| 1. |
- Abbas, Abdul-Karim, 1959, et al.
(författare)
-
Emetine treatment masks initial LTP without affecting long-term stability.
- 2011
-
Ingår i: Brain research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; 1426, s. 18-29
-
Tidskriftsartikel (refereegranskat)abstract
- Applying emetine, a protein synthesis inhibitor, at 20-40μM for 90-120min prior to LTP induction in hippocampal slices from young rats (2-3weeks) and washing it out afterwards revealed a slowly developing potentiation that reached maximum after 20-30min, distinct from the LTP observed under normal conditions. Nevertheless, the later phase of this potentiation was similar to standard LTP as judged by experiments lasting up to 8h after induction. Emetine preapplication for 3h without subsequent washout resulted in a substantial decay of evoked responses. By comparison between test and control pathways, LTP could still be assessed in these experiments for up to 4-6h after induction and was found not to differ from normal, except for the slow onset. The NMDA-R blocker AP5 fully blocked LTP; however, with emetine pretreatment there was an initial depression of responses with a gradual recovery during 20-30min. This depression involved not only the field EPSP but also the presynaptic fiber volley. However, when using the protein synthesis inhibitors cycloheximide and anisomycin there was essentially no such depression. In conclusion, the present results support the idea that preexisting proteins are sufficient for inducing stable LTP. Moreover, emetine but not anisomycin or cycloheximide impairs presynaptic action potentials, leading to an apparent slow onset of LTP. The emetine-dependent effect could be due to a characteristic blocking spectrum of the drug, preferred targeting of presynaptic compartments or effects unrelated to protein synthesis.
|
|
| 2. |
|
|
| 3. |
|
|
| 4. |
|
|
| 5. |
- Ansar, Saema, et al.
(författare)
-
Subarachnoid Hemorrhage Induces Enhanced Expression of Thromboxane A(2) Receptors in Rat Cerebral Arteries.
- 2010
-
Ingår i: Brain Research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; 1316, s. 163-172
-
Tidskriftsartikel (refereegranskat)abstract
- Cerebral ischemia remains the key cause of morbidity and mortality after subarachnoid hemorrhage (SAH) with a pathogenesis that is still poorly understood. The aim of the present study was to examine the involvement of thromboxane A(2) receptors (TP) in the patophysiology of cerebral ischemia after SAH in cerebral arteries. SAH was induced in rats by injecting 250 microl blood into the prechiasmatic cistern. Two days after the SAH, cerebral arteries were harvested and contractile responses to the TP receptor agonist U46619 were investigated with myographs. In addition, the contractile responses were examined after pretreatment with selective TP receptor antagonist GR3219b. The TP receptor RNA and protein levels were analyzed by quantitative real-time PCR and immunohistochemistry, respectively. The global and regional cerebral blood flows (CBF) were quantified with an autoradiographic technique. SAH resulted in enhanced contractile responses to U46619 as compared to sham. The TP receptor antagonist GR3219b abolished the enhanced contractile responses to U46619 observed after SAH. The TP receptor mRNA level was elevated after SAH as compared to sham. The level of TP receptor protein on the smooth muscle cells (SMC) was increased in SAH compared to sham, Global and regional CBF was reduced in SAH as compared to sham. The results demonstrate that SAH results in CBF reduction and this is associated with enhanced expression of TP receptors in the SMC of cerebral arteries and microvessels.
|
|
| 6. |
- Asser, Andres, et al.
(författare)
-
Increased striatal VMAT2 binding in mice after chronic administration of methcathinone and manganese
- 2016
-
Ingår i: Brain Research. - : Elsevier BV. - 0006-8993 .- 1872-6240. ; 1652, s. 97-102
-
Tidskriftsartikel (refereegranskat)abstract
- Intravenous use of a psychostimulant drug containing methcathinone (ephedrone) and manganese causes an irreversible extrapyramidal syndrome in drug abusers. We aimed to reproduce the syndrome in mice to evaluate dopaminergic damage. C57/B6 mice were intraperitoneally injected once a day with the study drug or saline for a period of 27 weeks. Motor activity was recorded in an automated motility-box. After 13 and 27 weeks of treatment, ex vivo digital autoradiography was performed using [C-11]dihydrotetrabenazine ([C-11]DTBZ). After 27 weeks of treatment [C-11]DTBZ autoradiography demonstrated a significant increase in the striatum to -cerebellum binding ratio compared with saline treated controls. At the same time point, there was no evident change in motor activity. Increased [C-11]DTBZ binding may indicate vesicular monoamine transporter type 2 (VMAT2) function is altered. The lack of extrapyramidal symptoms in animals could be attributed to low dosing regimen or high metabolic rate.
|
|
| 7. |
- Atis, Muge, et al.
(författare)
-
Effects of methyl-beta-cyclodextrin on blood-brain barrier permeability in angiotensin II-induced hypertensive rats
- 2019
-
Ingår i: Brain Research. - : ELSEVIER SCIENCE BV. - 0006-8993 .- 1872-6240. ; 1715, s. 148-155
-
Tidskriftsartikel (refereegranskat)abstract
- The blood-brain barrier (BBB) permeability primarily increases in cerebral venules during acute hypertension. Methyl-beta-cyclodextrin (M beta CD), a cholesterol-depleting agent, decreases the expression of caveolins disrupting caveolar structures. We aimed to determine the effects of M beta CD on the BBB permeability of angiotensin (ANG) II-induced hypertensive rats. Three minutes after M beta CD administration (5 mg/kg), acute hypertension was induced by ANG II (60 mu g/kg). Evans blue (EB) and horseradish peroxidase (HRP) tracers were used to assess BBB permeability. Immunohistochemistry for caveolin (Cav)-1 and tight junction protein claudin-5 was performed. EB dye content significantly increased in both cerebral cortices and left hippocampus in M beta CD (P < 0.05), right cerebral cortex and both hippocampi in ANG II (P < 0.05; P < 0.01), and both cerebral cortices and hippocampi in M beta CD plus ANG II groups compared with controls (P < 0.05; P < 0.01). A significant decrease in claudin-5 immunostaining intensity was observed in animals treated with M beta CD compared with controls (P < 0.05). Cav-1 immunostaining intensity increased in ANG II group (P < 0.05). Ultrastructurally, HRP reaction products were observed in endothelial cells of the microvessels in the hippocampus region in M beta CD group while the tracer was mainly localized in astrocytes and neurons in ANG II, and M beta CD plus ANG II groups. The endothelial cells of the venules in the cerebral cortex of the animals in the latter experimental groups also showed an abundance of caveolar vesicles devoid of HRP reaction products. Our results revealed that M beta CD did not provide overall protective effects on BBB integrity in acute hypertension and even led to BBB disruption in normotensive animals.
|
|
| 8. |
- Bagheri, Maryam, et al.
(författare)
-
Genistein inhibits aggregation of exogenous amyloid-beta(1-40) and alleviates astrogliosis in the hippocampus of rats
- 2012
-
Ingår i: Brain Research. - : Elsevier. - 0006-8993 .- 1872-6240. ; 1429, s. 145-154
-
Tidskriftsartikel (refereegranskat)abstract
- We addressed the question of whether injection of Amyloid beta (Aβ)(1-40) in the rat brain is associated with pathology in the hippocampus, and if genistein has any protective effect against the neuronal damage caused by Aβ(1-40). Genistein is a plant-derived compound with a structure similar to that of the female sex hormone estrogen and it was recently shown that pretreatment with a single dose of genistein ameliorated learning and memory deficits in an (Aβ)(1-40) rat model of Alzheimer's disease. Here, we report that injection of the amyloid peptide into the hippocampus of rats led to formation of Aβ(1-40) positive aggregates close to the lateral blade of the dentate gyrus (DGlb). We also observed the following in the hippocampus: extensive cell death in the DGlb (P<0.0001), CA1 (P=0.03), and CA3 (P=0.002); an increased number of iNOS-expressing cells (P=0.01) and gliosis. Genistein given to rats by gavage 1h before injection of Aβ(1-40) inhibited the formation of Aβ(1-40) positive aggregates in the brain tissue and led to increased number of nNOS(+) (P=0.0001) cells in the hippocampus compared to sham-operated genistein-treated controls. Treatment with genistein also alleviated the extensive astrogliosis that occurred in Aβ(1-40)-injected hippocampus to a level similar to that observed in sham-operated rats. We conclude that the neurons in the DGlb are most sensitive to Aβ(1-40), and a single dose of genistein can ameliorate Aβ(1-40) induced pathology.
|
|
| 9. |
- Bergamino, Maurizio, et al.
(författare)
-
Statistical differences in the white matter tracts in subjects with depression by using different skeletonized voxel-wise analysis approaches and DTI fitting procedures
- 2017
-
Ingår i: Brain Research. - : Elsevier. - 0006-8993 .- 1872-6240. ; 1669, s. 131-140
-
Tidskriftsartikel (refereegranskat)abstract
- Major depressive disorder (MDD) is one of the most significant contributors to the global burden of illness. Diffusion tensor imaging (DTI) is a procedure that has been used in several studies to characterize abnormalities in white matter (WM) microstructural integrity in MDD. These studies, however, have provided divergent findings, potentially due to the large variety of methodological alternatives available in conducting DTI research. In order to determine the importance of different approaches to coregistration of DTI-derived metrics to a standard space, we compared results from two different skeletonized voxel-wise analysis approaches: the standard TBBS pipeline and the Advanced Normalization Tools (ANTs) approach incorporating a symmetric image normalization (SyN) algorithm and a group-wise template (ANTs TBSS). We also assessed effects of applying twelve different fitting procedures for the diffusion tensor. For our dataset, lower fractional anisotropy (FA) and axial diffusivity (AD) in depressed subjects compared with healthy controls were found for both methods and for all fitting procedures. No group differences were found for radial and mean diffusivity indices. Importantly, for the AD metric, the normalization methods and fitting procedures showed reliable differences, both in the volume and in the number of significant between-groups difference clusters detected. Additionally, a significant voxel-based correlation, in the left inferior fronto-occipital fasciculus, between AD and self-reported stress was found only for one of the normalization procedure (ANTs TBSS). In conclusion, the sensitivity to detect group-level effects on DTI metrics might depend on the DTI normalization and/or tensor fitting procedures used.
|
|
| 10. |
- Bjartmar, Lisa, 1966-, et al.
(författare)
-
Long-term treatment with antidepressants, but not environmental stimulation, induces expression of NP2 mRNA in hippocampus and medial habenula
- 2010
-
Ingår i: Brain Research. - : Elsevier. - 0006-8993 .- 1872-6240. ; 1328, s. 24-33
-
Tidskriftsartikel (refereegranskat)abstract
- Neuronal Pentraxin 2 (NP2, Narp), known to mediate clustering of glutamatergic AMPA receptors at synapses, is involved in activity-dependent synaptogenesis and synaptic plasticity. In experimental settings, antidepressant treatment as well as a stimulating environment has a positive influence on cognition and hippocampal plasticity. This study demonstrates that NP2 mRNA is robustly expressed in the hippocampus and the medial habenula (MHb), both regions implicated in cognitive functions. Furthermore, NP2 mRNA expression is enhanced in the hippocampal subregions as well as in the MHb after long-term treatment with antidepressant drugs of various monoaminergic profiles, indicating a common mode of action of different antidepressant drugs. This effect occurs at the time frame where clinical response is normally achieved. In contrast, neither environmental enrichment nor deprivation has any influence on long-term NP2 mRNA expression. These findings support an involvement of NP2 in the pathway of antidepressant induced plasticity, but not EE induced plasticity; that NP2 might constitute a common link for the action of different types of antidepressant drugs and that the MHb could be a putative region for further studies of NP2.
|
|
