2013, Number 3
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Arch Neurocien 2013; 18 (3)
Effect of chronic undernutrition on postnatal expression of short-dystrophin in rat brain
Vargas FM, Guadarrama-Olmos JC, Mariscal S, Segura-Alegría B, Jiménez-Estrada I
Language: English
References: 44
Page: 113-119
PDF size: 134.98 Kb.
ABSTRACT
Maternal undernutrition results in impaired fetal and postnatal growth of the newborn and it is associated with
increased risks of developing cardiovascular and metabolic syndrome type diseases in adulthood. Undernourished
offsprings show altered electrophysiological and neurochemical properties producing behavioral, learning and memory
deficits. Dystrophin protein plays an important role as part of a scaffold-signaling associated protein complex
(DAPC), known to contribute to Na
+, K
+, and Ca
2+ ion channels modulation, in muscle and brain cells. Short dystrophin
of 71 kDal (Dp71) is the main form identified in neuronal and glial cells which covers most of the scaffolding
functions as shown in muscle cells. The goal of this study was to analyze the postnatal expression of this Dp71 as
a first approach to comprehend the many functional imbalances occurring during postnatal development in the brain
from rats subjected to chronic undernutrition (CU) treatment. We found that Dp71 is present at postnatal day 7
(P7) and attains maximal level of expression at 16 days of age (P16) in the brain of pup rats born from mothers fed
a control diet. In addition, Dp71 protein expression at P7 and P16 was significantly lower in brain samples of pup
rats born from dams under a CU feeding conditions as compared to the values of control groups or 58±13%
vs
24±7% and 98±2%
vs 57±24%, respectively, and practically no significant differences were observed at P26 and
P45. Our data shows that CU treatment delays expression of Dp71 in the rat brain during the first three wks
postnatally. Since the DAPC contribute to the ionic homeostasis in the cell it is plausible to suggest that Dp71
expression delay causes a rise in [Ca2+]i that disturbs brain cells maturation, thus contributing to the physiological
and neurochemical deficits observed in these CU treated rats.
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