| 1. |
|
|
| 2. |
- Arvidsson, Andreas, et al.
(författare)
-
Stroke induces widespread changes of gene expression for glial cell line-derived neurotrophic factor family receptors in the adult rat brain
- 2001
-
Ingår i: Neuroscience. - 1873-7544. ; 106:1, s. 27-41
-
Tidskriftsartikel (refereegranskat)abstract
- Gene expression for glial cell line-derived neurotrophic factor (GDNF) family ligands and receptors was analyzed with in situ hybridization after two focal ischemic insults of different severities. Focal ischemia was induced in rats by either 30 min or 2 h of middle cerebral artery occlusion (MCAO), causing damage to the striatum only, or involving also the parietal cortex, respectively. We found modest, transient elevation of GDNF mRNA in the dentate granule cell layer. In addition, the number of GDNF mRNA-expressing cells increased in the cortex and striatum after 2 h or 30 min of MCAO, respectively. No changes of neurturin or persephin mRNA expression were detected. Both c-Ret and GFRalpha1 mRNA levels were markedly increased in the ipsilateral cortex outside the ischemic lesion at 6-24 h after the 2-h insult, whereas GFRalpha2 expression was decreased in cortical areas both within and outside the lesion. Similar increases of c-Ret and GFRalpha1 mRNA levels were detected in the striatum, and to a lesser extent, in the cortex following 30 min of MCAO. The 2-h insult also gave rise to transient increases of c-Ret and GFRalpha1 mRNA in hippocampal subregions. Thirty minutes and 2 h of MCAO lead to elevated c-Ret, and GFRalpha1 or GFRalpha2 mRNA expression, respectively, in the ipsilateral ventroposterolateral thalamic nucleus. Both insults induced increased levels of GFRalpha1 mRNA in the subventricular zone of the lateral ventricle.Our data indicate major changes of GDNF family signaling in the forebrain, regulated mainly through altered receptor levels, in the post-ischemic phase. These changes could enhance neuroprotective and neuroregenerative responses both to endogenous and exogenous GDNF ligands.
|
|
| 3. |
- Collins, A., et al.
(författare)
-
Interference elimination in glutamate monitoring with chip integrated enzyme microreactors
- 2001
-
Ingår i: Electroanalysis. - 1040-0397. ; 13:6, s. 425-431
-
Tidskriftsartikel (refereegranskat)abstract
- On-chip enzyme reactors are often used in medical/pharmaceutical analysis due to their inherent advantages, such as high sample throughput, low reagent consumption, stability, reproducibility and low cost. The present work describes a different application of such microreactors, namely, elimination of interfering ascorbate signals in glutamate monitoring using ascorbate oxidase modified silicon chip microreactors of different sizes (5.3 and 0.95 muL). Glutamate was monitored with a previously developed redox hydrogel integrated bienzyme electrode, based on coupled glutamate oxidase and horseradish peroxidase, inserted in a miniaturized flow cell operated at -50 mV (vs. Ag/AgCl). The developed on-line analysis system was characterized with regard to dilution effects, detection limit, response time and interference ability using model solutions and real samples. Off-line in vivo glutamate measurements could be made by injecting rat brain microdialysate samples collected before and after KCl stimulation without any interference of ascorbate, I Within the studied flow rate range (2-25 muL/min), 1 mM and 200 muM ascorbate could he totally eliminated using the larger and the mailer microreactor, respectively.
|
|
| 4. |
- Rivera, C, et al.
(författare)
-
BDNF-induced TrkB activation down-regulates the K+-Cl- cotransporter KCC2 and impairs neuronal Cl- extrusion
- 2002
-
Ingår i: Journal of Cell Biology. - : Rockefeller University Press. - 0021-9525 .- 1540-8140. ; 159:5, s. 747-752
-
Tidskriftsartikel (refereegranskat)abstract
- Pathophysiological activity and various kinds of traumatic insults are known to have deleterious long-term effects on neuronal Cl- regulation, which can lead to a suppression of fast postsynaptic GABAergic responses. Brain-derived neurotrophic factor (BDNF) increases neuronal excitability through a conjunction of mechanisms that include regulation of the efficacy of GABAergic transmission. Here, we show that exposure of rat hippocampal slice cultures and acute slices to exogenous BDNF or neurotrophin-4 produces a TrkB-mediated fall in the neuron-specific K+-Cl- cotransporter KCC2 mRNA and protein, as well as a consequent impairment in neuronal Cl- extrusion capacity. After kindling-induced seizures in vivo, the expression of KCC2 is down-regulated in the mouse hippocampus with a spatio-temporal profile complementary to the up-regulation of TrkB and BDNF. The present data demonstrate a novel mechanism whereby BDNF/TrkB signaling suppresses chloride-dependent fast GABAergic inhibition, which most likely contributes to the well-known role of TrkB-activated signaling cascades in the induction and establishment of epileptic activity.
|
|
| 5. |
|
|
