Ablation of serotonergic nerves in the rat pancreas. Lack of effects on hormone secretion and intrinsic blood flow

Jansson, Leif; Leung, Pearl E.; McEvoy, Robert

doi:10.1530/acta.0.1100515

Cited by 5 publications

(4 citation statements)

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“…The levels of 5-HT in the pancreas of control rats were similar to those previously reported (Lundquist et al 1989). The injection of 5,7-DHT severely decreased the level of 5-HT (85%) in the rat pancreas 3 days after its injection in agreement with previously published values (Jansson et al 1985). Thus, 5-HT axon innervation in the pancreas was nearly abolished by 5,7-DHT.…”

Section: Discussionsupporting

confidence: 91%

“…The specific 5-HT neurotoxin, 5,7-DHT (Azmitia & Marovitz 1980), was dissolved to a final concentration of 5xl0~4M in Krebs Ringer buffer, pH 74, supple¬ mented with ascorbic acid (10 m) as an antioxidant and the monoamine oxidase inhibitor, pargyline (10~4 m) (Jansson et al 1985). Male Wistar rats weighing 225-250 g were anaesthetized with ether and the pancreas was exposed through a midline laparatomy.…”

Section: Experimental Animalsmentioning

confidence: 99%

“…Male Wistar rats weighing 225-250 g were anaesthetized with ether and the pancreas was exposed through a midline laparatomy. The pancreas was infiltrated completely with 2 ml 5,7-DHT solution in¬ jected into the substance of the gland through a 25 gauge needle as previously described (Jansson et al 1985). The abdominal wound was closed.…”

Section: Experimental Animalsmentioning

confidence: 99%

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Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Muñoz-Acedo

Alvaro-Alonso²,

Arilla³

1995

Journal of Endocrinology

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To date, it is unknown whether intrapancreatic serotonergic nerves can influence pancreatic somatostatin (SS) content and the SS receptor/effector system in the exocrine pancreas. In this study, the intrapancreatic serotonergic nerves were chemically ablated by injecting a specific serotonin (5-HT) neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into the substance of the gland. Three days after the injection, the 5-HT-like immunoreactive levels in the pancreas were reduced by more than 85% whereas somatostatin-like immunoreactive levels had increased (86%). The number of SS receptors in the pancreatic acinar cell membranes of the 5,7-DHT-treated rats was also increased (72%). No significant differences were seen in basal or forskolin-stimulated adenylate cyclase (AC) enzyme activities in the control and the 5,7-DHT-treated groups. In spite of the increase in the number of SS receptors in the pancreatic acinar cell membranes of 5,7-DHT-treated rats, SS caused a significantly lower inhibition of AC activity in these membranes. This finding is related to the observed decrease of a 41 kD pertussis toxin-sensitive substrate, presumably the alpha i subunit of the guanine nucleotide inhibitory protein, in pancreatic acinar cell membranes 3 days after intrapancreatic 5,7-DHT administration when compared with the corresponding controls. The functions of pancreatic serotonergic nerves seem to be associated with enteropancreatic communication. These data together with the present results suggest that pancreatic SS content and the SS receptor/effector system in the exocrine pancreas may be regulated by enteropancreatic serotonergic nerve fibers and may participate in enteropancreatic reflexes.

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Section: Discussionsupporting

confidence: 91%

Section: Experimental Animalsmentioning

confidence: 99%

Section: Experimental Animalsmentioning

confidence: 99%

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Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Muñoz-Acedo

Alvaro-Alonso²,

Arilla³

1995

Journal of Endocrinology

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“…Ablation of serotonergic nerves in the pancreas does not affect hormone secretion , and the islets have been found to lack dopaminergic innervation , but serotonin and dopamine may nevertheless modulate insulin secretion. β ‐Cells express high activity of aromatic l ‐amino acid decarboxylase (AADC) that converts 5‐hydroxytryptophane to serotonin .…”

Section: Pulsatile Insulin Release From Single β‐Cellsmentioning

confidence: 99%

Neurotransmitter control of islet hormone pulsatility

Gylfe

Tengholm

2014

Diabetes Obesity Metabolism

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Pulsatile secretion is an inherent property of hormone-releasing pancreatic islet cells. This secretory pattern is physiologically important and compromised in diabetes. Neurotransmitters released from islet cells may shape the pulses in auto/paracrine feedback loops. Within islets, glucose-stimulated β-cells couple via gap junctions to generate synchronized insulin pulses. In contrast, α-and δ-cells lack gap junctions, and glucagon release from islets stimulated by lack of glucose is non-pulsatile. Increasing glucose concentrations gradually inhibit glucagon secretion by α-cell-intrinsic mechanism/s. Further glucose elevation will stimulate pulsatile insulin release and co-secretion of neurotransmitters. Excitatory ATP may synchronize β-cells with δ-cells to generate coinciding pulses of insulin and somatostatin. Inhibitory neurotransmitters from β-and δ-cells can then generate antiphase pulses of glucagon release. Neurotransmitters released from intrapancreatic ganglia are required to synchronize β-cells between islets to coordinate insulin pulsatility from the entire pancreas, whereas paracrine intra-islet effects still suffice to explain coordinated pulsatile release of glucagon and somatostatin. The present review discusses how neurotransmitters contribute to the pulsatility at different levels of integration. Keywords: glucagon, insulin, neurotransmitters, oscillations, pulsatile secretion, somatostatin Date submitted 28 March 2014; date of final acceptance 15 April 2014 IntroductionInsulin is the major blood glucose-lowering hormone, and glucagon is most important for blood glucose elevation. The release of these hormones from the islets of Langerhans is therefore essential for normal glucose homeostasis, and secretion disturbances underlie development of type 2 diabetes (T2D), which is increasing worldwide in an almost epidemic manner. It has long been known that the concentration of circulating insulin shows regular oscillations in normal human subjects, and that this pattern does not reflect variations in blood glucose but is determined by a pancreatic pacemaker [1]. Studies in normal subjects and diabetic patients have shown that less insulin is required to maintain normoglycaemia if the hormone is infused in an oscillatory manner compared to a constant rate [2], which may reflect higher expression of insulin receptors. The oscillatory insulin pattern is early deteriorated in patients with T2D [1]. Loss of insulin oscillations may therefore contribute to insulin resistance and the resulting increased insulin demand may exhaust the β-cells and cause overt T2D in susceptible individuals.Although insufficient secretion of insulin is the generally accepted cause of diabetes, it was recently proposed that 'glucagon excess, rather than insulin deficiency, is the sine qua non of diabetes ' [3]. Also, circulating glucagon is oscillating due to pulsatile release of the hormone with insulin and glucagon in opposite phase [4]. Indeed, prediabetes is associated Correspondence to: E. Gylfe, Department of Medical C...

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Angioarchitecture of the atrophic pancreas

Weaver

1997

Microsc. Res. Tech.

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Ablation of serotonergic nerves in the rat pancreas. Lack of effects on hormone secretion and intrinsic blood flow

Cited by 5 publications

References 20 publications

Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Neurotransmitter control of islet hormone pulsatility

Angioarchitecture of the atrophic pancreas

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