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

Abstract

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.

Learning and memory disabilities in IUGR babies: Functional and molecular analysis in a rat model

“…In mammals, this process takes place in the CA1 region of the hippocampus, and the underlying cellular mechanism is a form of synaptic plasticity known as long‐term potentiation or LTP (Vann & Albasser, 2011), that requires Ca +2 signaling, gene expression changes and protein synthesis (Morgado‐Bernal, 2011). The neuropathological bases of learning and memory alterations in IUGR babies are not clear, but there is consensus that within the brain the hippocampus is one of the areas most susceptible to IUGR and hypoxic damage (Fung et al., 2012; Lodygensky et al., 2008; Mallard et al., 2000), which particularly affects CA1 pyramidal neurons in the hippocampus (Kovalenko et al., 2006; Lister et al., 2005). In this study, the ischemic and IUGR CMO groups presented a reduction in CA1 neuronal number, mild gliosis and paradoxical changes in PSD95 and synaptophysin expression.…”

“…In the same line, neuroimaging and histopathological studies of the IUGR brain in infants and animal models have shown that one of the areas most affected is the hippocampus (Dieni & Rees, 2003; Lister et al., 2005; Lodygensky et al., 2008). The hippocampus is a structure involved in codification, storage, and recovery mechanisms related to learning and memory processes (Vann & Albasser, 2011).…”

Functional Magnetic Resonance Study of Non-conventional Morphological Brains: malnourished rats

“…Malnutrition also affects structures involved in learning and memory processes, including the hippocampus and hypothalamus [2][3][4][5][6][7][8][9][10][11][12][13][14].…”

“…Studies of malnourished animal models, using postmortem histological and imaging analyses, have revealed a range of morphological changes, including a decrease in the prenatal brain size [2], a decrease in the postnatal brain size [3], fewer hippocampal neurons [4], diminished granular volume of cortex [5], abnormalities in the dendritic spines of the cerebellar cortex [6], reduced myelin content [7], and reduced synthesis of myelin-associated proteins [8].…”

Efeitos da desnutrição protéica precoce e da estimulação ambiental em medidas bioquímicas e comportamentais em ratos

“…No sistema nervoso central (SNC), a elevação de corticosterona mediada pelo estresse contribui para a atrofia hipocampal, mas não é suficiente para causar morte neuronal (Lister et al, 2005;Kehoe, et al 2001;Mesquita, et al 2003e Schertel et al 1991.…”