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J Satrústegui

Publications and source records attributed to J Satrústegui.

58 records · Page 4Linked to original sources
PubMed1980

Development of NADPH-producing pathways in rat heart.

The behaviours of the principal NADPH-producing enzymes (glucose 6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, cytoplasmic and mitochondrial 'malic' enzyme and NAPD+-dependent isocitrate dehydrogenase) were studied during the development of rat heart and compared with those in brain and liver. 1. The enzymes belonging to the pentose phosphate pathway exhibit lower activities in heart than in other tissues throughout development. 2. The pattern of induction of heart cytoplasmic and mitochondrial 'malic' enzymes does not parallel that found in liver. Heart mitochondrial enzyme is slowly induced from birth onwards. 3. NADP+-dependent isocitrate dehydrogenase has similar activities in all tissues in 18-day foetuses. 4. Heart mitochondrial NADP+-dependent isocitrate dehydrogenase is greatly induced in the adult, where it attains a 10-fold higher activity than in liver. 5. The physiological functions of mitochondrial 'malic' enzyme and NADP+-dependent isocitrate dehydrogenase are discussed.

Animals↗
PubMedDate not supplied

Age-related changes in calcium homeostatic mechanisms in synaptosomes in relation with working memory deficiency.

Aging is associated with alterations in different systems that govern neuronal calcium homeostasis. This study was designed to determine whether any of these alterations may contribute to the decline in spatial working memory that is observed in old rats. Several parameters [initial (5 s) and steady state (15 min) 45Ca2+ uptake, FCCP-releaseable 45Ca2+, [Ca2+]i levels, depolarization-induced phosphoprotein (P97, PP65, P42) dephosphorylation and acetylcholine levels and release) involved in calcium homeostasis/signaling were determined in whole brain synaptosomes derived from adult (9-month-old) and old (24-month-old) rats that were evaluated for spatial memory performance in the eight-arm radial maze. The neurochemical analysis indicated that both the 9- and 24-month-old rats were impaired with respect to 3-month-old animals. When learners (animals reaching criterion; RC) were compared to memory impaired rats (MI), it was found that the FCCP-releaseable 45Ca2+ of synaptosomes, that reflects mitochondrial calcium, was lower in the MI than the RC rats and was correlated with the behavioral performance of the rats in their first testing sessions. The results suggest that the loss of calcium uptake capacity in synaptic mitochondria during aging may be associated with impaired working memory in old animals.

Acetylcholine↗
PubMedDate not supplied

Altered cell calcium regulation in synaptosomes and brain cells of the 30-month-old rat: prominent effects in hippocampus.

A deficient regulation of neuronal cytosolic calcium levels has been suggested to play a role in the pathogenesis of neurodegeneration. However, evidence for an alteration in cytosolic calcium regulation in old age is at present controversial. The present work was aimed at studying whether changes in synaptosomal calcium homeostasis in 30-month-old rats are uniform throughout the brain or affect specific brain regions. A second question addressed in this work is whether the effect of ageing on calcium homeostasis is restricted to the nerve terminal or a more general process affecting also cell bodies. To study these questions cytosolic calcium regulation was studied in parallel in synaptosomes and a preparation of acutely dissociated brain cells obtained from different regions of 3- and 30-month-old rats. 45Ca2+ accumulation and distribution in mitochondria (assessed as FCCP-releasable 45Ca2+) was also studied. Mean [Ca2+]i obtained at rest and after high K+ depolarization were unchanged in cerebral cortex synaptosomes but increased in hippocampal synaptosomes at 30 months. Resting [Ca2+]i also increased with age in hippocampal, but not cerebral cortex cells, whereas the increase in [Ca2+]i obtained by depolarization was larger in both brain regions. Calcium compartmentation in mitochondria from hippocampal neurons incubated under high K+ conditions was also decreased with ageing. An altered calcium regulation in cell bodies and synaptic terminals in the hippocampus may be involved in the development of functional impairments in the hippocampal formation.

Aging↗