Generation of Local CA1 &amp;#947; Oscillations by Tetanic Stimulation

Hatch, Robert J.; Reid, Christopher A.; Petrou, Steven

doi:10.3791/52877

Cited by 2 publications

(2 citation statements)

References 27 publications

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“…Brain slices were prepared similar to those described previously [ 16 ]. SUS- and sham-treated mice were anaesthetized with 2% isoflurane (Attane) and transcardially perfused with cold cutting solution comprising (in mM) 125 choline-Cl, 2.5 KCl, 0.4 CaCl 2 , 6 MgCl 2 , 1.25 NaH 2 PO 4 , 26 NaHCO 3 and 20 D-glucose saturated with carbogen gas (95% O 2 /5% CO 2 ).…”

Section: Methodsmentioning

confidence: 99%

“…300 μm coronal hippocampal brain slices, from between approximately -1.34 to -2.54 mm of the Bregma, were cut on a vibratome (VT1000S, Leica). Slices were rested for 30 minutes at 35°C and then at room temperature (RT) for at least 30 minutes prior to recordings, which were conducted by an experimenter who was blinded to treatment [ 16 , 17 ].…”

Section: Methodsmentioning

confidence: 99%

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Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice

2016

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Scanning ultrasound (SUS) is a noninvasive approach that has recently been shown to ameliorate histopathological changes and restore memory functions in an Alzheimer's disease mouse model. Although no overt neuronal damage was reported, the short- and long-term effects of SUS on neuronal excitability and dendritic tree morphology had not been investigated. To address this, we performed patch-clamp recordings from hippocampal CA1 pyramidal neurons in wild-type mice 2 and 24 hours after a single SUS treatment, and one week and 3 months after six weekly SUS treatments, including sham treatments as controls. In both treatment regimes, no changes in CA1 neuronal excitability were observed in SUS-treated neurons when compared to sham-treated neurons at any time-point. For the multiple treatment groups, we also determined the dendritic morphology and spine densities of the neurons from which we had recorded. The apical trees of sham-treated neurons were reduced at the 3 month time-point when compared to one week; however, surprisingly, no longitudinal change was detected in the apical dendritic trees of SUS-treated neurons. In contrast, the length and complexity of the basal dendritic trees were not affected by SUS treatment at either time-point. The apical dendritic spine densities were reduced, independent of the treatment group, at 3 months compared to one week. Collectively, these data suggest that ultrasound can be employed to prevent an age-associated loss of dendritic structure without impairing neuronal excitability.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice

2016

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Hyperphosphorylated tau causes reduced hippocampal CA1 excitability by relocating the axon initial segment

et al. 2017

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Hyperphosphorylated tau has a critical role in tauopathies such as Alzheimer’s disease and frontotemporal dementia, impairing neuronal function and eventually leading to neurodegeneration. A critical role for tau is supported by studies in transgenic mouse models that express the P301L tau mutation found in cases of familial frontotemporal dementia, with the accumulation of hyperphosphorylated tau in the hippocampus causing reductions in hippocampal long-term potentiation and impairments in spatial learning and memory. However, what has remained unexplored is the role of hyperphosphorylated tau in reducing neuronal excitability. Here, we show in two complementary P301L tau transgenic mouse models that hyperphosphorylated tau induces a more depolarized threshold for action potential initiation and reduces firing in hippocampal CA1 neurons, which was rescued by the suppression of transgenic tau. Furthermore, using mutagenesis and primary hippocampal neuronal cultures, we reveal that this reduction in neuronal excitability results from the relocation of the axon initial segment (AIS) down the axon in a tau phosphorylation-dependent manner. We also demonstrate that this effect is microtubule-dependent. In addition, pharmacological stabilization was found to prevent both the structural and functional deficits caused by tau hyperphosphorylation. Finally, we demonstrate that the AIS of neurons from tau transgenic mice is further down the axon, which correlates with a reduction in excitability. We therefore propose that a reduction in hippocampal excitability due to a tau-mediated distal relocalization of the AIS contributes to the hippocampal dysfunction observed in tauopathies.Electronic supplementary materialThe online version of this article (doi:10.1007/s00401-017-1674-1) contains supplementary material, which is available to authorized users.

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Generation of Local CA1 γ Oscillations by Tetanic Stimulation

Cited by 2 publications

References 27 publications

Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice

Scanning Ultrasound (SUS) Causes No Changes to Neuronal Excitability and Prevents Age-Related Reductions in Hippocampal CA1 Dendritic Structure in Wild-Type Mice

Hyperphosphorylated tau causes reduced hippocampal CA1 excitability by relocating the axon initial segment

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