ABSTRACT
Objective To establish a Alzheimer dementia(AD) model in mice. Methods The C57BL/6 mice were lesioned with ibotenic acid in Nucleus basalis of Meynert(NBM). Behavioral tests by eight-arm radial maze were conducted 8 weeks, and immunohistochemical staining of choline acetyltransferase(ChAT), serotonin(5-HT), GAD(GABA), amyloid-?protein (AP) was conducted 12 weeks after NBM lesioning. Results In NBM lesioned mice, the ChAT-positive neurons, serotonin-positive neurons, and GAD-positive neurons in right NBM reduced, and ChAT-positive neurons reduced most evidently. At the same time, the ChAT-positive fibers in prefrontal and parietal cortices decreased significantly, serotonin-positive axons slightly, accompanied by heavily AP co-expression. On the contrary, there was no change of GAD-positive neurons in cortex. The working memory error increased significantly.Conclusion Ibotenic acid lesioning in NBM can provide as a model of AD in that it produces deafferentation of cholinergic system and recent memory disruption.
ABSTRACT
The present study was performed to explore the role of corticotropin releasing factor (CRF) in the nucleus basalis of Meynert (NBM) in spatial learning and memory of rats. The latency, distance and swimming path to find the platform were measured by Morris water maze after intra-NBM injections of 0, 0.01, 0.1 and 0.4 nmol of CRF. Intra-NBM injections of 0.1 or 0.4 nmol of CRF induced significant increase of the latency for spatial learning and memory, and there were no significant changes in the swimming speed in Morris water maze test. The results suggest that CRF plays an inhibitory role in spatial learning and memory consolidation in the NBM of rats.
ABSTRACT
Several lines of evidence show that decreased metabolic rate precedes cognitive impairment in Alzheimer s disease (AD). Decreased neuronal metabolism contributes to neuronal atrophy and functional impairment and is thus an early occurring hallmark of AD. Factors that may contribute to a diminishment in neuronal metabolism are age, sex, APOE-ε 4 and decreased levels of sex hormones or melatonin. Several observations in postmortem brain indicate that activated neurons are better able to withstand aging and AD, a phenomenon we paraphrased as use it or lose it. Moreover, a number of pharmacological and non-pharmacological studies support the concept that activation of the brain has beneficial effects and may to a certain degree restore several aspects of cognition and other central functions. For instance, the circadian system of Alzheimer patients may be restimulated by exposing them to more light or transcutaneous nerve stimulation. A procedure allowing testing of the efficacy of putative stimulatory compounds such as neurotrophins and precursor cells has been developed in order to be able to culture human postmortem brain tissue.
Subject(s)
Alzheimer Disease , Apoenzymes , Atrophy , Basal Nucleus of Meynert , Nerve Degeneration , Neurology , Neurons , Receptor, trkA , Suprachiasmatic NucleusABSTRACT
Objective To observe the age-related changes of brain-derived neurotrophic factor(BDNF) and investigate the effects of ginsenosides(GS) on BDNF in nucleus basalis of Meynert(NBM) and cerebral cortex of aged rats. Methods Twenty-four female Wistar rats were randomly divided into 3 groups: young group(3-5 months),aged groups(27 months) and GS group(27 months).GS group was fed with GS from 18 to 27 months.Immunohistochemistry and Imaging analysis were used to show the expression and distribution of BDNF in NBM and cerebral cortex of each group. Results BDNF level of aged group was much lower than that of young group in these two brain areas(P