastern traditional medicine. The efferent activity on the gastric vagus nerve was studied in the rat, and the activity was found to increase after administration of Hoelen into the duodenum. In addition, we examined the effect of Hoelen fractions. Both the fraction containing polysaccharide and the triterpenoid-rich fraction increased activity significantly. Hoelen would thus appear useful for treating gastric disease by activating efferent activity of the gastric vagus nerve through the action of triterpenoid and polysaccharide.

Analysis of Variance↗