Low levels of brain-derived neurotrophic factor and tyrosine kinase receptor B are related to loss of dentate granule cells after prolonged low-protein feeding in the rat

Mesquita, Rui; Pereira, Pedro; Andrade, José Paulo

doi:10.1016/s0304-3940(02)00743-7

Cited by 18 publications

(14 citation statements)

References 22 publications

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“…A recent study investigated the effects of postnatal protein malnutrition on the levels of the neurotrophin BDNF and its receptor TrkB in the dentate gyrus granule cells (Mesquita et al, 2002). These investigators reported a decrease in both the number of cells immunoreactive for the neurotrophin and its receptor and in the expression of their respective genes measured by in situ hybridization.…”

Section: Possible Mechanisms Of Cell Loss In Ca1mentioning

confidence: 99%

Effect of prenatal protein malnutrition on numbers of neurons in the principal cell layers of the adult rat hippocampal formation

et al. 2005

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Malnutrition has been associated with a variety of functional and anatomical impairments of the hippocampal formation. One of the more striking of these is widespread loss of hippocampal neurons in postnatally malnourished rats. In the present study we have investigated the effect of prenatal malnutrition on these same neuronal populations, neurons that are all generated during the period of the dietary restriction. In prenatally protein deprived rats, using design-based stereology, we have measured the regional volume and number of neurons in the hilus of the dentate gyrus and the pyramidal cell layers of CA3, CA2, CA1, and the subiculum of 90-day-old animals. These results demonstrated a statistically significant reduction of 20% in neuron numbers in the CA1 subfield, while numbers in the other subfields were unchanged. There was a corresponding significant reduction of 22% in the volume of the CA1 subfield and a significant 14% decrease in the volume of the pyramidal layer of the subiculum. The change in volume of the pyramidal layer of the subiculum without neuron loss may reflect loss of CA1 afferent input to the pyramidal layer. Although the effect of nutritional deprivation on the neuronal population appears to be different in pre- and postnatal malnutrition, both dietary paradigms highlight the vulnerability of key components of the hippocampal trisynaptic circuit (consisting of the dentate granule cell mossy fibers projection to CA3 pyramids and the CA3 projection to the CA1 pyramids), which is an essential circuit for memory and learning.

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Section: Possible Mechanisms Of Cell Loss In Ca1mentioning

confidence: 99%

Effect of prenatal protein malnutrition on numbers of neurons in the principal cell layers of the adult rat hippocampal formation

et al. 2005

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“…Malnutrition also contributes to hypothyroidism (Ramos, Lima, Teixeira, Brito, & Moura, 1997), low levels of brain derived neurotrophic factor (BDNF) (Mesquita, Pereira, & Andrade, 2002) and decreased activity of ornithine decarboxylase (ODC) (Schertel & Eichler, 1991), a regulatory, limiting of polyamine synthesis enzyme and a marker of cellular proliferation and differentiation (Pegg, 1988;Tabor & Tabor, 1984).…”

Section: Introductionmentioning

confidence: 99%

The effects of early protein malnutrition and environmental stimulation on behavioral and biochemical parameters in rats.

Sampaio

Oliveira

Almeida

et al. 2008

Psychology & Neuroscience

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The present study investigated the effects of protein malnutrition and environmental stimulation on biochemical and behavioral parameters in rats. The concentrations of polyamines in the frontal cortex, striatum, and hippocampus, as well as plasma corticosterone levels, were measured. The exploratory behavior was analyzed using the elevated plus-maze (EPM) test. Rats received either 16% (well-nourished -W) or 6% (malnourished -M) protein diets and were divided into stimulated or non-stimulated groups. Malnutrition increased corticosterone levels and decreased plasma protein and anxiety. Non-stimulated rats tested in the EPM had increased corticosterone levels and decreased frontal cortex, striatum and hippocampus protein and polyamines contents. Stimulation decreased open arm entries in the EPM in M animals and increased closed arm entries in the W ones. Stimulation increased frequency and time spent in risk-assessment behaviors. These results suggest that both malnutrition and EPM testing are distressing situations, as indicated by increased corticosterone levels. These results are consistent with lower anxiety and/or higher impulsiveness in M animals.

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“…A growing body of evidence has suggested that protein deprivation during adulthood can also cause important structural and biochemical alterations in the hippocampus, including a reduction in the number of pyramidal neurons, synapses and arborizations in the CA1 and CA3 regions (Andrade et al 1996a,b). Decreased expression of neurotrophic factors as well as a reduction in the number of cholinergic and GABAergic neurons has also been reported in the hippocampus (Andrade and PaulaBarbosa 1996;Mesquita et al 2002). The behavioural consequences have been less studied although in adult rats fed 8% casein diet for 8 months, performance in the open field and the water maze indicated significant impairments of hippocampal-dependent functions such as emotionality, habituation and spatial learning (Lukoyanov and Andrade 2000).…”

Section: Introductionmentioning

confidence: 94%

“…The nutritional model used in this series of studies (8% casein) was intended to induce protein deficiency, yet weight gain was unaltered and no biochemical evidence of protein deficiency was provided. Although food intake was reported to be unchanged (Andrade and PaulaBarbosa 1996;Andrade et al 1996a,b;Lukoyanov and Andrade 2000;Mesquita et al 2002), it is difficult to interpret these data because the low protein diet was of entirely different composition than that of the control diet and thus likely of different energy and micronutrient density. Further, since diets were not matched for nutrients other than protein, the structural and behavioural deficits cannot be specifically attributed to protein status.…”

Section: Introductionmentioning

confidence: 99%

Can a reward-based behavioural test be used to investigate the effect of protein–energy malnutrition on hippocampal function?

Prosser-Loose

Saucier

Paterson

2007

Nutritional Neuroscience

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Our laboratory is investigating the effects of protein-energy malnutrition (PEM) on cognitive outcome following global ischemia. Here, we investigated whether PEM independently impairs working memory in the T-maze and if the associated food reward reverses PEM. Gerbils were fed 12.5% (control diet) or 2% protein. A loss of body weight (20.1%) in the 2% protein group and decreased food intake and serum albumin concentration compared to controls (17.5% and 18.2%, respectively) indicated that PEM was achieved. Based on T-maze criterion frequently used in ischemia studies, no difference was observed in the mean (+/- SEM) number of trials required (control 5.2 +/- 0.7; PEM 4.9 +/- 0.4; p = 0.758) or the number of animals reaching criterion (control 10/12; PEM 12/12; p = 0.140). Using more stringent criterion, PEM animals required fewer trials (control 7.3 +/- 0.7; PEM 5.4 +/- 0.4; p = 0.035), and more reached criterion (control 8/12; PEM 12/12; p = 0.028). PEM may increase motivation to obtain a food reward.

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Low levels of brain-derived neurotrophic factor and tyrosine kinase receptor B are related to loss of dentate granule cells after prolonged low-protein feeding in the rat

Cited by 18 publications

References 22 publications

Effect of prenatal protein malnutrition on numbers of neurons in the principal cell layers of the adult rat hippocampal formation

Effect of prenatal protein malnutrition on numbers of neurons in the principal cell layers of the adult rat hippocampal formation

The effects of early protein malnutrition and environmental stimulation on behavioral and biochemical parameters in rats.

Can a reward-based behavioural test be used to investigate the effect of protein–energy malnutrition on hippocampal function?

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