Abstract
Altered neural excitability is considered a prominent contributing factor to cognitive decline during aging. A clear example is the excess neural activity observed in several temporal lobe structures of cognitively impaired older individuals in rodents and humans. At a cellular level, aging-related changes in mechanisms regulating intrinsic excitability have been well examined in pyramidal cells of the CA1 hippocampal subfield. Studies in the inbred Fisher 344 rat strain document an age-related increase in the slow afterhyperpolarization (AHP) that normally occurs after a burst of action potentials, and serves to reduce subsequent firing. We evaluated the status of the AHP in the outbred Long-Evans rat, a well-established model for studying individual differences in neurocognitive aging. In contrast to the findings reported in the Fisher 344 rats, in the Long-Evan rats we detected a selective reduction in AHP in cognitively impaired aged individuals. We discuss plausible scenarios to account for these differences and also discuss possible implications of these differences.
Original language | English (US) |
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Pages (from-to) | 43-48 |
Number of pages | 6 |
Journal | Neurobiology of aging |
Volume | 96 |
DOIs | |
State | Published - Dec 2020 |
Keywords
- Afterhyperpolarization
- CA1
- Cognitive decline
- Current clamp
- Intrinsic excitability
- sAHP
ASJC Scopus subject areas
- General Neuroscience
- Aging
- Developmental Biology
- Clinical Neurology
- Geriatrics and Gerontology