Journal
NEUROBIOLOGY OF AGING
Volume 32, Issue 5, Pages 956-965Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2009.05.006
Keywords
Kainate; GluR5; Ageing; Hippocampus; Interneuron; CA3; Gamma oscillation; BAY K 8644; Nimodipine; Fura-2; Slow-afterhyperpolarisation; Intracellular calcium concentration
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Funding
- Medical Research Council (UK)
- Wellcome Trust
- MRC [G0301020] Funding Source: UKRI
- Medical Research Council [G0301020] Funding Source: researchfish
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Normal ageing-associated spatial memory impairment has been linked to subtle changes in the hippocampal network. Here we test whether the age-dependent reduction in gamma oscillations can be explained by the changes in intrinsic properties of hippocampal interneurons. Kainate-induced gamma oscillations, but not spontaneous gamma oscillations, were reduced in slices from aged mice. CA3 interneurons were recorded in slices from young and aged mice using Fura-2-filled pipettes. Passive membrane properties, firing properties, medium- and slow-afterhyperpolarisation amplitudes, basal [Ca2+](i) and firing-induced [Ca2+](i) transients were not different with ageing. Kainate caused a larger depolarisation and increase in [Ca2+](i) signal in aged interneurons than in young ones. In contrast to young interneurons, kainate increased the medium- and slow-afterhyperpolarisation and underlying [Ca2+](i) transient in aged interneurons. Modulating the slow-afterhyperpolarisation by modulating L-type calcium channels with BAY K 8644 and nimodipine suppressed and potentiated, respectively, kainate-induced gamma oscillations in young slices. The age-dependent and stimulation-dependent increase in basal [Ca2+](i), firing-induced [Ca2+](i) transient and associated afterhyperpolarisation may reduce interneuron excitability and contribute to an age-dependent impairment of hippocampal gamma oscillations. (C) 2009 Elsevier Inc. All rights reserved.
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