Additionally, most researches have concentrated broadly on amyloid- deposits and neurofibrillary pathology in AD, while neuronal loss has been more difficult to assess. A common way for a large number of degenerative routes in AD is the neuronal loss and may be prompted by some factors, such as perturbed calcium regulation, inflammatory routes or oxidative stress, ischemia, amyloid- plaques and glutamate. The chronic systemic treatment with scopolamine significantly disrupted cell proliferation, differentiation and maturation, especially, impaired the dendrite maturation and complexity of neuronal progenitor cells in the mouse hippocampal dentate gyrus (DG). Moreover, scopolamine directly caused damage to the hippocampal circuits that might predominantly be responsible for cognitive and memory deficits. Also, scopolamine reduced dose-dependently the number of M1 muscarinic receptor-immunoreactive (ir) neurons in the male rats’ hippocampus. The post-training scopolamine dose-dependently decreased the step-through latency in the inhibitory avoidance task it shows scopolamine-induced amnesia. Scopolamine is well known for interfering with the methods of learning acquisition, memory performance and short-term memory in animals and humans. Previous studies reported the precognitive effects of M1 muscarinic receptor activators and have used models in which the cholinergic function is damaged with scopolamine, a non-selective muscarinic receptor antagonist. Because M1 muscarinic receptor plays a critical role in memory and is closely linked with AD, it has long been guessed as a target for therapy. Cognitive deficits and damage in long-term potentiation were shown in M1 muscarinic receptor-knockout mice, indicating that this receptor is physiologically related to multiple roles such as neuronal excitability, synaptic plasticity, and differentiation of neurons during early development, and memory. Indeed, M1 muscarinic receptors are highly concentrated in the brain areas related to Alzheimer’s disease (AD) but less in the periphery. So far, five muscarinic acetylcholine receptor subtypes (M1-M5) have been known and among them, the M1 subtype makes up more than a half of the total and mainly exists in all major zones of the forebrain, such as the cortex, the hippocampal formation, corpus striatum of basal nuclei, and thalamus. One kind of G-protein coupled receptors is muscarinic acetylcholine receptors.
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