Biomedical subjects

T Neumann-Haefelin

Publications and source records attributed to T Neumann-Haefelin.

39 records · Page 3Linked to original sources

PubMed1995

Cellular correlates of neuronal hyperexcitability in the vicinity of photochemically induced cortical infarcts in rats in vitro.

Intrinsic membrane properties and synaptic responses of neocortical neurons located lateral to photochemically induced ischemic lesions were investigated using neocortical slice preparation. In comparison to neurons from control slices, these neurons had a significantly less negative resting membrane potential without any significant change in input resistance. In addition, gamma-aminobutyric acid (GABA) mediated synaptic inhibition was found to be less efficient; the conductances of both the early and late inhibitory postsynaptic potentials (IPSPs) were significantly smaller, and the reversal potential of the early IPSP was shifted to a more positive value. In some of the neurons, 'epileptiform' postsynaptic potentials could be elicited, which were abolished after wash-in of the N-methyl-D-aspartic acid (NMDA)-receptor antagonist D-2-amino-5-phosphonovaleric acid (AP-5). The results provide a possible explanation for the hyperexcitability found in the vicinity of cortical infarcts.

2-Amino-5-phosphonovalerate↗

PubMed1995

Transient forebrain ischemia induces an immediate-early gene encoding the mitogen-activated protein kinase phosphatase 3CH134 in the adult rat brain.

In fibroblasts, serum stimulation has been shown to activate the immediate-early gene 3CH134 encoding a dual specificity protein phosphatase that regulates mitogen-activated protein kinase. We report here that 3CH134 messenger RNA levels increase during recirculation following 30 min forebrain ischemia in the rat brain. In normal rat brains, 3CH134 messenger RNA was found mainly in neurons of the cortex and thalamus. At recirculation periods up to 1 h after 30 min ischemia, 3CH134 messenger RNA increased in neurons and glial cells of all previously ischemic brain regions. After 3 and 6 h recirculation, a prominent increase of 3CH134 messenger RNA was observed in the pyramidal cell layer of all sectors of the hippocampus and the granule cells of the dentate gyrus, whereas in the other brain regions messenger RNA levels returned to control. Up to 6 h of recirculation the spatial induction pattern of 3CH134 was similar to the pattern observed for the immediate-early genes c-fos and c-jun. Within the hippocampus a similar pattern was also observed for the heat shock protein hsp70 messenger RNA. At 12 and 24 h after ischemia, increased levels of 3CH134 messenger RNA persisted in hippocampal neurons; at the same time a delayed increase of 3CH134 messenger RNA was observed in large neurons of the thalamus and in glial cells in damaged regions of the striatum. At later survival periods, 3CH134 messenger RNA returned to control levels. Our study shows that the mitogen-activated protein kinase phosphatase 3CH134 is induced in the brain after a period of global ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1994

Differential expression of the immediate early genes c-fos, c-jun, junB, and NGFI-B in the rat brain following transient forebrain ischemia.

The temporospatial expression pattern of four immediate early genes (IEGs) (c-fos, c-jun, junB, NGFI-B) following 30 min of global ischemia was investigated in rat brains by in situ hybridization and immunohistochemistry (c-fos). All examined IEG mRNAs, as well as Fos-like immunoreactivity, increased transiently in vulnerable and resistant brain regions following ischemia, but the induction profiles were distinct. Ischemia caused a post-ischemic early-onset, transient c-fos induction in wide-spread regions, as well as a late-onset induction restricted to vulnerable regions. Late-onset c-fos induction was observed in the CA1 region and the ventral thalamus but not in the striatum or neocortex, where neurons degenerate at a quicker pace. After recirculation, c-jun mRNA appeared to be initially coinduced with c-fos mRNA, but c-jun mRNA levels remained elevated or increased in various regions, including all vulnerable regions, when c-fos mRNA had already declined to near basal levels. Compared to c-fos and c-jun, junB induction was less pronounced and confined largely to the dentate gyrus. NGFI-B mRNA increased moderately and only in brain regions exhibiting the most dramatic c-fos increases and with similar kinetics. The differential activation of the investigated IEGs suggests that rather complex long-term adaptive processes may be initiated at the genomic level after global ischemia. The present findings provide further evidence that the activation of IEGs forms part of the brain's metabolic response to ischemia, but no simple correlation appears to exist between the induction of the investigated IEGs and the phenomenon of selective vulnerability.

Animals↗