In vivo and in vitro studies central cholinergic nervous system in the role and mechanism of the formation of vascular dementia (VaD) cognitive dysfunction . VaD model rat basal forebrain ischemic irreversible pathological changes under in vivo conditions , the development over time , cholinergic neuronal injury , nicotinic acetylcholine receptor the largest combined with volume reduction , cAMP response element binding protein . (CREB) phosphorylation of the lower level as well as the VaD rat learning and memory ability , application cholinesterase inhibitors can improve learning and memory in rats ; vitro hypoxia under experimental conditions , primary cultured hippocampal neurons CREB phosphorylation levels decreased and shorten the length of the protrusions , application of muscarinic and nicotinic acetylcholine receptor agonist , can improve the level of CREB phosphorylation and neurite length . Accordingly, we believe that chronic cerebral hypoperfusion central cholinergic neuronal damage, decline in ability to synthesis of acetylcholine molecules , the decrease in the number of receptors in the postsynaptic receptor subtype signal transduction pathway dysfunction , resulting in CREB phosphorylation levels reduce , thereby affecting synaptic plasticity and the formation of the neural network , which eventually led VaD cognitive dysfunction .
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