Differences in serotoninergic metabolism possibly contribute to differences in breathing phenotype of FVB/N and C57BL/6J mice

Menuet, Clément; Kourdougli, Nazim; Hilaire, Gérard; Voituron, Nicolas

doi:10.1152/japplphysiol.00117.2011

Cited by 14 publications

(16 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These mice have a significantly lower pCO 2 than C57BL/6 mice anesthetized under the same conditions (Supplementary Figure S3) and a trend toward a lower arterial pH. 12 In keeping with this, we maintained endtidal pCO 2 at values~20 to 30 mm Hg, which correspond to an arterial pH of 30 to 40 mm Hg, i.e., the physiologic value for FVB/N mice.…”

Section: Resultsmentioning

confidence: 69%

Dysfunction of Mouse Cerebral Arteries during Early Aging

Balbi

Ghosh²,

Longden

et al. 2015

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Aging leads to a gradual decline in the fidelity of cerebral blood flow (CBF) responses to neuronal activation, resulting in an increased risk for stroke and dementia. However, it is currently unknown when age-related cerebrovascular dysfunction starts or which vascular components and functions are first affected. The aim of this study was to examine the function of microcirculation throughout aging in mice. Microcirculation was challenged by inhalation of 5% and 10% CO 2 or by forepaw stimulation in 6-week, 8-month, and 12-month-old FVB/N mice. The resulting dilation of pial vessels and increase in CBF was measured by intravital fluorescence microscopy and laser Doppler fluxmetry, respectively. Neurovascular coupling and astrocytic endfoot Ca 2+ were measured in acute brain slices from 18-month-old mice. We did not reveal any changes in CBF after CO 2 reactivity up to an age of 12 months. However, direct visualization of pial vessels by in vivo microscopy showed a significant, age-dependent loss of CO 2 reactivity starting at 8 months of age. At the same age neurovascular coupling was also significantly affected. These results suggest that aging does not affect cerebral vessel function simultaneously, but starts in pial microvessels months before global changes in CBF are detectable.

show abstract

Section: Resultsmentioning

confidence: 69%

Dysfunction of Mouse Cerebral Arteries during Early Aging

Balbi

Ghosh²,

Longden

et al. 2015

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…Conversely, bigenic GSK3α.KOxTau.P301L mice (detailed below) did not survive longer than the parental Tau.P301L mice, notwithstanding an initial delay in precocious mortality (Figure 3B, arched area) [29,35]. Terminal Tau.P301L mice present with a rapid progression (2–3 weeks) of motor defects and loss in body-weight, upper-airway dysfunction with asphyxia and exhaustion, terminating in precocious death between age 8 and 11 months (mean 9.5 mo) [29,35-37]. The current data imply that GSK3α did not affect this terminal phase, but contributed negatively to the early phenotype of Tau.P301L mice, characterized by defective cognition and beginning motor problems [29,35,36].…”

Section: Resultsmentioning

confidence: 72%

Neurological characterization of mice deficient in GSK3α highlight pleiotropic physiological functions in cognition and pathological activity as Tau kinase

et al. 2013

View full text Add to dashboard Cite

BackgroundGSK3β is involved in a wide range of physiological functions, and is presumed to act in the pathogenesis of neurological diseases, from bipolar disorder to Alzheimer’s disease (AD). In contrast, the GSK3α isozyme remained largely ignored with respect to both aspects.ResultsWe generated and characterized two mouse strains with neuron-specific or with total GSK3α deficiency. Behavioral and electrophysiological analysis demonstrated the physiological importance of neuronal GSK3α, with GSK3β not compensating for impaired cognition and reduced LTP. Interestingly, the passive inhibitory avoidance task proved to modulate the phosphorylation status of both GSK3 isozymes in wild-type mice, further implying both to function in cognition. Moreover, GSK3α contributed to the neuronal architecture of the hippocampal CA1 sub-region that is most vulnerable in AD. Consequently, practically all parameters and characteristics indicated that both GSK3 isoforms were regulated independently, but that they acted on the same physiological functions in learning and memory, in mobility and in behavior.ConclusionsGSK3α proved to be regulated independently from GSK3β, and to exert non-redundant physiological neurological functions in general behavior and in cognition. Moreover, GSK3α contributes to the pathological phosphorylation of protein Tau.

show abstract

“…Besides age of onset, both models present regional differences in their intensity of eventual tauopathy [26], [27], [29], [46]–[50]. Nevertheless, the terminal phase was very similar in both models, despite the age difference, by combination of clinical indices that progress rapidly (2–3 weeks) leading to death: reduction in bodyweight, increased clasping of hind- and then fore-limbs, hyperkyphosis and inactivity, upper airway dysfunction caused by defective brainstem circuits [46], [50], [51]. The endpoint was invariably precocious death, for Tau.P301L mice mostly between age 8–12 months (average 9 months) without survivors beyond age 12 months [29].…”

Section: Resultsmentioning

confidence: 97%

“…The endpoint was invariably precocious death, for Tau.P301L mice mostly between age 8–12 months (average 9 months) without survivors beyond age 12 months [29]. The age of death of biGT mice was less sharply defined, ranging from 10 to 22 months [26], [27], [46], [50], [51]. The mechanistic contributions of GSK3β in the biGT model to the delay in tauopathy and to clinical phenotype are subject of ongoing studies.…”

Section: Resultsmentioning

confidence: 99%

Early Structural and Functional Defects in Synapses and Myelinated Axons in Stratum Lacunosum Moleculare in Two Preclinical Models for Tauopathy

Maurin¹,

Chong²,

Kraev

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

The stratum lacunosum moleculare (SLM) is the connection hub between entorhinal cortex and hippocampus, two brain regions that are most vulnerable in Alzheimer’s disease. We recently identified a specific synaptic deficit of Nectin-3 in transgenic models for tauopathy. Here we defined cognitive impairment and electrophysiological problems in the SLM of Tau.P301L mice, which corroborated the structural defects in synapses and dendritic spines. Reduced diffusion of DiI from the ERC to the hippocampus indicated defective myelinated axonal pathways. Ultrastructurally, myelinated axons in the temporoammonic pathway (TA) that connects ERC to CA1 were damaged in Tau.P301L mice at young age. Unexpectedly, the myelin defects were even more severe in bigenic biGT mice that co-express GSK3β with Tau.P301L in neurons. Combined, our data demonstrate that neuronal expression of protein Tau profoundly affected the functional and structural organization of the entorhinal-hippocampal complex, in particular synapses and myelinated axons in the SLM. White matter pathology deserves further attention in patients suffering from tauopathy and Alzheimer’s disease.

show abstract

Differences in serotoninergic metabolism possibly contribute to differences in breathing phenotype of FVB/N and C57BL/6J mice

Cited by 14 publications

References 64 publications

Dysfunction of Mouse Cerebral Arteries during Early Aging

Dysfunction of Mouse Cerebral Arteries during Early Aging

Neurological characterization of mice deficient in GSK3α highlight pleiotropic physiological functions in cognition and pathological activity as Tau kinase

Early Structural and Functional Defects in Synapses and Myelinated Axons in Stratum Lacunosum Moleculare in Two Preclinical Models for Tauopathy

Contact Info

Product

Resources

About