Effects of mild protein prenatal malnutrition and subsequent postnatal nutritional rehabilitation on noradrenaline release and neuronal density in the rat occipital cortex

Soto-Moyano, Rubén; Fernández, Vı́ctor; Sanhueza, Miguel; Belmar, Jorge; Kusch, Claudia; Pérez, Hernán; Ruíz, Samuel; Hernández, Alejandro

doi:10.1016/s0165-3806(99)00074-7

Cited by 28 publications

(21 citation statements)

References 63 publications

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“…1978; Soto‐Moyano et al . 1995), increased release of noradrenaline in the neocortex (Soto‐Moyano et al . 1994, 1995, 1998a,b, 1999), and decreased number of α and β adrenoceptors in total brain (Keller et al .…”

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confidence: 99%

Mild prenatal protein malnutrition increases α_2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Soto-Moyano

Valladares

Sierralta

et al. 2005

Journal of Neurochemistry

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Mild reduction in the protein content of the mother's diet from 25 to 8% casein, calorically compensated by carbohydrates, does not alter body and brain weights of rat pups at birth, but leads to significant enhancements in the concentration and release of cortical noradrenaline during early postnatal life. Since central noradrenaline and some of its receptors are critically involved in long-term potentiation (LTP) and memory formation, this study evaluated the effect of mild prenatal protein malnutrition on the a 2C -adrenoceptor density in the frontal and occipital cortices, induction of LTP in the same cortical regions and the visuo-spatial memory. Pups born from rats fed a 25% casein diet throughout pregnancy served as controls. At day 8 of postnatal age, prenatally malnourished rats showed a threefold increase in neocortical a 2C -adrenoceptor density. At 60 days-of-age, a 2C -adrenoceptor density was still elevated in the neocortex, and the animals were unable to maintain neocortical LTP and presented lower visuo-spatial memory performance. Results suggest that overexpression of neocortical a 2C -adrenoceptors during postnatal life, subsequent to mild prenatal protein malnutrition, could functionally affect the synaptic networks subserving neocortical LTP and visuo-spatial memory formation. Keywords: a 2C adrenoceptor, long-term potentiation, neocortex, protein malnutrition, visuo-spatial memory. Central nervous system noradrenaline critically influences long-term potentiation (LTP) in cerebral cortex (Nowicky et al. 1992;Kamatsu 1996) and hippocampus (Hopkins and Johnston 1988;Radisavljevic et al. 1994;Bramham et al. 1997), as well as memory formation (Sternberg et al. 1986;Crowe et al. 1990;Gibbs 1991), through balanced activation of specific receptors. For instance, animal studies have revealed that b adrenoceptor activation is associated with enhancement of LTP in the hippocampus (Hopkins and Johnston 1988;Radisavljevic et al. 1994;Bramham et al. 1997) and memory facilitation (Crowe et al. 1990;Gibbs 1991;Gibbs and Summers 2000), while activation of a 2 adrenoceptors (Sara and Devauges 1989;Devauges and Sara 1990;Bunsey and Strupp 1995), especially the a 2C subtype (Haapalinna et al. 1998 Björklund et al. 1998Björklund et al. , 1999Björklund et al. , 2000, is related to decreased memory formation. This role of b and a 2C adrenoceptors is consistent with the widespread distribution of these receptor subtypes in the hippocampus and the cerebral cortex (Lee et al. 1998;Gibbs and Summers 2000).It has been reported that perinatal malnutrition and severe forms of prenatal malnutrition in the rat, in addition to decrease body and brain weights of pups results in functional changes of central noradrenergic systems, including increased activity of brain tyrosine hydroxylase

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confidence: 99%

Mild prenatal protein malnutrition increases α_2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Soto-Moyano

Valladares

Sierralta

et al. 2005

Journal of Neurochemistry

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“…In infants who died of severe malnutrition during the first year of life, brain analysis showed decreased cellularity [81]. But also mild protein malnutrition in the prenatal phase induced altered neuronal density in rats [82]. In a study of premature infants, however, postnatal growth pattern during the first 9 months, rather than being small for gestational age at birth, was found to be significantly associated with adverse neurodevelopmental outcome at age 2, even after statistical correction of certain diseases [83].…”

Section: Outcomes Of Early Amino Acid Administrationmentioning

confidence: 97%

Nutritional support for extremely low-birth weight infants: abandoning catabolism in the neonatal intensive care unit

Akker

Vlaardingerbroek

Goudoever

2010

Current Opinion in Clinical Nutrition and Metabolic Care

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“…Una vez impregnados los encéfalos en celoidina y endurecido el material, se realizaron cortes coronales anteroposteriores, de 40 mm de espesor, los que fueron teñidos con Cresil Violeta (Nissl) al 1%, a fin de poder visualizar con mayor facilidad los somas neuronianos (Soto-Moyano et al, 1999). Se seleccionaron los cortes correspondientes a la región dorsomedial del área 17 y, dentro de éstos, las capas IV y V, tomando como referencia un mapa estereotáxico de la citoarquitectura de la corteza cerebral presente en roedor (Caviness, 1975) y la histología del área 17 de la corteza cerebral de rata (Peters & Kara, 1985a, 1985b.…”

Section: Materials Y Métodounclassified

Densidad Neuronal en la Corteza Visual Primaria (Área 17), en Ratas Sometidas a Estrés Crónico

et al. 2010

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RESUMEN:El estrés puede ser definido como una amenaza a la integridad psicológica o fisiológica de un individuo. Por otro lado, se ha verificado que el estrés tiene efecto sobre la morfología y función de diversas estructuras del Sistema Nervioso Central, relacionadas con el aprendizaje, memoria y respuestas emocionales, tales como el hipocampo, amígdala y corteza prefrontal. Es por lo anterior, que el objetivo del presente trabajo fue realizar un estudio de la anatomía de la corteza visual primaria (área 17), en ratas machos (n=9), de la cepa Sprague-Dawley, de 3 meses de edad (250-350g.), sometidas a estrés crónico por inmovilización. Es así como se observó que el grupo estrés (n=3) presentó una menor densidad neuronal que el grupo control (n=3) y una significativa menor densidad neuronal (p<0,05) que el grupo postestrés (n=3) el cual presentó la más alta densidad neuronal observada. Estableciendo una relación inversa entre densidad neuronal y tamaño de los somas neuronales y sus respectivas conexiones y ramificaciones dendríticas. Lo anterior podría tener incidencia en el procesamiento de la información visual.PALABRAS CLAVE: Estrés; Corteza Visual; Densidad neuronal; Rata. INTRODUCCIÓNEl estrés, se define como una respuesta general del organismo antes demandas externas o internas, inicialmente amenazantes, que consiste en movilizar recursos fisioló-gicos y psicológicos para poderlas afrontar. Es decir, será el desequilibrio entre las demandas del organismo y la capacidad de éste para sobrellevarlas, lo que caracteriza una situación estresante, el mantenimiento de esta situación caracteriza al estrés crónico o diestrés (Montoro et al., 2009).El estrés tiene un profundo efecto sobre la morfología y función de diversas estructuras del Sistema Nervioso Central. En ratas, se ha observado que los protocolos de estrés inducen alteraciones morfológicas en hipocampo, amígdala y corteza prefrontal, estructuras que están relacionadas con el aprendizaje, memoria y respuestas emocionales (Vyas et al., 2002).En humanos con depresión, estudios de neuroimágenes han evidenciado atrofia del volumen hipocampal, reducción de la sustancia gris y blanca en la corteza prefrontal y disminución del volumen amigdalino (Sheline et al., 1996;McEwen & Chattarji, 2004). Estudios postmortem en cerebros de pacientes con depresión mayor, mostraron reducción del tamaño neuronal y/o disminución de la densidad de las células gliales en la corteza orbitofrontal, dorsolateral y corteza prefrontal (Rajkowska et al., 1999;Manji et al., 2003).Adicionalmente, se ha demostrado el rol del estrés prenatal, sobre eventuales alteraciones en la morfología cerebral y en funciones cognitivas, emocionales y conductuales (Lemaire et al., 2000). En los últimos años, numerosos estudios indican que largos periodos de estrés afectan la plas-*

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Effects of mild protein prenatal malnutrition and subsequent postnatal nutritional rehabilitation on noradrenaline release and neuronal density in the rat occipital cortex

Cited by 28 publications

References 63 publications

Mild prenatal protein malnutrition increases α_2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Mild prenatal protein malnutrition increases α_2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Nutritional support for extremely low-birth weight infants: abandoning catabolism in the neonatal intensive care unit

Densidad Neuronal en la Corteza Visual Primaria (Área 17), en Ratas Sometidas a Estrés Crónico

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Effects of mild protein prenatal malnutrition and subsequent postnatal nutritional rehabilitation on noradrenaline release and neuronal density in the rat occipital cortex

Cited by 28 publications

References 63 publications

Mild prenatal protein malnutrition increases α2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Mild prenatal protein malnutrition increases α2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Nutritional support for extremely low-birth weight infants: abandoning catabolism in the neonatal intensive care unit

Densidad Neuronal en la Corteza Visual Primaria (Área 17), en Ratas Sometidas a Estrés Crónico

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Mild prenatal protein malnutrition increases α_2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats

Mild prenatal protein malnutrition increases α_2C‐adrenoceptor density in the cerebral cortex during postnatal life and impairs neocortical long‐term potentiation and visuo‐spatial performance in rats