Prenatal choline supplementation increases NGF levels in the hippocampus and frontal cortex of young and adult rats

Sandstrom, Noah J.; Loy, Rebekah; Williams, Christina L.

doi:10.1016/s0006-8993(02)02900-1

Cited by 76 publications

(59 citation statements)

References 90 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SUP rats showed enhanced baseline levels of several growth/neurotrophic factors (BDNF, NGF, IGF-1) in the hippocampus, compared to CON rats. This finding extends our previous demonstrations of higher BDNF protein in 8-month old (Glenn et al, 2007) and NGF protein in 20-and 90-day old (Sandstrom et al, 2002) female offspring of choline-supplemented dams. Infusions of BDNF or bFGF into the hippocampus prior to SE (Liu et al, 1993;Reibel et al, 2000) as well as exercise (Setkowicz & Mazur, 2006), which stimulates BDNF, NGF, and IGF-1 (Gomez-Pinilla et al, 1998;Cotman & Berchtold, 2002), have been shown to ameliorate the progression of excitotoxin-induced SE.…”

Section: Discussionsupporting

confidence: 91%

“…While the mechanism by which prenatal choline supplementation confers neuroprotection is not fully understood, choline is a vital nutrient important for several biological functions: acetylcholine synthesis, building biological membranes, cell signaling, and methyl donation (Blusztajn, 1998;Zeisel, 2004Zeisel, , 2006. Prenatal choline supplementation also enhances several features of adult hippocampal plasticity known to influence learning and memory function, such as increased baseline levels of neurogenesis, brain-derived neurotrophic factor (BDNF) (Glenn et al, 2007) and nerve growth factor (NGF) (Sandstrom et al, 2002); a reduced threshold to induce long-term potentiation (Pyapali et al, 1998;Jones et al, 1999); and enhanced depolarizationinduced mitogen-activated protein kinase (MAPK) and cAMP-response element binding protein (CREB) activation (Mellott et al, 2004). Enhanced hippocampal plasticity may underlie prenatal choline supplementation's neuroprotection of the hippocampus, rendering the hippocampus better able to withstand or recover from the deleterious effects of a neural insult.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

View full text Add to dashboard Cite

Prenatal choline supplementation (SUP) protects adult rats against spatial memory deficits observed after excitotoxin-induced status epilepticus (SE). To examine the mechanism underlying this neuroprotection, we determined the effects of SUP on a variety of hippocampal markers known to change in response to SE and thought to underlie ensuing cognitive deficits. Adult offspring from rat dams that received either a Control or SUP diet on embryonic days 12-17 were administered saline or kainic acid (i.p.) to induce SE and were euthanized 16 days later. SUP markedly attenuated seizure-induced hippocampal neurodegeneration, dentate cell proliferation, hippocampal GFAP mRNA expression levels, prevented the loss of hippocampal GAD65 protein and mRNA expression, and altered growth factor expression patterns. SUP also enhanced pre-seizure hippocampal levels of BDNF, NGF, and IGF-1, which may confer a neuroprotective hippocampal microenvironment that dampens the neuropathological response to and/or helps facilitate recovery from SE to protect cognitive function. Keywords choline; kainic acid; hippocampus; seizures; bromodeoxyuridine; growth factor; glutamic acid decarboxylase; glial fibrillary acidic protein; neuroprotection Status epilepticus (SE), a period of prolonged seizures, produces a host of plastic changes in the hippocampus that are thought to contribute to the development of temporal lobe epilepsy. SE results in substantial neuronal loss (Cavazos et al., 1994;Haas et al., 2001;Gorter et al., 2003), γ-aminobutyric acid (GABA) system alterations (e.g., Houser & Esclapez, 1996), reactive gliosis (Jorgensen et al. 1993; Niquet et al., 1994a;Kang et al., 2006), mossy fiber innervation of the dentate gyrus (Sutula et al., 1988;Ben-Ari & Represa, 1990), changes in levels of growth factors (Khrestchatisky et al., 1995;Mudo et al., 1996;Schmidt-Kastner et al., 1996;Shetty et al., 2004), and a transient increase in cell proliferation and neurogenesis (Bengzon et al., 1997;Parent et al., 1997;Scharfman et al., 2000;Hattiangady et al., 2004). These SE-induced degenerative and regenerative changes in the hippocampus are also Corresponding author: Dr. Christina L. Williams, Department of Psychology and Neuroscience, 572 Research Drive, Box 91050, GSRB-II, Room 3022, Duke University, Durham, NC 27708, USA, Phone: 919-660-5638, Fax: 919-660-5798, Email: williams@psych.duke.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. accompanied by deficits in hippocampal-dependent learning and memory (Stafstrom et al., 1993;Liu et al., 1994;Sarkisian et al., 1997;Hort et al., 1999;Mik...

show abstract

Section: Discussionsupporting

confidence: 91%

mentioning

confidence: 99%

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Wong-Goodrich¹,

Mellott²,

Glenn³

et al. 2008

Neurobiology of Disease

View full text Add to dashboard Cite

show abstract

“…Although the present results are most directly related to possible interactions of prenatal choline and α7-AChRs in the striatum (Cheng et al, 2007;Meck, 2006b;Mobley et al, 1985;Morley et al, 1977) it is also important to note that prenatal choline supplementation leads to increases in NGF levels in the frontal cortex and hippocampus (Sandstrom et al, 2002). These results suggest that increased NGF levels throughout development may contribute to higher α7-nAChR densities and influence corticostriatal circuits involved in adult timing behavior (e.g., Kawai et al, 2002;Matell and Meck, 2004;Summers et al, 2007).…”

Section: Discussionmentioning

confidence: 74%

Prenatal choline supplementation increases sensitivity to time by reducing non-scalar sources of variance in adult temporal processing

Cheng

Meck

2007

Brain Research

View full text Add to dashboard Cite

Choline supplementation of the maternal diet has a long-term facilitative effect on timing and temporal memory of the offspring. To further delineate the impact of early nutritional status on interval timing, we examined effects of prenatal-choline supplementation on the temporal sensitivity of adult (6 mo) male rats. Rats that were given sufficient choline in their chow (CON: 1.1 g/kg) or supplemental choline added to their drinking water (SUP: 3.5 g/kg) during embryonic days (ED) 12-17 were trained with a peak-interval procedure that was shifted among 75%, 50%, and 25% probabilities of reinforcement with transitions from 18s -> 36s ->72s temporal criteria. Prenatalcholine supplementation systematically sharpened interval-timing functions by reducing the associative/non-temporal response enhancing effects of reinforcement probability on the Start response threshold, thereby reducing non-scalar sources of variance in the left-hand portion of the Gaussian-shaped response functions. No effect was observed for the Stop response threshold as a function of any of these manipulations. In addition, independence of peak time and peak rate was demonstrated as a function of reinforcement probability for both prenatal-choline supplemented and control rats. Overall, these results suggest that prenatal-choline supplementation facilitates timing by reducing impulsive responding early in the interval, thereby improving the superimposition of peak functions for different temporal criteria.

show abstract

“…These choline-induced alterations in cognitive function are accompanied by changes in the size and shape of basal forebrain cholinergic neurons (e.g., Williams et al 1998;McKeon-O'Malley et al 2003); modifications in acetylcholine turnover and choline transporter expression in the septum and hippocampus (Cermak et al 1999;Mellott et al 2007b); modulation of hippocampal neurogenesis, gene expression, phospholipase D activity, NGF levels, and MAPK and CREB activation (e.g., Holler et al 1996;Sandstrom et al 2002;Mellott et al 2004Mellott et al , 2007aGlenn et al 2007); changes in dendritic fields and spine density in CA1 and dentate gyrus (DG) regions of the hippocampus ; as well as modification of the neuropathological response to status epilepticus (e.g., Holmes et al 2002;Wong-Goodrich et al 2008a) and thresholds for eliciting long-term potentiation (LTP) in the hippocampus (Pyapali et al 1998;Jones III et al 1999). Together, these findings suggest that alterations in choline availability during early development may have specific impact on the ontogeny and later functioning of basal forebrain cholinergic neurons as well as efferent neurons involved in hippocampal LTP (Montoya et al 2000).…”

mentioning

confidence: 99%

Prenatal choline availability alters the context sensitivity of Pavlovian conditioning in adult rats

Lamoureux¹,

Meck²,

Williams³

2008

Learn. Mem.

View full text Add to dashboard Cite

The effects of prenatal choline availability on Pavlovian conditioning were assessed in adult male rats (3-4 mo). Neither supplementation nor deprivation of prenatal choline affected the acquisition and extinction of simple Pavlovian conditioned excitation, or the acquisition and retardation of conditioned inhibition. However, prenatal choline availability significantly altered the contextual control of these learned behaviors. Both control and choline-deprived rats exhibited context specificity of conditioned excitation as exhibited by a loss in responding when tested in an alternate context after conditioning; in contrast, choline-supplemented rats showed no such effect. When switched to a different context following extinction, however, both choline-supplemented and control rats showed substantial contextual control of responding, whereas choline-deficient rats did not. These data support the view that configural associations that rely on hippocampal function are selectively sensitive to prenatal manipulations of dietary choline during prenatal development.There is increasing evidence that variations in maternal dietary choline intake during the second half of pregnancy cause structural, biochemical, and physiological changes in basal forebrain neurons and their projections to the hippocampal complex as well as long-term cognitive changes in the offspring (e.g., Meck and Williams 2003;McCann et al. 2006;Meck et al. 2008). We know, for instance, that the adult offspring of pregnant rats supplemented with 4.5 times the amount of choline in the standard laboratory diet display improved memory capacity and precision on the radial-arm maze (e.g., Meck et al.

show abstract

Prenatal choline supplementation increases NGF levels in the hippocampus and frontal cortex of young and adult rats

Cited by 76 publications

References 90 publications

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Prenatal choline supplementation attenuates neuropathological response to status epilepticus in the adult rat hippocampus

Prenatal choline supplementation increases sensitivity to time by reducing non-scalar sources of variance in adult temporal processing

Prenatal choline availability alters the context sensitivity of Pavlovian conditioning in adult rats

Contact Info

Product

Resources

About