It is well known that a variety of stressors induces a significant alteration in various putative neurotransmitters in the mammalian CNS. However, relatively little attention has been paid on the alteration of central glutamate neurotransmission, which is a major excitatory neurotransmitter in the brain. The present study aimed to determine whether acute restraint stress induces the changes in neurotransmitter level, especially glutamate, in rat brain and to examine whether 1-h recovery time after the termination of stress can revert to its pre-stress state. In vivo ¹H-NMR spectra were acquired from the cerebral cortex and hippocampus (control: N = 10, stress: N = 10, stress + 1 h rest: N = 10) immediately or after 1 h rest from restraint stress. All in vivo proton spectra were automatically analyzed using LCModel. We found that acute restraint stress induced significant increase in glutamate concentrations in the cerebral cortex and the hippocampus of rat. However, the level could not revert to its pre-stress state by the end of 1-h recovery period in cerebral cortex of rats. In addition, glutamine/glutamate ratio, which may function as an index of the glutamatergic neurotransmission, was significantly lower in the cerebral cortex of both stress and 1 h stress + 1 h recovery groups, as compared to control. Our finding may provide important evidence for altered glutamatergic activity after the stress and suggest a potential biochemical marker for eventual diagnosis and/or therapy monitoring in mood disorder.

Using urinary microalbumin radioimmunoassay, we evaluated the clinical utility of microalbumin excretion in nephrotic syndrome with complete remission, isolated microscopic hematuria and kidney donors in reanl transplantation. The highest value in normal controls was 10.86 μg/min, and the upper normal level was set to 15 μg/min.The range of microalbuminuria in patients with nephrotic syndrome with complete remission was 1.67 μg/min to 32.5 μg/min. There was no significant correlation between the recurrence rate and microlbuminuria level in nephrotic syndrome with complete remission. The range of microalbuminuria levels in isolated microscopic hematuric patients was between 2.37μg/min and 103.2 μg/min.There was no singificant correlation between the amount of the red blood cells in urine and the level of microalbuminuria in the isolated microscopic hematuric patients. Most renal transplantation donors showed a normal range of microalbuminuria after nephrectomy. The aim of this study was to evaluate the clinical utility of urinary microalbuminuria in diseases other than diabetes. We concluded that further extensive and specific study will be required to determine the clinical utility of microalbuminuria.

To study the effect of cyclosporin A (CsA) on glucose metabolism in peripheral insulin target cells, we studied the intraperitoneal glucose tolerance test (i.p. GTT), insulin binding, glucose transport and lipogenesis in isolated adipocytes of CsA-treated male Wistar rats. The rats were treated for 7 days with an intramuscular injection of vehicle (control group), or 5 (group I) or 50 mg/kg body weight (group II) of CsA dissolved in ethanol. The results of i.p. GTT in group II showed markedly impaired glucose tolerance with significantly decreased basal and glucose-stimulated serum insulin levels. In isolated adipocytes of CsA-treated rats, the insulin bindings were decreased by 26% in group I and 32% in group II. The maximum insulin-stimulated glucose transports were decreased by 34% in group I and 41% in group II. The maximum insulin-stimulated lipogenesis was decreased by 33% in group I and 37% in group II. There was a right shift of the dose response curves for insulin of glucose transport and lipogenesis of both CsA-treated groups.In conclusion, these results suggest that CsA produces significant functional changes of pancreatic B cells and also induces insulin resistance in adipocytes due to combined receptor and postreceptor defects in insulin action.