Reduced potassium currents in old rat CA1 hippocampal neurons
Potassium currents are an important factor in repolarizing the membrane potential and determining the level of neuronal excitability. We compared potassium currents in CA1 hippocampal neurons dissociated from young (2–3 months old) and old (26–30 months old) Sprague–Dawley rats. Whole‐cell patch‐cla...
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Veröffentlicht in: | Journal of neuroscience research 2001-01, Vol.63 (2), p.176-184 |
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Zusammenfassung: | Potassium currents are an important factor in repolarizing the membrane potential and determining the level of neuronal excitability. We compared potassium currents in CA1 hippocampal neurons dissociated from young (2–3 months old) and old (26–30 months old) Sprague–Dawley rats. Whole‐cell patch‐clamp techniques were used to measure the delayed rectifier (sustained) and the A‐type (transient) potassium currents. The delayed rectifier current was smaller in old (548 ± 57 pA) than in young (1193 ± 171 pA) neurons. In the absence of extracellular calcium, the delayed rectifier current was also smaller in old (427 ± 41 pA) than in young (946 ± 144 pA) neurons. The cell membrane capacitance was unchanged in old (13.3 ± 1.2 pF) compared to young (13.6 ± 1.2 pF). Therefore, the reduction in the delayed rectifier current was not due to a change in membrane surface area. Moreover, activation and inactivation of the delayed rectifier current were unchanged in old compared to young neurons. The slope of the current‐voltage relation, however, was smaller in old (B = 5.03) than in young (B = 9.62) neurons. Similarly, the A‐current was smaller in old (100 ± 16 pA) than in young (210 ± 44 pA) neurons in the presence of extracellular calcium. This reduction of potassium currents could account for the prolongation of action potentials reported previously for old rat CA1 hippocampal neurons. The age‐related reduction in potassium current indicates plasticity in neuronal function that can impact communication in the hippocampal neural network during aging. J. Neurosci. Res. 63:176–184, 2001. © 2001 Wiley‐Liss, Inc. |
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ISSN: | 0360-4012 1097-4547 |
DOI: | 10.1002/1097-4547(20010115)63:2<176::AID-JNR1009>3.0.CO;2-H |