CNS sites involved in sympathetic and parasympathetic control of the pancreas: a viral tracing study

Jansen, A.S.P.; Hoffman, Julie; Loewy, A.

doi:10.1016/s0006-8993(97)00532-5

Cited by 157 publications

(115 citation statements)

References 42 publications

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“…Given the human PET data showing medial prefrontal and orbital cortex activation during hypoglycemia, it is possible that these brain regions participate in hypoglycemia awareness, the conscious perception of the symptoms engendered by autonomic activation (including palpitations, hunger, sweating, tingling) (Teves et al, 2004). Alternatively, functional imaging in humans and neuroanatomic tracing studies in rats have consistently suggested a role of medial prefrontal cortex in visceral sensation and regulation (Terreberry and Neafsey, 1983;Jansen et al, 1997;Ter Horst and Postema, 1997;King et al, 1999;Buijs et al, 2001;Westerhaus and Loewy, 2001;Owens and Verberne, 2001;Floyd et al, 2001;Cameron and Minoshima, 2002). Thus, the loss of neurons in the medial prefrontal and orbital cortex may be one element contributing to reduced compensatory adrenomedullary responses to hypoglycemia in our model.…”

Section: Discussionmentioning

confidence: 99%

Cortical Fluoro-Jade Staining and Blunted Adrenomedullary Response to Hypoglycemia after Noncoma Hypoglycemia in Rats

Tkacs

Pan

Raghupathi

et al. 2005

J Cereb Blood Flow Metab

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Intensive insulin therapy in patients with type 1 diabetes mellitus reduces long-term complications; however, intensive therapy is also associated with a three-fold increase in hypoglycemic episodes. The present study in conscious rats characterizes the physiologic and neuropathologic consequences of a single episode of moderate hypoglycemia. In this model, intravenous insulin is used to reduce plasma glucose to 30 to 35 mg/dL for 75 mins. This single hypoglycemic insult acutely induces hypoglycemia-associated autonomic failure (HAAF), with epinephrine responses to hypoglycemia reduced more than 36% from control. Neuropathology after this insult includes the appearance of dying cells, assessed with the marker Fluoro-jade B (FJ). After hypoglycemic insult, FJ þ cells were consistently seen in subdivisions of the medial prefrontal cortex, the orbital cortex, and the piriform cortex. There was a significant correlation between depth of hypoglycemia and number of FJ þ cells, suggesting that there is a critical threshold below which vulnerable cells begin to die. These data suggest that there is a population of cells that are vulnerable to moderate levels of hypoglycemia commonly experienced by patients with insulin-treated diabetes. These cells, which may be neurons, are primarily found in cortical regions implicated in visceral perception and autonomic control, raising the possibility that their loss contributes to clinically reported deficits in autonomic and perceptual responses to hypoglycemia.

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Section: Discussionmentioning

confidence: 99%

Cortical Fluoro-Jade Staining and Blunted Adrenomedullary Response to Hypoglycemia after Noncoma Hypoglycemia in Rats

Tkacs

Pan

Raghupathi

et al. 2005

J Cereb Blood Flow Metab

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“…The PVH, perifornical hypothalamic region (PeF), A5 catecholamine cell group, rostal ventrolateral medulla (RVL) and lateral paragigantocellular reticular nucleus (LPGI) have been proposed to contain a considerable amount of neurons that project to both the sympathetic and parasympathetic pancreatic outflow systems as well as the sympathoadrenal outflow system in rats [74]. In addition, some hypothalamic nuclei including the dorsal hypothalamic area (DHA), DMH and LH have been proposed to contain neurons that project to the parasympathetic pancreatic outflow systems.…”

Section: Central Neural Pathways Of Sympathetic Effects On Glucose Anmentioning

confidence: 99%

“…In addition, some hypothalamic nuclei including the dorsal hypothalamic area (DHA), DMH and LH have been proposed to contain neurons that project to the parasympathetic pancreatic outflow systems. The MPA, DHA, LH and the posterior hypothalamic area have been proposed to contain neurons that project to the sympathetic pancreatic outflow system [74]. Brown adipose tissue is only innervated by sympathetic nerves.…”

Section: Central Neural Pathways Of Sympathetic Effects On Glucose Anmentioning

confidence: 99%

New insights into sympathetic regulation of glucose and fat metabolism

2000

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Since the observation by Claude Bernard in the 1850 s that puncture of the floor of the fourth ventricle in dogs results in the appearance of transient glucosuria, the central nervous system (CNS) has been implicated in the control of certain metabolic processes of energy homeostasis mainly through neuroendocrine systems. After its recent discovery, leptin, an adipocyte hormone, has been proposed to signal the CNS to modulate autonomic outflow and food intake, leading to alterations of energy metabolism [1,2]. Leptin has been suggested to increase sympathetic outflow and disturbances of leptin signalling lead to Diabetologia (2000) 43: 533±549 ReviewsNew insights into sympathetic regulation of glucose and fat metabolism AbstractThe autonomic nervous system modulates glucose and fat metabolism through both direct neural effects and hormonal effects. This review presents recent concepts on the sympathetic regulation of glucose and fat metabolism. Focally released norepinephrine from sympathetic nerves is likely to increase glucose uptake in skeletal muscle and adipose tissues independent of insulin but norepinephrine does not contribute so much as epinephrine to hepatic glucose production. Epinephrine increases hepatic glucose production and inhibits insulin secretion and the glucose uptake by tissues that is induced by insulin. Additionally, catecholamines can increase thermogenesis and lipolysis, leading to increased energy expenditure and decreased fat stores. It is likely that b-(b3)-adrenergic receptors mediate these responses. Alterations of central neurotransmission and environmental factors can change the relative contribution of sympathetic outflow to the pancreas, liver, adrenal medulla and adipose tissues, leading to the modulation of glucose and fat metabolism. Recent studies have proposed that leptin, an adipocyte hormone, affects the central nervous system to increase sympathetic outflow independent of feeding. The effects of leptin on glucose and fat metabolism could be in part mediated by the sympathetic nervous system. Studies using mice with a genetic disruption of serotonin 5-HT2 c receptor indicate that central neural mechanisms in the regulation of sympathetic outflow and satiety could be dissociated. Abnormalities of sympathetic effects, including disturbances of leptin and b3-adrenergic receptor signalling, are likely to cause obesity and impaired glucose tolerance in rodents and humans. These findings indicate that dysfunction of the sympathetic nervous system could predispose to obesity and Type II (non-insulin-dependent) diabetes mellitus. [Diabetologia (2000) 43: 533±549]

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“…With the development of neurotropic viruses as an alternative to traditional tract tracing tools, our understanding of complex neuronal circuitry, particularly the innervation of thoracic and abdominal viscera, has greatly advanced (Buijs et al, 2003;Cano et al, 2000Cano et al, , 2004Card et al, 1990;Glatzer et al, 2003;Hadziefendic and Haxhiu, 1999;Jansen et al, 1997;Nadelhaft et al, 1992;Schramm et al, 1993;Standish et al, 1995). Notwithstanding this progress, there is a paucity of knowledge concerning how neurotrauma, particularly spinal cord injury (SCI), affects neuronal circuitry and/or plasticity as demarcated with the use of neurotropic viruses (Bareyre et al, 2004;Duale et al, 2009;Kim et al, 2002;Lane et al, 2008;Pan et al, 2005;Yu et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Noxious Colorectal Distention in Spinalized Rats Reduces Pseudorabies Virus Labeling of Sympathetic Neurons

Duale

Lyttle²,

Smith³

et al. 2010

Journal of Neurotrauma

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The retrograde transsynaptic tracer pseudorabies virus (PRV) has been widely used as a marker for synaptic connectivity in the spinal cord. Notably, the PRV-152 construct expresses enhanced green fluorescent protein (EGFP). We recently reported a significant attenuation of PRV-152 labeling of the intermediolateral cell column (IML) and celiac ganglia after complete T4 spinal cord transection versus sham injury in rats at 96 h after PRV-152 inoculation of the left kidney. Here we found a significant increase in noxious colorectal distention (CRD)-evoked c-Fos expression in spinal cords of injured versus sham rats without PRV infection. In order to assess whether enhancing neuronal activity in spinalized rats might increase PRV-152 labeling, we subjected awake spinalized rats to 1.5 h of intermittent noxious CRD either: (1) just prior to inoculation, or (2) 96 h after inoculation (n ¼ 3/group). Equal numbers of spinalized rats in both groups received PRV-152 inoculations without CRD (non-stimulated; n ¼ 3/group). At 96 h post-inoculation fixed spinal cords and left celiac ganglionic tissues were assessed for the distribution and quantification of EGFP-labeled cells. The injured cohort that received CRD just prior to PRV injection showed a significant reduction in EGFP-labeled cells in both the IML and left celiac ganglion compared to non-stimulated injured rats. In contrast, the injured cohort that received CRD 96 h after PRV-152 inoculation showed no differences in EGFP-labeled cell numbers in the IML or celiac ganglia versus non-stimulated injured rats. Interestingly, microglia near c-Fos-positive cells after acute CRD appeared more reactive compared to non-stimulated spinalized rats, and activated microglial cells markedly reduce viral transduction and progression following PRV inoculation of the CNS. Hence our results imply that increased CRD-induced c-Fos expression in the injured paradigm, prior to but not after PRV injection, further attenuates PRV-152 uptake, perhaps through changes in neuronal activity and/or innate neuro-immune responses.

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CNS sites involved in sympathetic and parasympathetic control of the pancreas: a viral tracing study

Cited by 157 publications

References 42 publications

Cortical Fluoro-Jade Staining and Blunted Adrenomedullary Response to Hypoglycemia after Noncoma Hypoglycemia in Rats

Cortical Fluoro-Jade Staining and Blunted Adrenomedullary Response to Hypoglycemia after Noncoma Hypoglycemia in Rats

New insights into sympathetic regulation of glucose and fat metabolism

Noxious Colorectal Distention in Spinalized Rats Reduces Pseudorabies Virus Labeling of Sympathetic Neurons

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