Biomedical subjects

M H Maurer

Publications and source records attributed to M H Maurer.

8 recordsLinked to original sources

PubMed2007

Spatial learning induces predominant downregulation of cytosolic proteins in the rat hippocampus.

Spatial learning is known to depend on protein synthesis in the hippocampus. Whereas the role of the hippocampus in spatial memory is established, the biochemical and molecular mechanisms underlying this process are poorly understood. To comprehend the complex pattern of protein expression induced by spatial learning, we analyzed alterations in the rat hippocampus proteome after 7 days of spatial learning in the Morris water maze. Forty Wistar rats were randomized into two groups. Animals of group A learned to localize a hidden platform in the water maze. Animals of group B served as controls and spent exactly the same time in the water maze as animals of group A. However, no platform was used in this test and the rats could not learn to localize the target. After the last trial, hydrophilic proteins from the hippocampus were isolated. A proteome-wide study was performed, based on two-dimensional gel electrophoresis and mass spectrometry. Compared with non-learning animals, 53 (70%) proteins were downregulated and 23 (30%) proteins were upregulated after 7 days in rats with spatial learning. The overall changes in protein expression, as quantified by the induction factor, ranged from -1.62 (downregulation to 62%) to 2.10 (upregulation by 110%) compared with controls (100%). Most identified proteins exhibit known functions in vesicle transport, cytoskeletal architecture, and metabolism as well as neurogenesis. These findings indicate that learning in the Morris water maze has a morphological correlate on the proteome level in the hippocampus.

Animals↗

PubMed2006

Volatile anesthetics evoke prolonged changes in the proteome of the left ventricule myocardium: defining a molecular basis of cardioprotection?

BACKGROUND: Volatile anesthetics can alter cardiac gene and protein expression. Of those underlying molecular changes in gene and protein expression in the myocardium after exposure to volatile anesthetics that have been identified, some of them have been related to cardioprotection. METHODS: We used two-dimensional gel electrophoresis and mass spectrometry to identify changes in the protein expression of the left ventricle myocardium of anesthesized rats. We maintained anesthesia for 3 h using isoflurane, sevoflurane or desflurane, respectively, at 1.0 minimum alveolar concentration (MAC) and dissected the left ventricular myocardium either immediately or 72 h after the end of anesthesia. RESULTS: We found changes of at least twofold in 106 proteins of the more than 1.600 protein spots discriminated in each gel. These differentially expressed proteins are associated with functions in glycolysis, mitochondrial respiration and stress response. No obvious difference could be observed between the patterns of differential expression of the three volatile anesthetics. CONCLUSION: We provide the first study of post-anesthetic protein expression profiles associated with three common volatile anesthetics. These volatile anesthetics promote a distinct change in the myocardial protein expression profile, whereby changes in the expression pattern still exist 72 h after anesthesia. These proteome changes are closely related to cardioprotection and ischemic preconditioning, indicating a common functional signaling of volatile anesthestics.

Anesthetics, Inhalation↗

PubMed2004

[Cerebral microdialysis in stroke].

Cerebral microdialysis is an invasive technique for neurochemical monitoring that has been established for neuro-critical disorders such as subarachnoid hemorrhage and severe brain injury. We present data on cerebral microdialysis in stroke patients which were obtained in an ongoing study supported by the German Ministry for Education and Research. So far, 50 patients have been included who required critical care due to massive stroke of the middle cerebral artery territory. By correlating the microdialysis results with follow-up CT scans, we could define the neurochemical characteristics of three different brain compartments: (1) noninfarcted brain tissue with normal microdialysis values, (2) brain areas adjacent to the infarct core which were not hypodense in CT scans but caused reversible neurochemical alterations, and (3) the infarct core with massive concentration changes which did not normalize over the measuring period of 3 to 5 days. Microdialysis values averaged over time and correlated with initial PET scans helped to describe neurochemical predictors of a malignant, i.e., life-threatening, space-occupying course of the ischemic stroke. We discuss the value of this method in guiding therapy and predicting clinical outcome in the context of other neurological critical care disorders and describe the pros and cons of cerebral microdialysis as an invasive monitoring technique.

Brain Edema↗

PubMed2001

Correlation between local glucose transporter densities and local 3-O-methylglucose transport in rat brain.

The present study addresses the question whether local glucose transport kinetics are correlated with local glucose transporter densities in the brain. In 47 brain structures the local rate constants for 3-O-[(14)C]methylglucose (3-O-MG) transport, K(1) and k(2,) were quantified, and local glucose Glut1 and Glut3 transporter densities were determined by immuno-autoradiographic methods. Statistically significant correlations were found between the rate constants for glucose transport and the transporter densities. The correlations were tighter for Glut1 than for Glut3. Inasmuch as 3-O-MG is transported by the same transporter as glucose, these results indicate that the local densities of glucose transporters determine local glucose transport rates in the brain.

3-O-Methylglucose↗

PubMed2000

Increased cerebral glucose utilization and decreased glucose transporter Glut1 during chronic hyperglycemia in rat brain.

Whereas acute hyperglycemia has been shown to result in an unchanged local cerebral glucose utilization (LCGU) the changes of LCGU during chronic hyperglycemia are a matter of dispute. The present study had three aims: (1) To compare the effects of acute and chronic hyperglycemia on LCGU and to investigate in vivo the lactate level as a potential indicator of glycolytic flux. (2) To investigate local changes in brain Glut1 and/or Glut3 glucose transporter densities during chronic hyperglycemia. (3) To analyze the relationship between LCGU and local Glut densities during chronic hyperglycemia. To induce chronic hyperglycemia in rats steptozotocin was given i.p. and experiments were performed 3 weeks later. LCGU was measured by the 2-[14C]deoxyglucose method and intraparenchymal lactate concentration by MR-spectroscopy. Local densities of the glucose transport proteins were determined by immunoautoradiographic methods. During chronic hyperglycemia weighted average of LCGU increased by 13.9% whereas it remained unchanged during acute hyperglycemia. The cerebral lactate/choline ratio was increased by 143% during chronic hyperglycemia. The average density of glucose transporters Glut1 decreased by 7.5%. Local densities of Glut1 were decreased in 12 of 28 brain structures. Glut3 remained unchanged. Positive correlations were found between LCGU and local Glut densities during control conditions and during chronic hyperglycemia. It was concluded that (1) Chronic, but not acute hyperglycemia is followed by an increased LCGU. (2) The capacity to transport glucose is decreased during chronic hyperglycemia. (3) Increased LCGU and decreased densities of Glut1 are matched on a local level.

Animals↗

PubMed1999

Brain water content, glucose transporter densities and glucose utilization after 3 days of water deprivation in the rat.

After 3 days of water deprivation, the following parameters were measured in rats: (i) brain water content (apparent diffusion coefficient); (ii) local cerebral glucose utilization (LCGU) ([14C]deoxyglucose method) and (iii) densities of glucose transporters Glut1 and Glut3 (immunoautoradiography). The results show that brain water content is maintained after water deprivation. Densities of glucose transporters Glut1 and Glut3 increased in parallel to increased LCGU in some of the osmoregulatory structures indicating a long-term local adaptation of glucose transporters to LCGU.

Animals↗

PubMed1998

Decreased glucose transporter densities, rate constants and glucose utilization in visual structures of rat brain during chronic visual deprivation.

The question was investigated whether local changes in glucose transporter densities and transport kinetics can occur when local cerebral glucose utilization (LCGU) is decreased in some brain structures. Unilateral visual deprivation was induced by monocular enucleation in 25 rats. After 1 week, the contralateral structures of the visual system were analyzed for (1) densities of glucose transporters Glut1 and Glut3 (immunoautoradiography), (2) LCGU (2-[14C]deoxyglucose method) and (3) local rate constants (3-O[14C]methylglucose method). The ipsilateral structures served as controls. During chronic visual deprivation Glut1 and Glut3 densities, LCGU and rate constants were significantly decreased in some structures of the visual system and remained unchanged in others. These results indicate a moderate degree of downregulation of glucose transporters, LCGU and rate constants in the visual system during visual deprivation.

Animals↗

PubMed1998

Local transport kinetics of glucose during acute and chronic nicotine infusion in rat brains.

Acute and chronic infusion of nicotine is known to result in a distinct increase in local cerebral glucose utilization (LCGU) in several brain structures. The present study addresses the question whether this increase in LCGU is paralleled by a local change in glucose transport in rat brain. Nicotine was infused either acutely for 3 hours or chronically by osmotic minipumps for one week. Local rate constants for glucose transport were measured in brain cryosections using the 3-O-[14C]methylglucose method. Local rate constants K1 and k2 were lower in part of the brain structures during acute (-10% to -20%) and in nearly all structures during chronic (-39% to -41%) nicotine. The finding of a decreased glucose transport during chronic nicotine was confirmed by additional experiments of 3-O-[14C]methylglucose transfer in an epithelial cell culture. It is concluded that acute and chronic nicotine infusion results in decreased glucose transport although LCGU is either unchanged or increased.

3-O-Methylglucose↗