Prenatal dietary choline availability alters postnatal neurotoxic vulnerability in the adult rat

Guo‐Ross, Shirley X.; Jones, Katherine H.; Shetty, Ashok K.; Wilson, Wilkie A.; Swartzwelder, H. Scott

doi:10.1016/s0304-3940(03)00119-8

Cited by 25 publications

(21 citation statements)

References 15 publications

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“…When histones are deacetylated they are less permissive to gene transcription and therefore preventing deacetylation can promote gene transcription. This is a provocative target for future investigations into the mechanisms of choline’s antidepressant properties, demonstrated in the present report, but also its more general neuroprotective properties, which are well-documented (Glenn et al, 2008; Guo-Ross et al, 2003; Holmes et al, 2003; Moon et al, 2010; Nag & Berger-Sweeney, 2007; Thomas et al, 2000; 2007; Wong-Goodrich et al, 2008a; 2011). …”

Section: Discussionmentioning

confidence: 56%

“…Fitting extraordinarily well with these behavioral results are physiological and neural findings that the basal forebrain-hippocampal cholinergic system’s function and morphology are altered by the levels of choline in utero (Albright et al, 1999; Blusztajn et al, 1998; Craciunescu et al, 2003; Pyapali et al, 1998; Williams et al, 1998; also see Loy et al, 1991). Extending this work are findings that prenatal choline supplementation is neuroprotective against a variety of neural insults (Guo-Ross et al, 2003; Holmes et al, 2001; Thomas et al, 2000; 2007; Wong-Goodrich et al, 2008a; Yang et al, 2000) and that prenatal choline deficiency may reduce the capacity for neuroplastic changes in adult brains (Glenn et al, 2007). …”

Section: Introductionmentioning

confidence: 83%

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Supplemental dietary choline during development exerts antidepressant-like effects in adult female rats

2012

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Perinatal choline supplementation in rats is neuroprotective against insults such as fetal alcohol exposure, seizures, and advanced age. In the present study we explored whether dietary choline supplementation may also confer protection from psychological challenges, like stress, and act as a natural buffer against stress-linked psychological disorders, like depression. We previously found that choline supplementation increased adult hippocampal neurogenesis, a function compromised by stress, lowered in depression, and boosted by antidepressants; and increased levels of growth factors linked to depression, like brain-derived neurotrophic factor. Together, these were compelling reasons to study the role of choline in depressed mood. To do this, we treated rats with a choline supplemented diet (5 mg/kg choline chloride in AIN76A) prenatally on embryonic days 10–22, on postnatal days (PD) 25–50, or as adults from PD75 onward. Outside of these treatment periods rats were fed a standard diet (1.1 mg/kg choline chloride in AIN76A); control rats consumed only this diet throughout the study. Starting on PD100 rats’ anxiety-like responses to an open field, learning in a water maze, and reactivity to forced swimming were assessed. Rats given choline supplementation during pre- or post-natal development, but not adult-treated rats, were less anxious in the open field and less immobile in the forced swim test than control rats. These effects were not mediated by a learning deficit as all groups performed comparably and well in the water maze. Thus, we offer compelling support for the hypothesis that supplemental dietary choline, at least when given during development, may inoculate an individual against stress and major psychological disorders, like depression.

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Section: Discussionmentioning

confidence: 56%

Section: Introductionmentioning

confidence: 83%

Supplemental dietary choline during development exerts antidepressant-like effects in adult female rats

2012

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“…In addition to the beneficial cognitive effects of MCS in normal rats and mice, this early dietary intervention provides lasting neuroprotective effects and attenuates cognitive impairment in a wide variety of rodent disease models including aging [73, 82, 97–99], prenatal alcohol exposure [100–102], epilepsy [103–105], excitotoxicity [106, 107], Rett syndrome [108–111], and notably, DS [74–76, 112]. …”

Section: Effects Of Mcs On Spatial Cognition Hippocampal Neurogenesimentioning

confidence: 99%

Maternal Choline Supplementation: A Potential Prenatal Treatment for Down Syndrome and Alzheimer's Disease

Strupp

Powers²,

Velázquez³

et al. 2015

CAR

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Although Down syndrome (DS) can be diagnosed prenatally, currently there are no effective treatments to lessen the intellectual disability (ID) which is a hallmark of this disorder. Furthermore, starting as early as the third decade of life, DS individuals exhibit the neuropathological hallmarks of Alzheimer’s disease (AD) with subsequent dementia, adding substantial emotional and financial burden to their families and society at large. A potential therapeutic strategy emerging from the study of trisomic mouse models of DS is to supplement the maternal diet with additional choline during pregnancy and lactation. Studies demonstrate that maternal choline supplementation (MCS) markedly improves spatial cognition and attentional function, as well as normalizes adult hippocampal neurogenesis and offers protection to basal forebrain cholinergic neurons (BFCNs) in the Ts65Dn mouse model of DS. These effects on neurogenesis and BFCNs correlate significantly with spatial cognition, suggesting functional relationships. In this review, we highlight some of these provocative findings, which suggest that supplementing the maternal diet with additional choline may serve as an effective and safe prenatal strategy for improving cognitive, affective, and neural functioning in DS. In light of growing evidence that all pregnancies would benefit from increased maternal choline intake, this type of recommendation could be given to all pregnant women, thereby providing a very early intervention for DS fetuses, and include babies born to mothers unaware that they are carrying a DS fetus.

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“…Early life choline supplementation in rats, either prenatally, neonatally, or post-weaning, exerts neuroprotection in a wide array of disease models, including epilepsy (Wong-Goodrich et al, 2008b; 2011), Down syndrome (Strupp et al, 2016), Rett syndrome (Nag and Berger-Sweeney et al, 2007; Nag et al, 2009), fetal alcohol syndrome (Thomas et al, 2003; 2007; Schneider and Thomas, 2016), depression (Glenn et al, 2012; McCall et al, 2015: Schulz et al, 2014), and schizophrenia (Corriveau and Glenn, 2012; Stevens et al, 2008; 2014). In addition to these disease models, early life choline supplementation also attenuates the effects of exposure to the neurotoxin, MK-801 (Guo-Ross et al, 2002; 2003). MK-801 is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist (Wong et al, 1986) that blocks the activity of the excitatory neurotransmitter, glutamate, preventing it from activating the NMDA receptor.…”

Section: Introductionmentioning

confidence: 99%

“…Because glutamate is the primary excitatory neurotransmitter in the nervous system, the disruption of its activity by MK-801 causes a variety of problems. In rats, chronic or large acute doses of MK-801 induce motor deficits (Andiné et al, 1999), anhedonia (Vardigan et al, 2010), and neuronal degeneration (Guo-Ross et al, 2002; 2003), while low acute doses induce cognitive impairment in both spatial memory (Åhlander et al, 1999) and object recognition memory (de Lima et al, 2005). These are symptoms frequently observed in psychological disorders for which pathology is associated with reduced excitatory neurotransmission, such as schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

Prenatal choline supplementation attenuates MK-801-induced deficits in memory, motor function, and hippocampal plasticity in adult male rats

Nickerson

Brown

et al. 2017

Neuroscience

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Choline is essential to the development and function of the central nervous system and supplemental choline during development is neuroprotective against a variety of insults, including neurotoxins like dizocilpine (MK-801). MK-801 is an NMDA receptor antagonist that is frequently used in rodent models of psychological disorders, particularly schizophrenia. At low doses, it causes cognitive impairments, and at higher doses it induces motor deficits, anhedonia, and neuronal degeneration. The primary goals of the present study were to investigate whether prenatal choline supplementation protects against the cognitive impairments, motor deficits, and neuropathologies that are precipitated by MK-801 administration in adulthood. Adult male Sprague Dawley rats were fed a standard or supplemented choline diet prenatally. Using the novelty preference test of object recognition, we found that only prenatal standard-fed rats displayed memory consolidation deficits induced by low-dose MK-801 administered immediately following study of sample objects; all other groups, including prenatal choline supplemented rats given MK-801, showed intact memory. Following high-dose MK-801, prenatal choline supplementation significantly alleviated rats’ motor response to MK-801, particularly ataxia. Using doublecortin and Ki67 to mark neurogenesis and cell division, respectively, in the hippocampus, we found that prenatal choline supplementation, in the face of MK-801 toxicity, protected against reduced hippocampal plasticity. Taken together, the current findings suggest that prenatal choline supplementation protects against a variety of behavioral and neural pathologies induced by the neurotoxin, MK-801. This research contributes to the growing body of evidence supporting the robust neuroprotective capacity of choline.

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Prenatal dietary choline availability alters postnatal neurotoxic vulnerability in the adult rat

Cited by 25 publications

References 15 publications

Supplemental dietary choline during development exerts antidepressant-like effects in adult female rats

Supplemental dietary choline during development exerts antidepressant-like effects in adult female rats

Maternal Choline Supplementation: A Potential Prenatal Treatment for Down Syndrome and Alzheimer's Disease

Prenatal choline supplementation attenuates MK-801-induced deficits in memory, motor function, and hippocampal plasticity in adult male rats

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