scholarly journals Lifespan extension by dietary intervention in a mouse model of Cockayne Syndrome uncouples early postnatal development from segmental progeria

Aging Cell ◽  
2013 ◽  
Vol 12 (6) ◽  
pp. 1144-1147 ◽  
Author(s):  
Lear E. Brace ◽  
Sarah C. Vose ◽  
Dorathy F. Vargas ◽  
Shuangyun Zhao ◽  
Xiu-Ping Wang ◽  
...  
Keyword(s):  
Mouse Model ◽  
Postnatal Development ◽  
Dietary Intervention ◽  
Cockayne Syndrome ◽  
Lifespan Extension ◽  
Early Postnatal Development

scholarly journals Early intrinsic hyperexcitability does not contribute to motoneuron degeneration in amyotrophic lateral sclerosis

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Félix Leroy ◽  
Boris Lamotte d'Incamps ◽  
Rebecca D Imhoff-Manuel ◽  
Daniel Zytnicki
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Superoxide Dismutase ◽  
Mouse Model ◽  
Postnatal Development ◽  
Superoxide Dismutase 1 ◽  
Critical Test ◽  
Early Postnatal Development ◽  
Contracting Muscle ◽  
Lateral Sclerosis ◽  
Motoneuron Degeneration

In amyotrophic lateral sclerosis (ALS) the large motoneurons that innervate the fast-contracting muscle fibers (F-type motoneurons) are vulnerable and degenerate in adulthood. In contrast, the small motoneurons that innervate the slow-contracting fibers (S-type motoneurons) are resistant and do not degenerate. Intrinsic hyperexcitability of F-type motoneurons during early postnatal development has long been hypothesized to contribute to neural degeneration in the adult. Here, we performed a critical test of this hypothesis by recording from identified F- and S-type motoneurons in the superoxide dismutase-1 mutant G93A (mSOD1), a mouse model of ALS at a neonatal age when early pathophysiological changes are observed. Contrary to the standard hypothesis, excitability of F-type motoneurons was unchanged in the mutant mice. Surprisingly, the S-type motoneurons of mSDO1 mice did display intrinsic hyperexcitability (lower rheobase, hyperpolarized spiking threshold). As S-type motoneurons are resistant in ALS, we conclude that early intrinsic hyperexcitability does not contribute to motoneuron degeneration.

scholarly journals Choroid plexus NKCC1 mediates cerebrospinal fluid clearance during mouse early postnatal development

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Huixin Xu ◽  
Ryann M. Fame ◽  
Cameron Sadegh ◽  
Jason Sutin ◽  
Christopher Naranjo ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Pressure ◽  
Mouse Model ◽  
Choroid Plexus ◽  
Postnatal Development ◽  
Critical Period ◽  
Obstructive Hydrocephalus ◽  
Early Postnatal Development ◽  
Atp Production ◽  
The Brain

AbstractCerebrospinal fluid (CSF) provides vital support for the brain. Abnormal CSF accumulation, such as hydrocephalus, can negatively affect perinatal neurodevelopment. The mechanisms regulating CSF clearance during the postnatal critical period are unclear. Here, we show that CSF K+, accompanied by water, is cleared through the choroid plexus (ChP) during mouse early postnatal development. We report that, at this developmental stage, the ChP showed increased ATP production and increased expression of ATP-dependent K+ transporters, particularly the Na+, K+, Cl−, and water cotransporter NKCC1. Overexpression of NKCC1 in the ChP resulted in increased CSF K+ clearance, increased cerebral compliance, and reduced circulating CSF in the brain without changes in intracranial pressure in mice. Moreover, ChP-specific NKCC1 overexpression in an obstructive hydrocephalus mouse model resulted in reduced ventriculomegaly. Collectively, our results implicate NKCC1 in regulating CSF K+ clearance through the ChP in the critical period during postnatal neurodevelopment in mice.

scholarly journals Impact of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behaviors and BDNF mRNA expression in the adult Sprague–Dawley rats exposed to glutathione deficit during early postnatal development of the brain

2021 ◽  
Author(s):  
Marta A. Lech ◽  
Kinga Kamińska ◽  
Monika Leśkiewicz ◽  
Elżbieta Lorenc-Koci ◽  
Zofia Rogóż
Keyword(s):  
Mrna Expression ◽  
Postnatal Development ◽  
Repeated Treatment ◽  
Sprague Dawley ◽  
Biochemical Tests ◽  
Bdnf Mrna ◽  
Adult Rats ◽  
Behavioral Deficits ◽  
Glutathione Synthesis ◽  
Early Postnatal Development

Abstract Background Preclinical and clinical studies have indicated that impaired endogenous synthesis of glutathione during early postnatal development plays a significant role in the pathophysiology of schizophrenia. Moreover, some studies have suggested that antidepressants are able to increase the activity of atypical antipsychotics which may efficiently improve the treatment of negative and cognitive symptoms of schizophrenia. Methods In the present study, we investigated the influence of repeated co-treatment with escitalopram and aripiprazole on the schizophrenia-like behavior and BDNF mRNA expression in adult rats exposed to glutathione deficit during early postnatal development. Male pups between the postnatal days p5–p16 were treated with the inhibitor of glutathione synthesis, BSO (L-buthionine-(S,R)-sulfoximine) and the dopamine uptake inhibitor, GBR 12,909 alone or in combination. Escitalopram and aripiprazole were given repeatedly for 21 days before the tests. On p90–92 rats were evaluated in the behavioral and biochemical tests. Results BSO given alone and together with GBR 12,909 induced deficits in the studied behavioral tests and decreased the expression of BDNF mRNA. Repeated aripiprazole administration at a higher dose reversed these behavioral deficits. Co-treatment with aripiprazole and an ineffective dose of escitalopram also abolished the behavioral deficits in the studied tests. Conclusion The obtained data indicated that the inhibition of glutathione synthesis in early postnatal development induced long-term deficits corresponding to schizophrenia-like behavior and decreased the BDNF mRNA expression in adult rats, and these behavioral deficits were reversed by repeated treatment with a higher dose of aripiprazole and also by co-treatment with aripiprazole and ineffective dose of escitalopram.

scholarly journals Glutathione Deficiency during Early Postnatal Development Causes Schizophrenia-Like Symptoms and a Reduction in BDNF Levels in the Cortex and Hippocampus of Adult Sprague–Dawley Rats

2021 ◽  
Vol 22 (12) ◽  
pp. 6171
Author(s):  
Marta Anna Lech ◽  
Monika Leśkiewicz ◽  
Kinga Kamińska ◽  
Zofia Rogóż ◽  
Elżbieta Lorenc-Koci
Keyword(s):  
Postnatal Development ◽  
Time Course ◽  
Postnatal Life ◽  
Positive Symptoms ◽  
Gbr 12909 ◽  
Sprague Dawley ◽  
Bdnf Mrna ◽  
Synthesis Inhibitor ◽  
Early Postnatal Development ◽  
Middle Adolescence

Growing body of evidence points to dysregulation of redox status in the brain as an important factor in the pathogenesis of schizophrenia. The aim of our study was to evaluate the effects of l-buthionine-(S,R)-sulfoximine (BSO), a glutathione (GSH) synthesis inhibitor, and 1-[2-Bis(4-fluorophenyl)methoxy]ethyl]-4-(3-phenylpropyl)piperazine dihydrochloride (GBR 12909), a dopamine reuptake inhibitor, given alone or in combination, to Sprague–Dawley pups during early postnatal development (p5–p16), on the time course of the onset of schizophrenia-like behaviors, and on the expression of brain-derived neurotrophic factor (BDNF) mRNA and its protein in the prefrontal cortex (PFC) and hippocampus (HIP) during adulthood. BSO administered alone decreased the levels of BDNF mRNA and its protein both in the PFC and HIP. Treatment with the combination of BSO + GBR 12909 also decreased BDNF mRNA and its protein in the PFC, but in the HIP, only the level of BDNF protein was decreased. Schizophrenia-like behaviors in rats were assessed at three time points of adolescence (p30, p42–p44, p60–p62) and in early adulthood (p90–p92) using the social interaction test, novel object recognition test, and open field test. Social and cognitive deficits first appeared in the middle adolescence stage and continued to occur into adulthood, both in rats treated with BSO alone or with the BSO + GBR 12909 combination. Behavior corresponding to positive symptoms in humans occurred in the middle adolescence period, only in rats treated with BSO + GBR 12909. Only in the latter group, amphetamine exacerbated the existing positive symptoms in adulthood. Our data show that rats receiving the BSO + GBR 12909 combination in the early postnatal life reproduced virtually all symptoms observed in patients with schizophrenia and, therefore, can be considered a valuable neurodevelopmental model of this disease.

scholarly journals An Xpd mouse model for the combined xeroderma pigmentosum/Cockayne syndrome exhibiting both cancer predisposition and segmental progeria

Cancer Cell ◽  
2006 ◽  
Vol 10 (2) ◽  
pp. 121-132 ◽  
Author(s):  
Jaan-Olle Andressoo ◽  
James R. Mitchell ◽  
Jan de Wit ◽  
Deborah Hoogstraten ◽  
Marcel Volker ◽  
...  
Keyword(s):  
Mouse Model ◽  
Xeroderma Pigmentosum ◽  
Cockayne Syndrome ◽  
Cancer Predisposition

Early postnatal development of the mandibular permanent first molar in infants with isolated cleft palate

2011 ◽  
Vol 22 (4) ◽  
pp. 280-285 ◽  
Author(s):  
NUNO V. HERMANN ◽  
MOSTAFA ZARGHAM ◽  
TRON A. DARVANN ◽  
IB J. CHRISTENSEN ◽  
SVEN KREIBORG
Keyword(s):  
Cleft Palate ◽  
Postnatal Development ◽  
Early Postnatal Development ◽  
Isolated Cleft Palate
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