Intracardiac Injection of Dental Pulp Stem Cells After Neonatal Hypoxia-Ischemia Prevents Cognitive Deficits in Rats.

Neonatal hypoxia-ischemia (HI) is associated to cognitive and motor impairments and until the moment there is no proven treatment. The underlying neuroprotective mechanisms of stem cells are partially understood and include decrease in excitotoxicity, apoptosis and inflammation suppression. This study was conducted in order to test the effects of intracardiac transplantation of human dental pulp stem cells (hDPSCs) for treating HI damage.

Effects of pre- and postnatal protein malnutrition in hypoxic-ischemic rats.

Neonatal hypoxic-ischemic encephalopathy (HI) is a major cause of nervous system damage and neurological morbidity. Perinatal malnutrition affects morphological, biochemical and behavioral aspects of neural development, including pathophysiological cascades of cell death triggered by ischemic events, so modifying resulting brain damage. Female Wistar rats were subjected to protein restriction during pregnancy and lactation (control group: 25% soybean protein; malnourished group: 7%).

Neonatal handling impairs spatial memory and leads to altered nitric oxide production and DNA breaks in a sex specific manner.

Early life events lead to behavioral and neurochemical changes in adulthood. The aim of this study is to verify the effects of neonatal handling on spatial memory, nitric oxide (NO) production, antioxidant enzymatic activities and DNA breaks in the hippocampus of male and female adult rats. Litters of rats were non-handled or handled (10 min/day, days 1-10 after birth).

Effects of daily environmental enrichment on memory deficits and brain injury following neonatal hypoxia-ischemia in the rat.

Environmental enrichment (EE) results in improved learning and spatial memory, as well as attenuates morphological changes resulting from cerebral ischemia in adult animals. This study examined the effects of daily EE on memory deficits in the water maze and cerebral damage, assessed in the hippocampus and cerebral cortex, caused by neonatal hypoxia-ischemia. Male Wistar rats in the 7th postnatal day were submitted to the Levine-Rice model of neonatal hypoxia-ischemia (HI), comprising permanent occlusion of the right common carotid artery and a period of hypoxia (90 min, 8%O(2)-92%N(2)).

Tactile stimulation and maternal separation prevent hippocampal damage in rats submitted to neonatal hypoxia-ischemia.

Unilateral neonatal hypoxia-ischemia causes important damage to the hippocampus of the hemisphere ipsilateral to carotid artery occlusion; two forms of neonatal handling, tactile stimulation and maternal separation for a short period, have been shown to produce functional/behavioral protection in distinct models of CNS challenge. In this paper we investigated whether neonatal handling could alter the hippocampal damage caused by neonatal hypoxia-ischemia (HI) in the Wistar rat. Pups at postnatal day 7, P7, received HI (8% O(2)-92% N(2)) for 90 min and were submitted to neonatal handling, tactile stimulation of maternal separation daily, from P8 to P21, for 10 min.

Perturbations in the thiol homeostasis following neonatal cerebral hypoxia-ischemia in rats.

Changes in the thiol/disulphide status in the neonatal rat brain were evaluated after an episode of neonatal hypoxia-ischemia (HI) in 7-day-old rats. The glutathione level decreased in the post-HI period. The lowest values (43-68%) were obtained 24 h post-HI.

Neonatal hypoxia-ischemia reduces ganglioside, phospholipid and cholesterol contents in the rat hippocampus.

Hypoxia-ischemia is a common cause of neonatal brain damage producing serious impact on cerebral maturation. This report demonstrates that rats submitted to hypoxia-ischemia present a marked decrease in hippocampal gangliosides, phospholipids and cholesterol contents as from 7 days after the injury. Although chromatographic profiles of the different ganglioside species (GM1, GD1a, GD1b, and GT1b) from the hippocampus of hypoxic-ischemic hippocampi groups (HI) were apparently unaffected, as compared with controls, there were quantitative absolute reductions in HI.

Neonatal cerebral hypoxia-ischemia causes lateralized memory impairments in the adult rat.

Neonatal hypoxia-ischemia (HI) has been extensively studied in a rat model characterized by unilateral brain damage (Rice-Vannucci Model). However, as well as in humans, each rat brain hemisphere is distinctly involved in cognitive functions, as for example retrieval of emotionally based memory, and neurochemical asymmetries have been described. In this paper we investigated whether hypoxia-ischemia could cause distinct cognitive deficits depending on which hemisphere is damaged.

Agmatine induces anxiolysis in the elevated plus maze task in adult rats.

Agmatine is an endogenous released polyamine recently proposed to be a putative neurotransmitter, however its physiological role is still to be determined. We investigated the hypothesis that agmatine, systemically administered to adult Wistar rats, might exert anxiolytic-like behavior in the elevated plus maze (EPM) and the open field. Agmatine (1, 10, 20, 40 and 100 mg/kg) and saline were administered i.

Agmatine facilitates memory of an inhibitory avoidance task in adult rats.

Agmatine is a new putative neurotransmitter; however, the physiological role(s) of this endogenous released polyamine is still to be determined. We investigated its cognitive effect in an inhibitory avoidance task in adult rats. Agmatine (0.