Modification of ion channels and calcium homeostasis of basal forebrain neurons during aging

In this paper we review the last several years of work from our lab with attention to changes in the properties of basal forebrain neurons during aging. These neurons play a central role in behavioral functions, such as: attention, arousal, cognition and autonomic activity, and these functions can b...

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Bibliographic Details
Published in:Behavioural brain research 2000-11, Vol.115 (2), p.219-233
Main Authors: Griffith, William H, Jasek, Mark C, Bain, Stacey H, Murchison, David
Format: Article
Language:English
Subjects:
Aging - physiology
Animals
Basal Ganglia - cytology
Basal Ganglia - physiology
Calcium - physiology
Compensatory mechanisms
Diagonal band
Electrophysiology
GABA
Glutamate
Homeostasis - physiology
Humans
Ion Channels - physiology
Mammalia
Prosencephalon - cytology
Prosencephalon - physiology
Septum
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Summary:In this paper we review the last several years of work from our lab with attention to changes in the properties of basal forebrain neurons during aging. These neurons play a central role in behavioral functions, such as: attention, arousal, cognition and autonomic activity, and these functions can be adversely affected during aging. Therefore, it is fundamental to define the cellular mechanisms of aging in order to understand the basal forebrain and to correct deficits associated with aging. We have examined changes in the physiological properties of basal forebrain neurons during aging with whole-cell and single-channel patch-clamp, as well as, microfluorimetric measurements of intracellular calcium concentrations. These studies contribute to the understanding of integration within the basal forebrain and to the identification of age-related changes within central mammalian neurons. Although extensive functional/behavioral decline is often assumed to occur during aging, our data support an interpretation of compensatory increases in function for excitatory amino acid receptors, GABA A receptors, voltage-gated calcium currents and calcium homeostatic mechanisms. We believe that these changes occur to compensate for decrements accruing with age, such as decreased synaptic contacts, ion imbalances or neuronal loss. The basal forebrain must retain functionality into late aging if senescence is to be productive. Thus, it is critical to recognize the potential cellular and subcellular targets for therapeutic interventions intended to correct age-related behavioral deficits.
ISSN:0166-4328
1872-7549
DOI:10.1016/S0166-4328(00)00260-6