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- Abbas, Abdul-Karim, 1959, et al.
(author)
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Emetine treatment masks initial LTP without affecting long-term stability.
- 2011
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In: Brain research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; 1426, s. 18-29
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Journal article (peer-reviewed)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.
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| 5. |
- Allard, Per, et al.
(author)
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[3H]WIN 35,428 binding in the human brain.
- 1996
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In: Brain Research. - 0006-8993 .- 1872-6240. ; 706:2, s. 347-50
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Journal article (peer-reviewed)abstract
- The binding of [3H]WIN 35,428 was studied in post-mortem human brain, including extrastriatal regions. In the putamen, dopamine almost completely inhibited the [3H]WIN 35,428 binding. Paroxetine inhibited the binding with similar affinity as cocaine, in the range 200-300 nM. In the frontal cortex, [3H]WIN 35,428 labelled cocaine- and alaproclate sensitive binding sites, of which a major fraction was of protein nature. The elucidation of the cocaine sensitive sites in the frontal cortex should be the subject of further research.
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| 6. |
- Allard, Per, et al.
(author)
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Dopamine uptake sites in Parkinson's disease and in dementia of the Alzheimer type.
- 1994
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In: Brain Research. - 0006-8993 .- 1872-6240. ; 637:1-2, s. 262-6
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Journal article (peer-reviewed)abstract
- The binding of [3H]GBR-12935 to dopamine (DA) uptake sites was studied in post-mortem putamen from a control group and from patients with Parkinson's disease (PD) or dementia of the Alzheimer type (DAT). The specific binding (Bmax) was almost completely abolished in the PD group and reduced by 65% in the DAT group. There were no significant differences in apparent binding affinity (Kd) between the DAT group and controls. The decreases in [3H]GBR-12935 binding to DA uptake sites in this study indicate a marked degeneration of DA neurites in the putamen in PD and also in DAT.
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| 7. |
- Andersson, Claes, et al.
(author)
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Intervention for hazardous alcohol use and high level of stress in university freshmen A comparison between an intervention and a control University.
- 2009
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In: Brain Research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; Aug 20, s. 61-71
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Journal article (peer-reviewed)abstract
- BACKGROUND: The first year of university studies is associated with increased levels of alcohol drinking and stress. This study examines the one-year outcome of both primary and secondary interventions of one alcohol programme and one stress intervention programme at an intervention university in comparison with a control university. METHODS: At the intervention university all freshmen were offered a primary prevention programme for hazardous alcohol use and stress management and, in addition, those who had high ratings for stress and/or hazardous alcohol use were offered a secondary intervention programme for alcohol consumption and/or stress management. Freshmen still attending the two universities one year later responded to follow-up questionnaires. RESULTS: The primary alcohol and stress interventions were associated with lower alcohol expectancies and mental symptoms, but no differences in AUDIT scores (-0.2, CI 95% -0.5 to 0.1), estimated blood alcohol concentrations or stress in comparison to freshmen at the control university. The secondary alcohol interventions were associated with decreased AUDIT (-1.1, CI 95% -2.0 to -0.2) as well as alcohol expectancies, blood alcohol concentrations, stress and mental symptoms in comparison to high-risk freshmen at the control university. The secondary stress interventions were associated with decreased mental symptoms and alcohol expectancies, but not stress, AUDIT scores (-0.6, CI 95% -1.4 to 0.2) and blood alcohol concentrations in comparison to high-risk freshmen at the control university. CONCLUSION: This study suggests that both primary and secondary alcohol and stress interventions have 1-year effects in university freshmen and could be implemented in university settings.
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| 8. |
- Andin, Josefine, 1979-, et al.
(author)
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Influence of environmental enrichment on steady-state mRNA levels for EAAC1, AMPA1 and NMDA2A receptor subunits in rat hippocampus
- 2007
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In: Brain Research. - : Elsevier BV. - 0006-8993 .- 1872-6240. ; 1174:1, s. 18-27
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Journal article (peer-reviewed)abstract
- Interaction with the environment has a key role in refining the neuronal circuitry required for normal brain function throughout life. Profound effects of enriched environment have been shown on neuronal structure and chemistry in experimental animals. Epidemiological studies imply that this is true also in man, thus cognitive stimulation has a protective effect on neurodegeneration, e.g., in Alzheimer's disease. Glutamatergic pathways are imperative for cognitive functions, such as memory, learning and long-term potentiation, and relies on the AMPA and NMDA glutamate receptors and the hippocampus, with its specific subregions, is an important anatomical substrate in this. The glutamate signalling is also dependent on a fine-tuned transport system, in the hippocampus primarily achieved by the glutamate transporter EAAC1. In this study we show how environmental enrichment modulates these parts of the glutamatergic system using quantitative in situ hybridisation. This work demonstrates for the first time that environmental enrichment modulates the mRNA expression of EAAC1 which is significantly and region specifically decreased in the hippocampus. We also provide evidence for regional and hemisphere-specific upregulation of NMDA mRNA in the hippocampus after environmental enrichment. The current work also shows that AMPA mRNA of the hippocampus is not per se changed by environmental enrichment in adult animals. Taken together, our results extend the knowledge of the glutamatergic system of specific regions of the hippocampus and its modulation by environmental enrichment and could contribute to the development of strategies aimed at limiting pathological changes associated with glutamatergic dysfunctions. © 2007.
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| 9. |
- Ansar, Saema, et al.
(author)
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Subarachnoid Hemorrhage Induces Enhanced Expression of Thromboxane A(2) Receptors in Rat Cerebral Arteries.
- 2010
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In: Brain Research. - : Elsevier BV. - 1872-6240 .- 0006-8993. ; 1316, s. 163-172
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Journal article (peer-reviewed)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.
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