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Updated: Sep 20, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology
Published on: March 23, 2011
Effects of cholinergic depletion on evoked activity in the cortex of young and aged rats
P Herron1, Z Li, J B Schweitzer
1Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163, USA. pherron@utmeml.utmem.edu
Abstract:
Degeneration of cholinergic neurons in the basal forebrain is a neural marker of Alzheimer's disease and is associated with perceptual and cognitive deficits. An idea that has attracted scientific scutiny is that aging makes the brain more susceptible to neurodegenerative diseases such as Alzheimer's. The purpose of this study was to compare the effects of the loss of cholinergic input from nucleus basalis of Meynert on evoked activity in the posteromedial barrel subfield of the somatosensory cortex in young (2-2.5 months) and aged (28-30 months) male Fisher hybrid rats. The mean firing rate and receptive fields of single neurons in the posteromedial barrel subfield of the somatosensory cortex were examined after selective lesions of cholinergic neurons in the nucleus basalis of Meynert with an immunotoxin. IgG 192-saporin. Functional properties of single neurons in young animals were affected much more significantly by cholinergic depletion than those in aged animals. In cholinergic-depleted young animals, the mean firing rate of evoked activity and receptive field of posteromedial barrel subfield neurons were significantly decreased. Cholinergic depletion caused a 14% decrease in evoked activity and a 33% increase in receptive field size in young animals. The mean firing rate and receptive field of single neurons were not affected by cholinergic depletion in aged animals. It is concluded that functional properties of cortical sensory neurons in young animals are more vulnerable to cholinergic depletion than are those of aged animals and that cholinergic depletion does not further impact the properties of neurons exposed to the processes of aging.
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