Simultaneous Silencing of<i>Npy</i>and<i>Dbh</i>Expression in Hindbrain A1/C1 Catecholamine Cells Suppresses Glucoprivic Feeding

Li, Ai Jun; Wang, Qing; Dinh, Thu; Ritter, Sue

doi:10.1523/jneurosci.4267-08.2009

Cited by 51 publications

(40 citation statements)

References 56 publications

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“…65), there is growing evidence that NPY endogenous to the lower brain stem promotes food intake as well. Thus, infusions of NPY into the 4th ventricle lead to increased food consumption, similar to that observed following third ventricular infusions (12, 13, 53) Likewise, glucoprivation-induced feeding appears to depend on intact brain stem catecholamine-containing NPY neurons (CA/NPY) (35,36,46) and glucoprivation-induced feeding can be elicited in decerebrate preparations (15,21). Thus, a parsimonious argument might simply hold that brain stem CA/NPY neurons augment food intake by direct action on preoromotor neurons.…”

Section: Discussionmentioning

confidence: 57%

Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem

Chen

Travers

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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Chen Z, Travers SP, Travers JB. Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem. Am J Physiol Regul Integr Comp Physiol 302: R1401-R1410, 2012. First published April 18, 2012 doi:10.1152/ajpregu.00536.2011.-Consummatory responses to taste stimuli are modulated by visceral signals processed in the caudal nucleus of the solitary tract (cNST) and ventrolateral medulla. On the basis of decerebrate preparations, this modulation can occur through local brain stem pathways. Among the large number of neuropeptides and neuromodulators implicated in these visceral pathways is neuropeptide Y (NPY), which is oftentimes colocalized in catecholaminergic neurons themselves implicated in glucoprivic-induced feeding and satiety. In addition to the cNST and ventrolateral medulla, noradrenergic and NPY receptors are found in circumscribed regions of the medullary reticular formation rich in preoromotor neurons. To test the hypothesis that NPY may act as a neuromodulator on preoromotor neurons, we recorded the effects of bath application of NPY and specific Y1 and Y2 agonists on currents elicited from electrical stimulation of the rostral (taste) NST in prehypoglossal neurons in a brain stem slice preparation. A high proportion of NST-driven responses were suppressed by NPY, as well as Y1 and Y2 agonists. On the basis of paired pulse ratios and changes in membrane resistance, we concluded that Y1 receptors influence these neurons both presynaptically and postsynaptically and that Y2 receptors have a presynaptic locus. To test the hypothesis that NPY may act in concert with norepinephrine (NE), we examined neurons showing suppressed responses in the presence of a Y2 agonist and demonstrated a greater degree of suppression to a Y2 agonist/NE cocktail. These suppressive effects on preoromotoneurons may reflect a satiety pathway originating from A2 neurons in the caudal brain stem.oromotor; ingestion; reticular formation; norepinephrine CIRCUITS CONTROLLING THE CONSUMMATORY behaviors of ingestion are located in the lower brain stem (7,38,40,56). These circuits extend from the pons to the spinal medullary junction to encompass both sensory and motor nuclei, as well as specific regions of the reticular formation (RF). One region, immediately subjacent to the nucleus of the solitary tract (NST), which includes both the intermediate subdivision of the medullary RF (IRt) and the more lateral parvocellular RF (PCRt), contains a dense constellation of preoromotor neurons (29, 37, 58) that provide a potent source of excitatory drive to the oromotor nuclei (59, 60). Functional inactivation of the IRt/PCRt with either the GABA agonist muscimol or glutamatergic antagonists suppresses consummatory behavior in the awake freely moving rat (10,11,57).An additional, integrative role for the IRt/PCRt is suggested by input from forebrain sites involved in homeostatic, regulatory, and motor function (9, 43, 50, 61), as well as overlapping input from brain stem orosensory and vis...

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Section: Discussionmentioning

confidence: 57%

Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem

Chen

Travers

2012

American Journal of Physiology-Regulatory, Integrative and Comp

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“…Fos and gene expression data have shown that specific subpopulations of catecholamine neurons are potently activated by 2DG-induced glucoprivation (21,24,37). Gene silencing results have indicated that neuropeptide Y/catecholamine coexpressing neurons are required for the glucoprivic feeding response (22). Previous work has also shown that food intake can be evoked by third ventricle injections of GcA (45), third ventricle (44) and 4V (11) injections of Phl, and both LV and 4V injections of 5TG (34).…”

Section: Discussionmentioning

confidence: 99%

Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons

Wang

Dinh

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Li AJ, Wang Q, Dinh TT, Powers BR, Ritter S. Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons. Am J Physiol Regul Integr Comp Physiol 306: R257-R264, 2014. First published December 31, 2013 doi:10.1152/ajpregu.00451.2013-Previous work has shown that hindbrain catecholamine neurons are required components of the brain's glucoregulatory circuitry. However, the mechanisms and circuitry underlying their glucoregulatory functions are poorly understood. Here we examined three drugs, glucosamine (GcA), phloridzin (Phl) and 5-thio-D-glucose (5TG), that stimulate food intake but interfere in different ways with cellular glucose utilization or transport. We examined feeding and blood glucose responses to each drug in male rats previously injected into the hypothalamic paraventricular nucleus with anti-dopamine-␤-hydroxylase conjugated to saporin (DSAP), a retrogradely transported immunotoxin that selectively lesions noradrenergic and adrenergic neurons, or with unconjugated saporin (SAP) control. Our major findings were 1) that GcA, Phl, and 5TG all stimulated feeding in SAP controls whether injected into the lateral or fourth ventricle (LV or 4V), 2) that each drug's potency was similar for both LV and 4V injections, 3) that neither LV or 4V injection of these drugs evoked feeding in DSAP-lesioned rats, and 4) that only 5TG, which blocks glycolysis, stimulated a blood glucose response. The antagonist of the MEK/ERK signaling cascade, U0126, attenuated GcA-induced feeding, but not Phl-or 5TG-induced feeding. Thus GcA, Phl, and 5TG, although differing in mechanism and possibly activating different neural populations, stimulate feeding in a catecholamine-dependent manner. Although results do not exclude the possibility that catecholamine neurons possess glucose-sensing mechanisms responsive to all of these agents, currently available evidence favors the possibility that the feeding effects result from convergent neural circuits in which catecholamine neurons are a required component.glucosamine; phloridzin; 5-thio-D-glucose; catecholamine neurons; feeding HINDBRAIN CATECHOLAMINE NEURONS are required components of the brain's glucoregulatory circuitry. Pharmacological (29), chemical (26, 43), or immunotoxic (35, 40) disruption of these neurons impairs or abolishes key protective responses to glucose deficiency induced by hypoglycemic doses of insulin or by central or peripheral blockade of glycolysis using the antimetabolic glucose analogue 2-deoxy-D-glucose (2DG). Dissection of the hindbrain catecholamine system using the retrogradely transported immunotoxin anti-dopamine-␤-hydroxylase conjugated to saporin (DSAP) has revealed distinct responses to glucoprivation that are dependent on hypothalamically and spinally projecting norepinephrine (NE) and/or epinephrine (E) neurons. Specifically, some of those NE and E neurons with processes that innervate the medial hypothalamic region are required for feeding (35), corticosterone (40), and reproductive responses (15)...

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“…NPY released along with GABA by the nerve terminals of arcuate neurons in the PVH appears to stimulate food intake by inhibiting a subset of melanocortin-4 receptor (MC4R)-expressing oxytocinergic neurons that innervate the dorsal medulla and the parabrachial region (16,60,61). The same mechanism could conceivably contribute to glucoprivic feeding, a response that is mediated by the C1 and or the A1 neurons and is attenuated by silencing NPY expression in these cells, albeit only if D␤H is also downregulated (97). The effects of catecholamines on bulbospinal presympathetic PVH neurons have been investigated in rat brain slices.…”

Section: Signaling By the C1 Neuronsmentioning

confidence: 99%

“…C1 cell-derived peptides and catecholamines have detectable effects in the regions innervated by the C1 cells. However, the only physiological deficit that has been associated with the downregulation of a peptide (NPY) made by the C1 cells is a reduction of the glucoprivic response, and even in this case, the deficit was observable only when catecholamine synthesis was simultaneously downregulated (97). The conditions under which the C1 cells release peptides or catecholamines and the effects that these substances produce need clarification.…”

Section: Signaling By the C1 Neuronsmentioning

confidence: 99%

C1 neurons: the body's EMTs

Guyenet

Stornetta

Bochorishvili

et al. 2013

American Journal of Physiology-Regulatory, Integrative and Comp

248

262

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The C1 neurons reside in the rostral and intermediate portions of the ventrolateral medulla (RVLM, IVLM). They use glutamate as a fast transmitter and synthesize catecholamines plus various neuropeptides. These neurons regulate the hypothalamic pituitary axis via direct projections to the paraventricular nucleus and regulate the autonomic nervous system via projections to sympathetic and parasympathetic preganglionic neurons. The presympathetic C1 cells, located in the RVLM, are probably organized in a roughly viscerotopic manner and most of them regulate the circulation. C1 cells are variously activated by hypoglycemia, infection or inflammation, hypoxia, nociception, and hypotension and contribute to most glucoprivic responses. C1 cells also stimulate breathing and activate brain stem noradrenergic neurons including the locus coeruleus. Based on the various effects attributed to the C1 cells, their axonal projections and what is currently known of their synaptic inputs, subsets of C1 cells appear to be differentially recruited by pain, hypoxia, infection/inflammation, hemorrhage, and hypoglycemia to produce a repertoire of stereotyped autonomic, metabolic, and neuroendocrine responses that help the organism survive physical injury and its associated cohort of acute infection, hypoxia, hypotension, and blood loss. C1 cells may also contribute to glucose and cardiovascular homeostasis in the absence of such physical stresses, and C1 cell hyperactivity may contribute to the increase in sympathetic nerve activity associated with diseases such as hypertension. C1 neurons; blood pressure; brain stem BEST KNOWN for their contribution to the control of arterial pressure (AP), the C1 neurons have also been implicated in many other physiological processes ranging from neuroendocrine responses to infection and inflammation, glucose homeostasis, reproduction, breathing, thermoregulation, hypothalamo-pituitary axis (HPA)-mediated stress responses, and food consumption. The purpose of this review is to summarize the most salient information concerning the C1 cells, to point out some of the remaining gaps in our current knowledge, and to suggest a few unifying physiological principles that could account for these seemingly disparate observations. Based on the various effects attributed to the C1 cells and what is currently known of their synaptic inputs, we propose that these neurons are, figuratively speaking, the body's "emergency medical technicians." By this we imply that these neurons produce stereotyped autonomic, metabolic, and neuroendocrine responses designed to help the organism survive major acute physical stresses such as accidental, pathological, or dive-related hypoxia or physical injury and its associated cohort of acute infection, blood loss, and hypotension. These emergency responses include, in the short term and depending on the stress, vasoconstriction, cardioinhibition, or acceleration, breathing stimulation, antidiuresis, changes in metabolism, and gastrointestinal (GI) functions designed to conserve pe...

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Simultaneous Silencing ofNpyandDbhExpression in Hindbrain A1/C1 Catecholamine Cells Suppresses Glucoprivic Feeding

Cited by 51 publications

References 56 publications

Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem

Activation of NPY receptors suppresses excitatory synaptic transmission in a taste-feeding network in the lower brain stem

Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons

C1 neurons: the body's EMTs

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