ABSTRACT
It is widely known that prenatal stress (PS) exposure causes depression-like behaviour to offspring, as well as maladaptive responses including neurobiological and physiological changes. However, the underlying mechanism of PS induced juvenile-onset depression remains largely unravelled. The inadequacies of monoamine deficiency hypothesis, the emerging evidence of altered glutamate neurotransmission in mood disorders, as well as our previous studies inspired us to assess the potential role of glutamatergic system in the pathogenesis of juvenile depression. In this research, we examined the expression of phosphorylated GluR1 subunit of ionotropic receptor alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR), the Na+-dependent glutamate transporters excitatory amino acid transporter 2 (EAAT2) and EAAT3 in the hippocampus, striatum and frontal cortex of 1-month-old rat offspring after mid and late PS exposure. Prenatally stressed offspring rats showed significantly prolonged duration of immobility and shortened immobility latency in tail suspension test. We also detected that PS significantly altered the expression of glutamate receptor and glutamate transporters of these depressed rats. In brief, the changes of phosphorylated GluR1 subunit of AMPAR protein level in the hippocampus and frontal cortex, as well as markedly decreased EAAT2 mRNA expression in the hippocampus, striatum and frontal cortex and EAAT3 mRNA expression in the hippocampus of stressed rats were both observed. These results underpinned that glutamate receptors and glutamate transporters might be involved in the progress of depression-like behaviour in juvenile rat offspring induced by PS.
Subject(s)
Depression/psychology , Excitatory Amino Acid Transporter 2/physiology , Excitatory Amino Acid Transporter 3/physiology , Prenatal Exposure Delayed Effects/psychology , Receptors, AMPA/physiology , Animals , Blotting, Western , Depression/etiology , Female , Glutamic Acid/physiology , Hindlimb Suspension , Hippocampus/metabolism , Neostriatum/metabolism , Prefrontal Cortex/metabolism , Pregnancy , RNA/biosynthesis , RNA/isolation & purification , Rats , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Restraint, PhysicalABSTRACT
The origin of the magnetism in some oxide-based diluted magnetic semiconductors is still a puzzle. In this work, significantly ferromagnetic states of the oxygen-depleted In(2)O(3)(001) surfaces are investigated on the basis of first-principles density functional calculations. Our results show that the perfect oxygen-depleted surfaces are nonmagnetic; however, the surface states become ferromagnetic with the appearance of vacancies on the most outward In sites. The origin of the surface state magnetization can be explained using the Stoner model, and the exchange coupling between surfaces In s-p hybridization orbitals implies a ferromagnetic ground state. Our investigation gives a reasonable explanation for the source of the magnetism in oxygen-depleted In(2)O(3) nanostructures observed in previous experiments.
ABSTRACT
BACKGROUND: There is increasing evidence of therapeutic benefits from bone marrow (BM)-derived mesenchymal stromal cells (MSC) in various animal models with neurologic disorders. It is of great interest to apply the approach to clinical patients, i.e. to take the investigations from laboratory bench to the patient's bedside. This clinical trial was performed to assess the safety and feasibility of a combined procedure to deliver autologous MSC to patients with traumatic brain injury. METHODS: MSC were isolated by BM aspiration and expanded in culture. Seven patients received autologous cell transplantation. A primary administration of 10(7)-10(9) cells was applied directly to the injured area during the cranial operation; a second dose of 10(8)-10(10) cells was infused intravenously. All patients were followed up regularly for 6 months. RESULTS: There was no immediate or delayed toxicity related to the cell administration within the 6-month follow-up period. Neurologic function was significantly improved at 6 months after cell therapy. DISCUSSION: The procedure used is safe and feasible at ordinary medical facilities without additional invasive procedures for the patient. The combined cell delivery procedure is expected to enhance the engraftment efficacy of transplanted cells at injured brain tissue, thereby promoting neurologic recover.
