| 1. |
- Lindqvist, Andreas, et al.
(author)
-
High-fat diet impairs hippocampal neurogenesis in male rats.
- 2006
-
In: European Journal of Neurology. - : Wiley. - 1351-5101 .- 1468-1331. ; 13:12, s. 1385-1388
-
Journal article (peer-reviewed)abstract
- High fat diets and obesity pose serious health problems, such as type II diabetes and cardiovascular disease. Impaired cognitive function is also associated with high fat intake. In this study, we show that just 4 weeks of feeding a diet rich in fat ad libitum decreased hippocampal neurogenesis in male, but not female, rats. There was no obesity, but male rats fed a diet rich in fat exhibited elevated serum corticosterone levels compared with those fed standard rat chow. These data indicate that high dietary fat intake can disrupt hippocampal neurogenesis, probably through an increase in serum corticosterone levels, and that males are more susceptible than females.
|
|
| 2. |
- Mohapel, Paul, et al.
(author)
-
Working memory training decreases hippocampal neurogenesis.
- 2006
-
In: Neuroscience. - : Elsevier BV. - 1873-7544 .- 0306-4522. ; 142:3, s. 609-613
-
Journal article (peer-reviewed)abstract
- The relationship between adult hippocampal neurogenesis and cognition appears more complex than suggested by early reports. We aimed to determine if the duration and task demands of spatial memory training differentially affect hippocampal neurogenesis. Adult male rats were trained in the Morris water maze in a reference memory task for 4 days, or alternatively working memory for either 4 or 14 days. Four days of maze training did not impact neurogenesis regardless of whether reference or working memory paradigms were used. Interestingly, 2 weeks of working memory training using a hidden platform resulted in fewer newborn hippocampal neurons compared with controls that received either cue training or no maze exposure. Stress is a well-established negative regulator of hippocampal neurogenesis. We found that maze training in general, and a working memory task in particular, increased levels of circulating corticosterone after 4 days of training. Our study indicates that working memory training over a prolonged period of time reduces neurogenesis, and this reduction may partially be mediated by increased stress.
|
|
| 3. |
- Westin, Jenny, et al.
(author)
-
Endothelial proliferation and increased blood-brain barrier permeability in the basal ganglia in a rat model of 3,4-dihydroxyphenyl-L-alanine-induced dyskinesia.
- 2006
-
In: JNeurosci. - 1529-2401. ; 26:37, s. 9448-9461
-
Journal article (peer-reviewed)abstract
- 3,4-Dihydroxyphenyl-(L)-alanine ((L)-DOPA)-induced dyskinesia is associated with molecular and synaptic plasticity in the basal ganglia, but the occurrence of structural remodeling through cell genesis has not been explored. In this study, rats with 6-hydroxydopamine lesions received injections of the thymidine analog 5-bromo-2'-deoxyuridine (BrdU) concomitantly with (L)-DOPA for 2 weeks. A large number of BrdU-positive cells were found in the striatum and its output structures (globus pallidus, entopeduncular nucleus, and substantia nigra pars reticulata) in (L)-DOPA-treated rats that had developed dyskinesia. The vast majority (60-80%) of the newborn cells stained positively for endothelial markers. This endothelial proliferation was associated with an upregulation of immature endothelial markers (nestin) and a downregulation of endothelial barrier antigen on blood vessel walls. In addition, dyskinetic rats exhibited a significant increase in total blood vessel length and a visible extravasation of serum albumin in the two structures in which endothelial proliferation was most pronounced (substantia nigra pars reticulata and entopeduncular nucleus). The present study provides the first evidence of angiogenesis and blood-brain barrier dysfunction in an experimental model of (L)-DOPA-induced dyskinesia. These microvascular changes are likely to affect the kinetics of (L)-DOPA entry into the brain, favoring the occurrence of motor complications.
|
|
