The afferent and preganglionic parasympathetic innervation of the rat liver, demonstrated by the retrograde transport of horseradish peroxidase

Magni, F.; Carobi, C.

doi:10.1016/0165-1838(83)90108-x

Cited by 67 publications

(33 citation statements)

References 53 publications

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“…The present study indicates that the vagal motoneurones which innervate the liver are located mainly in the left dorsal motor nucleus of the vagus. This is supported by the results of a histological study using the horseradish peroxidase method (Rogers & Hermann, 1983;Magni & Carbi, 1983).…”

Section: Discussionsupporting

confidence: 65%

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

Niijima¹

1985

The Journal of Physiology

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SUMMARY1. Efferent discharges were recorded from nerve filaments dissected from the hepatic branch of the vagus nerve in the rat.2. Intravenous administration of D-glucose enhanced efferent activity in the hepatic branch of the vagus nerve, whereas 2-deoxyglucose and insulin suppressed this activity.3. The rate at which these fibres fire was found to be related to the concentration of glucose in the blood.4. 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.5. 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.

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Section: Discussionsupporting

confidence: 65%

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

Niijima¹

1985

The Journal of Physiology

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“…Since that time, a substantial amount of evidence has accumulated for the existence of glucose-sensitive afferents within the hepatic vagus that play a significant role in mediating feeding responses to changes in portal glucose concentrations. Anterograde and retrograde tracing studies from the nodose ganglia reveal extensive innervation of the portal vein, hepatic artery, and bile ducts by vagal afferents (36,(41)(42)(43), with little or no innervation of the liver parenchyma (36,42). Sectioning the celiac branch of the vagus nerve blocks the anorexic response induced by intraperitoneal injections of epinephrine (44).…”

Section: Discussionmentioning

confidence: 99%

Celiac-Superior Mesenteric Ganglionectomy, but Not Vagotomy, Suppresses the Sympathoadrenal Response to Insulin-Induced Hypoglycemia

Fujita

Donovan

2005

Diabetes

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Afferent innervation of the portal vein has been shown to be critical in hypoglycemic detection, but the neural pathway by which these afferents ascend remains unknown. To ascertain the role of vagal afferents versus spinal afferents in hypoglycemic detection, the catecholamine response to hypoglycemia was assessed in male Wistar rats undergoing hepatic vagotomy (HV), total subdiaphragmatic vagotomy (TSV), or celiac-superior mesenteric ganglionectomy (CSMG). After recovering from the surgery, the animals were exposed to a hyperinsulinemic-hypoglycemic clamp, with glucose infused peripherally via the jugular vein. In all animals, systemic hypoglycemia (2.64 ؎ 0.03 mmol/l) was induced via jugular vein insulin infusion (25 mU ⅐ kg ؊1 ⅐ min ؊1 ). No significant differences were observed among the groups with respect to arterial glucose or insulin concentration. When hypoglycemia was induced in shamoperated control animals, epinephrine was observed to rise from a basal value of 0.84 ؎ 0.10 to 25.18 ؎ 1.24 nmol/l. Neither HV nor TSV had any significant impact on the epinephrine response to hypoglycemia. In contrast, CSMG animals demonstrated a significant suppression in the epinephrine response to whole-body hypoglycemia (11.25 ؎ 1.21 vs. 22.32 ؎ 0.86 nmol/l in CSMG vs. controls; P < 0.05). The norepinephrine response for controls, 2.00 ؎ 0.22 at basal and rising to 8.95 ؎ 0.20 nmol/l in hypoglycemia, was not significantly different from that of the HV and TSV animals. As with epinephrine, the norepinephrine response to hypoglycemia was significantly suppressed in CSMG compared with control animals (4.72 ؎ 0.48 vs. 7.15 ؎ 0.76 nmol/l; P < 0.05). These findings are consistent with the idea that hypoglycemic detection at the portal vein is mediated by spinal, and not vagal, glucose-sensitive afferents. Diabetes 54:3258 -3264, 2005

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“…This indicates that not all parasympathetic innervation reaches the liver along this left branch. Therefore, in the following experiments (including the physiological experiments), we also dissected the nerves running over the stomach to the left lobe of the liver as described by Magni and Carobi (1983). This resulted in complete absence of any staining in the DMV in HPx rats.…”

Section: Virus Pattern In Hpx Ratsmentioning

confidence: 99%

Suprachiasmatic GABAergic Inputs to the Paraventricular Nucleus Control Plasma Glucose Concentrations in the Rat via Sympathetic Innervation of the Liver

Kalsbeek¹,

Fleur²,

Heijningen³

et al. 2004

J. Neurosci.

216

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Daily peak plasma glucose concentrations are attained shortly before awakening. Previous experiments indicated an important role for the biological clock, located in the suprachiasmatic nuclei (SCN), in the genesis of this anticipatory rise in plasma glucose concentrations by controlling hepatic glucose production. Here, we show that stimulation of NMDA receptors, or blockade of GABA receptors in the paraventricular nucleus of the hypothalamus (PVN) of conscious rats, caused a pronounced increase in plasma glucose concentrations. The local administration of TTX in brain areas afferent to the PVN revealed that an important part of the inhibitory inputs to the PVN was derived from the SCN. Using a transneuronal viral-tracing technique, we showed that the SCN is connected to the liver via both branches of the autonomic nervous system (ANS). The combination of a blockade of GABA receptors in the PVN with selective removal of either the sympathetic or parasympathetic branch of the hepatic ANS innervation showed that hyperglycemia produced by PVN stimulation was primarily attributable to an activation of the sympathetic input to the liver. We propose that the daily rise in plasma glucose concentrations is caused by an SCN-mediated withdrawal of GABAergic inputs to sympathetic preautonomic neurons in the PVN, resulting in an increased hepatic glucose production. The remarkable resemblance of the presently proposed control mechanism to that described previously for the control of daily melatonin rhythm suggests that the GABAergic control of sympathetic preautonomic neurons in the PVN is an important pathway for the SCN to control peripheral physiology.

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The afferent and preganglionic parasympathetic innervation of the rat liver, demonstrated by the retrograde transport of horseradish peroxidase

Cited by 67 publications

References 53 publications

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

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

Celiac-Superior Mesenteric Ganglionectomy, but Not Vagotomy, Suppresses the Sympathoadrenal Response to Insulin-Induced Hypoglycemia

Suprachiasmatic GABAergic Inputs to the Paraventricular Nucleus Control Plasma Glucose Concentrations in the Rat via Sympathetic Innervation of the Liver

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