High levels of Aβ impair neuronal function at least in part by disrupting normal synaptic transmission and causing dysfunction of neural networks. This network dysfunction includes abnormal synchronization of neuronal activity resulting in epileptiform activity. Over time, this aberrant network activity can lead to the depletion of calcium-dependent proteins, such as calbindin, Fos, and Arc, and compensatory inhibitory remodeling of hippocampal circuits, including GABAergic sprouting and ectopic expression of the inhibitory neuropeptide Y (NPY) in dentate granule cells. Here we present detailed protocols for detecting and quantifying these alterations in mouse models of Alzheimer’s disease (AD) by immunohistochemistry. These methods are useful as surrogate measures for detecting chronic aberrant network activity in models of AD and epilepsy. In addition, since we have found that the severity of these changes relates to the degree of Aβ-dependent cognitive impairments, the protocols are useful for quantifying biomarkers of cognitive impairment in mouse models of AD.

Expression of herpes simplex virus 1 glycoprotein B in human cells and protection of mice against lethal herpes simplex virus 1 infection

MANSERVIGI, Roberto;NEGRINI, Massimo;BARBANTI BRODANO, Giuseppe
1989

Abstract

High levels of Aβ impair neuronal function at least in part by disrupting normal synaptic transmission and causing dysfunction of neural networks. This network dysfunction includes abnormal synchronization of neuronal activity resulting in epileptiform activity. Over time, this aberrant network activity can lead to the depletion of calcium-dependent proteins, such as calbindin, Fos, and Arc, and compensatory inhibitory remodeling of hippocampal circuits, including GABAergic sprouting and ectopic expression of the inhibitory neuropeptide Y (NPY) in dentate granule cells. Here we present detailed protocols for detecting and quantifying these alterations in mouse models of Alzheimer’s disease (AD) by immunohistochemistry. These methods are useful as surrogate measures for detecting chronic aberrant network activity in models of AD and epilepsy. In addition, since we have found that the severity of these changes relates to the degree of Aβ-dependent cognitive impairments, the protocols are useful for quantifying biomarkers of cognitive impairment in mouse models of AD.
1989
0-306-43360-5
Hippocampus, Dentate gyrus, Granule cell, Mossy fiber, Hilus, Neuropeptide Y, NPY, Calbindin, Seizure, Epilepsy, Excitability, GABA, GABAergic sprouting, Ectopic expression, Excitatory, Inhibitory ,Immunohistochemistry, Aβ, Alzheimer’s disease, Biomarkers, Immediate early gene, Fos, Arc, Neuronal activity
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/522843
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