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Article ; Online: Feeding signals to the hungry mind.

Balthasar, Nina

2009 Volume 94, Issue 8, Page(s) 857–866

Abstract: Obesity, due to its associated co-morbidities, including type 2 diabetes and cardiovascular disease, is at the forefront of today's health care concerns. Our need for novel, multifaceted approaches to tackle the global increase of waistlines is urgent, ... ...

Abstract	Obesity, due to its associated co-morbidities, including type 2 diabetes and cardiovascular disease, is at the forefront of today's health care concerns. Our need for novel, multifaceted approaches to tackle the global increase of waistlines is urgent, and understanding the physiological processes underlying our vulnerability to weight gain is an important one of them. Evidence for considerable heritability of body weight indicates genetic influences in the susceptibility to our obesogenic environment. Here, we will focus on neurons in brain structures such as the hypothalamus, which sense the body's metabolic state and, through an intricate cascade of events, elicit an appropriate response. We will explore the use of genetically modified mouse models in the investigation of physiological functions of genes and pathways in neuronal regulation of metabolic balance. Use of these techniques allows us to make manipulations at the molecular level (e.g. in the neuronal metabolic sensing mechanism) and combine this with systems-level physiological analysis (e.g. body weight). Recent technological advances also enable the investigation of the contributions of genes to the co-morbidities of obesity, such as obesity-induced hypertension. Reviewing examples of improvements as well as large gaps in our knowledge, this lecture aims to incite interest in whole body physiological research.
MeSH term(s)	AMP-Activated Protein Kinases/physiology ; Animals ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Homeostasis/genetics ; Homeostasis/physiology ; Hunger ; Hypertension/etiology ; Hypothalamus/physiology ; Mice ; Neurons/physiology ; Obesity/complications ; Obesity/genetics ; Pro-Opiomelanocortin/physiology ; Receptor, Melanocortin, Type 4/physiology
Chemical Substances	Receptor, Melanocortin, Type 4 ; Pro-Opiomelanocortin (66796-54-1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2009-08
Publishing country	England
Document type	Lectures ; Research Support, Non-U.S. Gov't
ZDB-ID	1016295-1
ISSN	1469-445X ; 0958-0670
ISSN (online)	1469-445X
ISSN	0958-0670
DOI	10.1113/expphysiol.2008.042226
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Article: Genetic dissection of neuronal pathways controlling energy homeostasis.

Balthasar, Nina

Obesity (Silver Spring, Md.)

2006 Volume 14 Suppl 5, Page(s) 222S–227S

Abstract: Recent research has identified a number of genes playing critical roles in the central regulation of energy homeostasis. Subsequently, models of the neurocircuitry regulating energy balance have been suggested, although their physiological relevance ... ...

Abstract	Recent research has identified a number of genes playing critical roles in the central regulation of energy homeostasis. Subsequently, models of the neurocircuitry regulating energy balance have been suggested, although their physiological relevance remains mostly untested. Using the Cre/loxP system, we can now genetically dissect these neurocircuits and establish the specific roles of these genes in small neuronal subpopulations. Here we focus on two receptors shown to be critical in the central regulation of energy homeostasis: leptin (LepR) and melanocortin-4 receptors (MC4R). Mice and humans deficient in either leptin or melanocortin signaling are severely obese. A prominent model of leptin action places the arcuate nucleus of the hypothalamus, and in particular arcuate proopiomelanocortin (POMC) neurons, at the center stage of energy balance regulation. By deleting LepR specifically from POMC neurons in mice, we showed that LepR on POMC neurons are required but not solely responsible for leptin's regulation of body weight homeostasis. Thus, LepR on other neurons must also be critically important in leptin-mediated regulation of body weight homeostasis. Data from MC4R-deficient mice have shown that MC4Rs regulate both sides of the energy intake/energy expenditure balance. Our recent experiments used MC4R-deficient mice with restored MC4R expression only in the paraventricular hypothalamus and a subpopulation of amygdala neurons. We showed that MC4Rs in the paraventricular hypothalamus and/or amygdala are sufficient to control food intake but that MC4Rs elsewhere control energy expenditure, thereby discovering the novel concept of functional and anatomical divergence of MC4Rs.
MeSH term(s)	Animals ; Eating/genetics ; Eating/physiology ; Energy Intake/genetics ; Energy Intake/physiology ; Energy Metabolism/genetics ; Energy Metabolism/physiology ; Homeostasis/genetics ; Homeostasis/physiology ; Humans ; Mice ; Mice, Knockout ; Neurons ; Obesity, Morbid/etiology ; Obesity, Morbid/genetics ; Obesity, Morbid/metabolism ; Receptor, Melanocortin, Type 4/deficiency ; Receptor, Melanocortin, Type 4/physiology ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/physiology ; Receptors, Leptin
Chemical Substances	Receptor, Melanocortin, Type 4 ; Receptors, Cell Surface ; Receptors, Leptin
Language	English
Publishing date	2006-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2230457-5
ISSN	1930-739X ; 1930-7381 ; 1071-7323
ISSN (online)	1930-739X
ISSN	1930-7381 ; 1071-7323
DOI	10.1038/oby.2006.313
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Article ; Online: Sexual dimorphism in offspring glucose-sensitive hypothalamic gene expression and physiological responses to maternal high-fat diet feeding.

Dearden, Laura / Balthasar, Nina

Endocrinology

2014 Volume 155, Issue 6, Page(s) 2144–2154

Abstract: A wealth of animal and human studies demonstrate that early life environment significantly influences adult metabolic balance, however the etiology for offspring metabolic misprogramming remains incompletely understood. Here, we determine the effect of ... ...

Abstract	A wealth of animal and human studies demonstrate that early life environment significantly influences adult metabolic balance, however the etiology for offspring metabolic misprogramming remains incompletely understood. Here, we determine the effect of maternal diet per se on offspring sex-specific outcomes in metabolic health and hypothalamic transcriptome regulation in mice. Furthermore, to define developmental periods of maternal diet misprogramming aspects of offspring metabolic balance, we investigated offspring physiological and transcriptomic consequences of maternal high-fat/high-sugar diet feeding during pregnancy and/or lactation. We demonstrate that female offspring of high-fat/high-sugar diet-fed dams are particularly vulnerable to metabolic perturbation with body weight increases due to postnatal processes, whereas in utero effects of the diet ultimately lead to glucose homeostasis dysregulation. Furthermore, glucose- and maternal-diet sensitive gene expression modulation in the paraventricular hypothalamus is strikingly sexually dimorphic. In summary, we uncover female-specific, maternal diet-mediated in utero misprogramming of offspring glucose homeostasis and a striking sexual dimorphism in glucose- and maternal diet-sensitive paraventricular hypothalamus gene expression adjustment. Notably, female offspring metabolic vulnerability to maternal high-fat/high-sugar diet propagates a vicious cycle of obesity and type 2 diabetes in subsequent generations.
MeSH term(s)	Adiposity/drug effects ; Animals ; Body Weight/drug effects ; Diet, High-Fat/adverse effects ; Female ; Gene Expression Regulation ; Glucose/pharmacology ; Hypothalamus/drug effects ; Hypothalamus/metabolism ; Insulin/blood ; Male ; Mice ; Sex Characteristics ; Sweetening Agents/pharmacology
Chemical Substances	Insulin ; Sweetening Agents ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2014-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2014-1131
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Article: Growth hormone secretagogue receptor deficiency in mice protects against obesity-induced hypertension.

Harris, Louise E / Morgan, David G / Balthasar, Nina

Physiological reports

2014 Volume 2, Issue 3, Page(s) e00240

Abstract: Abstract Growth hormone secretagogue receptor (GHS-R) signaling has been associated with growth hormone release, increases in food intake and pleiotropic cardiovascular effects. Recent data demonstrated that acute GHS-R antagonism leads to increases in ... ...

Abstract	Abstract Growth hormone secretagogue receptor (GHS-R) signaling has been associated with growth hormone release, increases in food intake and pleiotropic cardiovascular effects. Recent data demonstrated that acute GHS-R antagonism leads to increases in mean arterial pressure mediated by the sympathetic nervous system in rats; a highly undesirable effect if GHS-R antagonism was to be used as a therapeutic approach to reducing food intake in an already obese, hypertensive patient population. However, our data in conscious, freely moving GHS-R deficient mice demonstrate that chronic absence of GHS-R signaling is protective against obesity-induced hypertension. GHS-R deficiency leads to reduced systolic blood pressure variability (SBPV); in response to acute high-fat diet (HFD)-feeding, increases in the sympathetic control of SBPV are suppressed in GHS-R KO mice. Our data further suggest that GHS-R signaling dampens the immediate HFD-mediated increase in spontaneous baroreflex sensitivity. In diet-induced obesity, absence of GHS-R signaling leads to reductions in obesity-mediated hypertension and tachycardia. Collectively, our findings thus suggest that chronic blockade of GHS-R signaling may not result in adverse cardiovascular effects in obesity.
Language	English
Publishing date	2014-03-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2724325-4
ISSN	2051-817X
ISSN	2051-817X
DOI	10.1002/phy2.240
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Article: Genetic Dissection of Neuronal Pathways Controlling Energy Homeostasis

Balthasar, Nina

Obesity. 2006 Aug., v. 14, Suppl. 005

2006

Abstract	Recent research has identified a number of genes playing critical roles in the central regulation of energy homeostasis. Subsequently, models of the neurocircuitry regulating energy balance have been suggested, although their physiological relevance remains mostly untested. Using the Cre/loxP system, we can now genetically dissect these neurocircuits and establish the specific roles of these genes in small neuronal subpopulations. Here we focus on two receptors shown to be critical in the central regulation of energy homeostasis: leptin (LepR) and melanocortin-4 receptors (MC4R). Mice and humans deficient in either leptin or melanocortin signaling are severely obese. A prominent model of leptin action places the arcuate nucleus of the hypothalamus, and in particular arcuate proopiomelanocortin (POMC) neurons, at the center stage of energy balance regulation. By deleting LepR specifically from POMC neurons in mice, we showed that LepR on POMC neurons are required but not solely responsible for leptin's regulation of body weight homeostasis. Thus, LepR on other neurons must also be critically important in leptin-mediated regulation of body weight homeostasis. Data from MC4R-deficient mice have shown that MC4Rs regulate both sides of the energy intake/energy expenditure balance. Our recent experiments used MC4R-deficient mice with restored MC4R expression only in the paraventricular hypothalamus and a subpopulation of amygdala neurons. We showed that MC4Rs in the paraventricular hypothalamus and/or amygdala are sufficient to control food intake but that MC4Rs elsewhere control energy expenditure, thereby discovering the novel concept of functional and anatomical divergence of MC4Rs.
Keywords	genes ; neurons ; neural pathways ; energy balance ; homeostasis ; leptin ; melanocyte-stimulating hormone ; hormone receptors ; obesity ; pro-opiomelanocortin ; mice ; animal models ; humans ; amygdala
Language	English
Dates of publication	2006-08
Size	p. 222S-227S.
Publishing place	The North American Association for the Study of Obesity
Document type	Article
Note	In the special issue: The neurobiology of obesity / edited by D. Richard and P. Boisvert. Paper presented at a symposium held on November 4-5, 2005, in Quebec City, Quebec, Canada.
ZDB-ID	1201744-9
ISSN	1550-8528 ; 1071-7323
ISSN (online)	1550-8528
ISSN	1071-7323
Database	NAL-Catalogue (AGRICOLA)

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Article: SIRT3: A Central Regulator of Mitochondrial Adaptation in Health and Disease.

Weir, Heather J M / Lane, Jon D / Balthasar, Nina

Genes & cancer

2013 Volume 4, Issue 3-4, Page(s) 118–124

Abstract: SIRT3 is a NAD(+)-dependent deacetylase that regulates the function of numerous mitochondrial proteins with roles in metabolism, oxidative stress, and cell survival. It is emerging as an instrumental regulator of the mitochondrial adaptive responses to ... ...

Abstract	SIRT3 is a NAD(+)-dependent deacetylase that regulates the function of numerous mitochondrial proteins with roles in metabolism, oxidative stress, and cell survival. It is emerging as an instrumental regulator of the mitochondrial adaptive responses to stress, including metabolic reprogramming and enhancing antioxidant defense mechanisms. Here, we discuss the role that SIRT3 plays at both a cellular and physiological level and consider its involvement in disease. Mitochondrial dysfunction is a key contributing factor in many diseases; however, the mechanisms involved are often not well understood, and few targeted therapies exist. If manipulation of SIRT3 proves to be beneficial in disease states, then it could be a promising target for novel therapies.
Language	English
Publishing date	2013-01-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2538519-7
ISSN	1947-6027 ; 1947-6019
ISSN (online)	1947-6027
ISSN	1947-6019
DOI	10.1177/1947601913476949
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Article ; Online: Activation of Brainstem Pro-opiomelanocortin Neurons Produces Opioidergic Analgesia, Bradycardia and Bradypnoea.

Cerritelli, Serena / Hirschberg, Stefan / Hill, Rob / Balthasar, Nina / Pickering, Anthony E

PloS one

2016 Volume 11, Issue 4, Page(s) e0153187

Abstract: Opioids are widely used medicinally as analgesics and abused for hedonic effects, actions that are each complicated by substantial risks such as cardiorespiratory depression. These drugs mimic peptides such as β-endorphin, which has a key role in ... ...

Abstract	Opioids are widely used medicinally as analgesics and abused for hedonic effects, actions that are each complicated by substantial risks such as cardiorespiratory depression. These drugs mimic peptides such as β-endorphin, which has a key role in endogenous analgesia. The β-endorphin in the central nervous system originates from pro-opiomelanocortin (POMC) neurons in the arcuate nucleus and nucleus of the solitary tract (NTS). Relatively little is known about the NTSPOMC neurons but their position within the sensory nucleus of the vagus led us to test the hypothesis that they play a role in modulation of cardiorespiratory and nociceptive control. The NTSPOMC neurons were targeted using viral vectors in a POMC-Cre mouse line to express either opto-genetic (channelrhodopsin-2) or chemo-genetic (Pharmacologically Selective Actuator Modules). Opto-genetic activation of the NTSPOMC neurons in the working heart brainstem preparation (n = 21) evoked a reliable, titratable and time-locked respiratory inhibition (120% increase in inter-breath interval) with a bradycardia (125±26 beats per minute) and augmented respiratory sinus arrhythmia (58% increase). Chemo-genetic activation of NTSPOMC neurons in vivo was anti-nociceptive in the tail flick assay (latency increased by 126±65%, p<0.001; n = 8). All effects of NTSPOMC activation were blocked by systemic naloxone (opioid antagonist) but not by SHU9119 (melanocortin receptor antagonist). The NTSPOMC neurons were found to project to key brainstem structures involved in cardiorespiratory control (nucleus ambiguus and ventral respiratory group) and endogenous analgesia (periaqueductal gray and midline raphe). Thus the NTSPOMC neurons may be capable of tuning behaviour by an opioidergic modulation of nociceptive, respiratory and cardiac control.
MeSH term(s)	Analgesia ; Analgesics, Opioid/metabolism ; Animals ; Arcuate Nucleus of Hypothalamus/cytology ; Arcuate Nucleus of Hypothalamus/drug effects ; Arcuate Nucleus of Hypothalamus/metabolism ; Bradycardia/metabolism ; Brain Stem/cytology ; Brain Stem/drug effects ; Brain Stem/metabolism ; Channelrhodopsins ; Female ; Male ; Melanocyte-Stimulating Hormones/pharmacology ; Mice, Transgenic ; Microscopy, Confocal ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Neurons/drug effects ; Neurons/metabolism ; Pro-Opiomelanocortin/metabolism ; Respiratory Insufficiency/metabolism ; Solitary Nucleus/cytology ; Solitary Nucleus/drug effects ; Solitary Nucleus/metabolism
Chemical Substances	Analgesics, Opioid ; Channelrhodopsins ; Narcotic Antagonists ; SHU 9119 (168482-23-3) ; Naloxone (36B82AMQ7N) ; Pro-Opiomelanocortin (66796-54-1) ; Melanocyte-Stimulating Hormones (9002-79-3)
Language	English
Publishing date	2016-04-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0153187
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Article ; Online: Activation of Brainstem Pro-opiomelanocortin Neurons Produces Opioidergic Analgesia, Bradycardia and Bradypnoea.

Serena Cerritelli / Stefan Hirschberg / Rob Hill / Nina Balthasar / Anthony E Pickering

PLoS ONE, Vol 11, Iss 4, p e

2016 Volume 0153187

Abstract	Opioids are widely used medicinally as analgesics and abused for hedonic effects, actions that are each complicated by substantial risks such as cardiorespiratory depression. These drugs mimic peptides such as β-endorphin, which has a key role in endogenous analgesia. The β-endorphin in the central nervous system originates from pro-opiomelanocortin (POMC) neurons in the arcuate nucleus and nucleus of the solitary tract (NTS). Relatively little is known about the NTSPOMC neurons but their position within the sensory nucleus of the vagus led us to test the hypothesis that they play a role in modulation of cardiorespiratory and nociceptive control. The NTSPOMC neurons were targeted using viral vectors in a POMC-Cre mouse line to express either opto-genetic (channelrhodopsin-2) or chemo-genetic (Pharmacologically Selective Actuator Modules). Opto-genetic activation of the NTSPOMC neurons in the working heart brainstem preparation (n = 21) evoked a reliable, titratable and time-locked respiratory inhibition (120% increase in inter-breath interval) with a bradycardia (125±26 beats per minute) and augmented respiratory sinus arrhythmia (58% increase). Chemo-genetic activation of NTSPOMC neurons in vivo was anti-nociceptive in the tail flick assay (latency increased by 126±65%, p<0.001; n = 8). All effects of NTSPOMC activation were blocked by systemic naloxone (opioid antagonist) but not by SHU9119 (melanocortin receptor antagonist). The NTSPOMC neurons were found to project to key brainstem structures involved in cardiorespiratory control (nucleus ambiguus and ventral respiratory group) and endogenous analgesia (periaqueductal gray and midline raphe). Thus the NTSPOMC neurons may be capable of tuning behaviour by an opioidergic modulation of nociceptive, respiratory and cardiac control.
Keywords	Medicine ; R ; Science ; Q
Subject code	590
Language	English
Publishing date	2016-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: The Paraventricular Hypothalamus Regulates Satiety and Prevents Obesity via Two Genetically Distinct Circuits.

Li, Monica M / Madara, Joseph C / Steger, Jennifer S / Krashes, Michael J / Balthasar, Nina / Campbell, John N / Resch, Jon M / Conley, Nicholas J / Garfield, Alastair S / Lowell, Bradford B

Neuron

2019 Volume 102, Issue 3, Page(s) 653–667.e6

Abstract: SIM1-expressing paraventricular hypothalamus (PVH) neurons are key regulators of energy balance. Within the ... ...

Abstract	SIM1-expressing paraventricular hypothalamus (PVH) neurons are key regulators of energy balance. Within the PVH
MeSH term(s)	Agouti-Related Protein/metabolism ; Animals ; Arcuate Nucleus of Hypothalamus/cytology ; Arcuate Nucleus of Hypothalamus/metabolism ; Arcuate Nucleus of Hypothalamus/physiology ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Energy Metabolism ; Enkephalins/metabolism ; Feeding Behavior/physiology ; Locus Coeruleus/cytology ; Locus Coeruleus/metabolism ; Locus Coeruleus/physiology ; Mice ; Neurons/cytology ; Neurons/metabolism ; Neurons/physiology ; Obesity/physiopathology ; Parabrachial Nucleus/cytology ; Parabrachial Nucleus/metabolism ; Parabrachial Nucleus/physiology ; Paraventricular Hypothalamic Nucleus/cytology ; Paraventricular Hypothalamic Nucleus/metabolism ; Paraventricular Hypothalamic Nucleus/physiology ; Protein Precursors/metabolism ; Receptor, Melanocortin, Type 4/metabolism ; Repressor Proteins/metabolism ; Satiety Response/physiology
Chemical Substances	Agouti-Related Protein ; Agrp protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Enkephalins ; MC4R protein, mouse ; Protein Precursors ; Receptor, Melanocortin, Type 4 ; Repressor Proteins ; Sim1 protein, mouse ; preproenkephalin (93443-35-7)
Language	English
Publishing date	2019-03-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	808167-0
ISSN	1097-4199 ; 0896-6273
ISSN (online)	1097-4199
ISSN	0896-6273
DOI	10.1016/j.neuron.2019.02.028
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Article ; Online: The generation of knock-in mice expressing fluorescently tagged galanin receptors 1 and 2.

Kerr, Niall / Holmes, Fiona E / Hobson, Sally-Ann / Vanderplank, Penny / Leard, Alan / Balthasar, Nina / Wynick, David

Molecular and cellular neurosciences

2015 Volume 68, Page(s) 258–271

Abstract: The neuropeptide galanin has diverse roles in the central and peripheral nervous systems, by activating the G protein-coupled receptors Gal1, Gal2 and the less studied Gal3 (GalR1-3 gene products). There is a wealth of data on expression of Gal1-3 at the ...

Abstract	The neuropeptide galanin has diverse roles in the central and peripheral nervous systems, by activating the G protein-coupled receptors Gal1, Gal2 and the less studied Gal3 (GalR1-3 gene products). There is a wealth of data on expression of Gal1-3 at the mRNA level, but not at the protein level due to the lack of specificity of currently available antibodies. Here we report the generation of knock-in mice expressing Gal1 or Gal2 receptor fluorescently tagged at the C-terminus with, respectively, mCherry or hrGFP (humanized Renilla green fluorescent protein). In dorsal root ganglia (DRG) neurons expressing the highest levels of Gal1-mCherry, localization to the somatic cell membrane was detected by live-cell fluorescence and immunohistochemistry, and that fluorescence decreased upon addition of galanin. In spinal cord, abundant Gal1-mCherry immunoreactive processes were detected in the superficial layers of the dorsal horn, and highly expressing intrinsic neurons of the lamina III/IV border showed both somatic cell membrane localization and outward transport of receptor from the cell body, detected as puncta within cell processes. In brain, high levels of Gal1-mCherry immunofluorescence were detected within thalamus, hypothalamus and amygdala, with a high density of nerve endings in the external zone of the median eminence, and regions with lesser immunoreactivity included the dorsal raphe nucleus. Gal2-hrGFP mRNA was detected in DRG, but live-cell fluorescence was at the limits of detection, drawing attention to both the much lower mRNA expression than to Gal1 in mice and the previously unrecognized potential for translational control by upstream open reading frames (uORFs).
MeSH term(s)	Animals ; Brain/metabolism ; Cells, Cultured ; Ganglia, Spinal/cytology ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Luminescent Proteins/genetics ; Luminescent Proteins/metabolism ; Mice ; Mice, Transgenic ; Microscopy, Confocal ; Neurons/physiology ; RNA, Messenger/metabolism ; Receptor, Galanin, Type 1/genetics ; Receptor, Galanin, Type 1/metabolism ; Receptor, Galanin, Type 2/genetics ; Receptor, Galanin, Type 2/metabolism ; Spinal Cord/metabolism ; Red Fluorescent Protein
Chemical Substances	Luminescent Proteins ; RNA, Messenger ; Receptor, Galanin, Type 1 ; Receptor, Galanin, Type 2 ; Green Fluorescent Proteins (147336-22-9)
Language	English
Publishing date	2015-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2015.08.006
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