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Article ; Online: Local Drd1-neurons input to subgroups of arcuate AgRP/NPY-neurons.

Chadwick, Sean R / Güler, Ali D

iScience

2022 Volume 25, Issue 7, Page(s) 104605

Abstract: Obesity is a pandemic afflicting more than 300 million people worldwide, driven by consumption of calorically dense and highly rewarding foods. Dopamine (DA) signaling has been implicated in neural responses to highly palatable nutrients, but the exact ... ...

Abstract	Obesity is a pandemic afflicting more than 300 million people worldwide, driven by consumption of calorically dense and highly rewarding foods. Dopamine (DA) signaling has been implicated in neural responses to highly palatable nutrients, but the exact mechanisms through which DA modulates homeostatic feeding circuits remains unknown. A subpopulation of arcuate (ARC) agouti-related peptide (AgRP)/neuropeptide Y (NPY) (ARC
Language	English
Publishing date	2022-06-15
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2022.104605
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Food preference assay in male and female C57BL/6 mice.

Rainwater, Aundrea / Güler, Ali D

Journal of neuroscience methods

2021 Volume 365, Page(s) 109384

MeSH term(s)	Animals ; Choice Behavior ; Diet ; Eating ; Female ; Food Preferences ; Male ; Mice ; Mice, Inbred C57BL
Language	English
Publishing date	2021-10-08
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	282721-9
ISSN	1872-678X ; 0165-0270
ISSN (online)	1872-678X
ISSN	0165-0270
DOI	10.1016/j.jneumeth.2021.109384
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Zs.A 1486: Show issues

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Article: Altered circadian behavior and light sensing in mouse models of Alzheimer's disease.

Weigel, Thaddeus K / Guo, Cherry L / Güler, Ali D / Ferris, Heather A

bioRxiv : the preprint server for biology

2023

Abstract: Circadian symptoms have long been observed in Alzheimer's disease (AD) and often appear before cognitive symptoms, but the mechanisms underlying circadian alterations in AD are poorly understood. We studied circadian re-entrainment in AD model mice using ...

Abstract	Circadian symptoms have long been observed in Alzheimer's disease (AD) and often appear before cognitive symptoms, but the mechanisms underlying circadian alterations in AD are poorly understood. We studied circadian re-entrainment in AD model mice using a "jet lag" paradigm, observing their behavior on a running wheel after a six hour advance in the light:dark cycle. Female 3xTg mice, which carry mutations producing progressive amyloid beta and tau pathology, re-entrained following jet lag more rapidly than age-matched wild type controls at both 8 and 13 months of age. This re-entrainment phenotype has not been previously reported in a murine AD model. Because microglia are activated in AD and in AD models, and inflammation can affect circadian rhythms, we hypothesized that microglia contribute to this re-entrainment phenotype. To test this, we used the colony stimulating factor 1 receptor (CSF1R) inhibitor PLX3397, which rapidly depletes microglia from the brain. Microglia depletion did not alter re-entrainment in either wild type or 3xTg mice, demonstrating that microglia activation is not acutely responsible for the re-entrainment phenotype. To test whether mutant tau pathology is necessary for this behavioral phenotype, we repeated the jet lag behavioral test with the 5xFAD mouse model, which develops amyloid plaques, but not neurofibrillary tangles. As with 3xTg mice, 7-month-old female 5xFAD mice re-entrained more rapidly than controls, demonstrating that mutant tau is not necessary for the re-entrainment phenotype. Because AD pathology affects the retina, we tested whether differences in light sensing may contribute to altered entrainment behavior. 3xTg mice demonstrated heightened negative masking, an SCN-independent circadian behavior measuring responses to different levels of light, and re-entrained dramatically faster than WT mice in a jet lag experiment performed in dim light. 3xTg mice show a heightened sensitivity to light as a circadian cue that may contribute to accelerated photic re-entrainment. Together, these experiments demonstrate novel circadian behavioral phenotypes with heightened responses to photic cues in AD model mice which are not dependent on tauopathy or microglia.
Language	English
Publishing date	2023-05-03
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.05.02.539086
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Article: Altered circadian behavior and light sensing in mouse models of Alzheimer's disease.

Weigel, Thaddeus K / Guo, Cherry L / Güler, Ali D / Ferris, Heather A

Frontiers in aging neuroscience

2023 Volume 15, Page(s) 1218193

Abstract	Circadian symptoms have long been observed in Alzheimer's disease (AD) and often appear before cognitive symptoms, but the mechanisms underlying circadian alterations in AD are poorly understood. We studied circadian re-entrainment in AD model mice using a "jet lag" paradigm, observing their behavior on a running wheel after a 6 h advance in the light:dark cycle. Female 3xTg mice, which carry mutations producing progressive amyloid beta and tau pathology, re-entrained following jet lag more rapidly than age-matched wild type controls at both 8 and 13 months of age. This re-entrainment phenotype has not been previously reported in a murine AD model. Because microglia are activated in AD and in AD models, and inflammation can affect circadian rhythms, we hypothesized that microglia contribute to this re-entrainment phenotype. To test this, we used the colony stimulating factor 1 receptor (CSF1R) inhibitor PLX3397, which rapidly depletes microglia from the brain. Microglia depletion did not alter re-entrainment in either wild type or 3xTg mice, demonstrating that microglia activation is not acutely responsible for the re-entrainment phenotype. To test whether mutant tau pathology is necessary for this behavioral phenotype, we repeated the jet lag behavioral test with the 5xFAD mouse model, which develops amyloid plaques, but not neurofibrillary tangles. As with 3xTg mice, 7-month-old female 5xFAD mice re-entrained more rapidly than controls, demonstrating that mutant tau is not necessary for the re-entrainment phenotype. Because AD pathology affects the retina, we tested whether differences in light sensing may contribute to altered entrainment behavior. 3xTg mice demonstrated heightened negative masking, a circadian behavior measuring responses to different levels of light, and re-entrained dramatically faster than WT mice in a jet lag experiment performed in dim light. 3xTg mice show a heightened sensitivity to light as a circadian cue that may contribute to accelerated photic re-entrainment. Together, these experiments demonstrate novel circadian behavioral phenotypes with heightened responses to photic cues in AD model mice which are not dependent on tauopathy or microglia.
Language	English
Publishing date	2023-06-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1218193
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Article: Dopamine systems and biological rhythms: Let's get a move on.

Tang, Qijun / Assali, Dina R / Güler, Ali D / Steele, Andrew D

Frontiers in integrative neuroscience

2022 Volume 16, Page(s) 957193

Abstract: How dopamine signaling regulates biological rhythms is an area of emerging interest. Here we review experiments focused on delineating dopamine signaling in the suprachiasmatic nucleus, nucleus accumbens, and dorsal striatum to mediate a range of ... ...

Abstract	How dopamine signaling regulates biological rhythms is an area of emerging interest. Here we review experiments focused on delineating dopamine signaling in the suprachiasmatic nucleus, nucleus accumbens, and dorsal striatum to mediate a range of biological rhythms including photoentrainment, activity cycles, rest phase eating of palatable food, diet-induced obesity, and food anticipatory activity. Enthusiasm for causal roles for dopamine in the regulation of circadian rhythms, particularly those associated with food and other rewarding events, is warranted. However, determining that there is rhythmic gene expression in dopamine neurons and target structures does not mean that they are bona fide circadian pacemakers. Given that dopamine has such a profound role in promoting voluntary movements, interpretation of circadian phenotypes associated with locomotor activity must be differentiated at the molecular and behavioral levels. Here we review our current understanding of dopamine signaling in relation to biological rhythms and suggest future experiments that are aimed at teasing apart the roles of dopamine subpopulations and dopamine receptor expressing neurons in causally mediating biological rhythms, particularly in relation to feeding, reward, and activity.
Language	English
Publishing date	2022-07-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452962-X
ISSN	1662-5145
ISSN	1662-5145
DOI	10.3389/fnint.2022.957193
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Article ; Online: Dopamine Signaling in Circadian Photoentrainment: Consequences of Desynchrony.

Grippo, Ryan M / Güler, Ali D

The Yale journal of biology and medicine

2019 Volume 92, Issue 2, Page(s) 271–281

Abstract: Circadian rhythms, or biological oscillations of approximately 24 hours, impact almost all aspects of our lives by regulating the sleep-wake cycle, hormone release, body temperature fluctuation, and timing of food consumption. The molecular machinery ... ...

Abstract	Circadian rhythms, or biological oscillations of approximately 24 hours, impact almost all aspects of our lives by regulating the sleep-wake cycle, hormone release, body temperature fluctuation, and timing of food consumption. The molecular machinery governing these rhythms is similar across organisms ranging from unicellular fungi to insects, rodents, and humans. Circadian entrainment, or temporal synchrony with one's environment, is essential for survival. In mammals, the central circadian pacemaker is located in the suprachiasmatic nucleus (SCN) of the hypothalamus and mediates entrainment to environmental conditions. While the light:dark cycle is the primary environmental cue, arousal-inducing, non-photic signals such as food consumption, exercise, and social interaction are also potent synchronizers. Many of these stimuli enhance dopaminergic signaling suggesting that a cohesive circadian physiology depends on the relationship between circadian clocks and the neuronal circuits responsible for detecting salient events. Here, we review the inner workings of mammalian circadian entrainment, and describe the health consequences of circadian rhythm disruptions with an emphasis on dopamine signaling.
MeSH term(s)	Animals ; Circadian Clocks/physiology ; Circadian Rhythm/physiology ; Dopamine/metabolism ; Dopamine/physiology ; Dopaminergic Neurons/physiology ; Humans ; Photoperiod ; Signal Transduction/physiology ; Suprachiasmatic Nucleus/metabolism ; Suprachiasmatic Nucleus/physiopathology
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2019-06-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	200515-3
ISSN	1551-4056 ; 0044-0086
ISSN (online)	1551-4056
ISSN	0044-0086
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Ua VI Zs.197: Show issues

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Article ; Online: Metabolic homeostasis via BDNF and its receptors.

Podyma, Brandon / Parekh, Kavya / Güler, Ali D / Deppmann, Christopher D

Trends in endocrinology and metabolism: TEM

2021 Volume 32, Issue 7, Page(s) 488–499

Abstract: Metabolic disorders result from dysregulation of central nervous system and peripheral metabolic energy homeostatic pathways. To maintain normal energy balance, neural circuits must integrate feedforward and feedback signals from the internal metabolic ... ...

Abstract	Metabolic disorders result from dysregulation of central nervous system and peripheral metabolic energy homeostatic pathways. To maintain normal energy balance, neural circuits must integrate feedforward and feedback signals from the internal metabolic environment to orchestrate proper food intake and energy expenditure. These signals include conserved meal and adipocyte cues such as glucose and leptin, respectively, in addition to more novel players including brain-derived neurotrophic factor (BDNF). In particular, BDNF's two receptors, tropomyosin related kinase B (TrkB) and p75 neurotrophin receptor (p75NTR), are increasingly appreciated to be involved in whole body energy homeostasis. At times, these two receptors even seem to functionally oppose one another's actions, providing the framework for a potential neurotrophin mediated energy regulatory axis, which we explore further here.
MeSH term(s)	Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Energy Metabolism ; Homeostasis ; Humans ; Protein Transport
Chemical Substances	Brain-Derived Neurotrophic Factor
Language	English
Publishing date	2021-05-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2021.04.005
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Zs.A 2999: Show issues

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Article ; Online: Dorsal motor vagal neurons can elicit bradycardia and reduce anxiety-like behavior.

Strain, Misty M / Conley, Nicholas J / Kauffman, Lily S / Espinoza, Liliana / Fedorchak, Stephanie / Martinez, Patricia Castro / Crook, Maisie E / Jalil, Maira / Hodes, Georgia E / Abbott, Stephen B G / Güler, Ali D / Campbell, John N / Boychuk, Carie R

iScience

2024 Volume 27, Issue 3, Page(s) 109137

Abstract: Cardiovagal neurons (CVNs) innervate cardiac ganglia through the vagus nerve to control cardiac function. Although the cardioinhibitory role of CVNs in nucleus ambiguus ( ... ...

Abstract	Cardiovagal neurons (CVNs) innervate cardiac ganglia through the vagus nerve to control cardiac function. Although the cardioinhibitory role of CVNs in nucleus ambiguus (CVN
Language	English
Publishing date	2024-02-06
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2024.109137
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Article ; Online: Long-term high fat diet consumption reversibly alters feeding behavior via a dopamine-associated mechanism in mice.

Altherr, Everett / Rainwater, Aundrea / Kaviani, Darian / Tang, Qijun / Güler, Ali D

Behavioural brain research

2021 Volume 414, Page(s) 113470

Abstract: Obesity is a costly, global epidemic that is perpetuated by an unhealthy diet. A significant factor in the initial consumption and maintenance of an unhealthy diet is the abundance of highly palatable, calorically dense foods. The aim of the present ... ...

Abstract	Obesity is a costly, global epidemic that is perpetuated by an unhealthy diet. A significant factor in the initial consumption and maintenance of an unhealthy diet is the abundance of highly palatable, calorically dense foods. The aim of the present study is to better understand the effects of high fat diet (HFD) consumption on food valuation and preference, and to elucidate the neurobiological mechanisms mediating these effects. By using a novel food preference assay, we found that prolonged consumption of a HFD diminishes preference for and consumption of the more calorically dense food choice when two lab diets are presented. Additionally, we demonstrated that prolonged HFD consumption dampens ventral tegmental c-fos induction during hedonic feeding, implicating the mesolimbic dopamine signaling pathway as a target of HFD. Notably, both the changes in food preference and this reduced c-fos induction were reversed during withdrawal from HFD. Further, HFD-induced alterations in food preference were attenuated by exercise. Our findings suggest that prolonged HFD consumption leads to anhedonia and altered feeding choices, and this is associated with changes in mesolimbic dopamine signaling.
MeSH term(s)	Anhedonia/physiology ; Animals ; Behavior, Animal/physiology ; Diet, High-Fat ; Dopamine/metabolism ; Feeding Behavior/physiology ; Food Preferences/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Physical Conditioning, Animal/physiology ; Signal Transduction/physiology ; Ventral Striatum/metabolism ; Ventral Tegmental Area/metabolism
Chemical Substances	Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2021-07-16
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2021.113470
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Zs.A 1599: Show issues

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Article ; Online: Reply to: Magneto is ineffective in controlling electrical properties of cerebellar Purkinje cells, Assessing the utility of Magneto to control neuronal excitability in the somatosensory cortex and Revaluation of magnetic properties of Magneto.

Wheeler, Michael A / Deppmann, Christopher D / Patel, Manoj K / Güler, Ali D

Nature neuroscience

2019 Volume 23, Issue 9, Page(s) 1051–1054

MeSH term(s)	Action Potentials ; Magnetic Phenomena ; Neurons ; Purkinje Cells ; Somatosensory Cortex
Language	English
Publishing date	2019-09-30
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	1420596-8
ISSN	1546-1726 ; 1097-6256
ISSN (online)	1546-1726
ISSN	1097-6256
DOI	10.1038/s41593-019-0472-6
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Zs.A 4891: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 67: Show issues

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