Age-dependent reduction of γ oscillations in the mouse hippocampus in vitro

M Vreugdenhil, EC Toescu - Neuroscience, 2005 - Elsevier
M Vreugdenhil, EC Toescu
Neuroscience, 2005Elsevier
Normal brain ageing is associated with a decline in hippocampal memory functions.
Neuronal oscillations in the γ frequency band have been implicated in various cognitive
tasks. In this study we test the effect of normal brain ageing on γ oscillations in the mouse
hippocampus in vitro. γ Oscillations were evoked by either 10 μM carbachol or 100 nM
kainate in ventral hippocampus slices from young (> 5 month) and aged (> 22 month)
C57Bl/J6 mice. In slices from young mice carbachol-induced γ oscillations were more …
Normal brain ageing is associated with a decline in hippocampal memory functions. Neuronal oscillations in the γ frequency band have been implicated in various cognitive tasks. In this study we test the effect of normal brain ageing on γ oscillations in the mouse hippocampus in vitro. γ Oscillations were evoked by either 10 μM carbachol or 100 nM kainate in ventral hippocampus slices from young (>5 month) and aged (>22 month) C57Bl/J6 mice. In slices from young mice carbachol-induced γ oscillations were more regular and more coherent than those induced by kainate. Compared with young, the power in the 20–80 Hz frequency range in area CA3 of slices from aged mice was reduced to 14% for kainate-induced oscillations and to 7% for carbachol-induced oscillations, whereas waveform, dominant frequency and coherence of the oscillation were unchanged. Local network properties were assessed by paired-pulse stimulation of Schaffer collateral/commissural fibers. The excitatory synaptic response in stratum radiatum of CA3 was reduced, in correlation with the antidromic population spike, but functional inhibition in CA3 and CA1 was unaffected. Changes in local network properties could not explain the reduced γ oscillation strength. Since oscillations driven by two different pathways are similarly affected with age, an age-dependent effect on tonic depolarizing drive of principal cells is unlikely to explain the current results. Other mechanisms, including a change with age in the use-dependent modulation of synaptic strength, should account for the impaired γ oscillations in the aged hippocampus that may contribute to age-dependent memory impairment.
Elsevier