Journal
JOURNAL OF NEUROSCIENCE
Volume 29, Issue 15, Pages 4750-4755Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0384-09.2009
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Funding
- National Institutes of Health [F31 NS053434, R37 AG08796]
- Northwestern University
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Normal aging is usually accompanied by increased difficulty learning new information. One contributor to aging-related cognitive decline is decreased intrinsic excitability in aged neurons, leading to more difficulty processing inputs and remodeling synapses to store new memories. Two measures of excitability known to be altered by learning are the slow afterhyperpolarization (sAHP) after a burst of action potentials and the fast AHP (fAHP) after individual action potentials. Using rats trained in trace eyeblink conditioning, we examined how these two measures of excitability were modulated in CA1 hippocampal neurons from young (3-4 months) and aged (29-31 months) animals. Although both the sAHP and the fAHP were reduced by successful learning in both age groups, only the sAHP showed aging-related increases. The dichotomy of learning-related and aging-related effects on two very similar calcium-dependent potassium-driven hyperpolarizations suggests several interesting hypotheses for how cellular excitability is modulated by aging and learning.
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