Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Ceftriaxone improves impairments in synaptic plasticity and cognitive behavior in APP/PS1 mouse model of Alzheimer's disease by inhibiting extrasynaptic NMDAR‐STEP61 signaling

“…The freshly separated hippocampi were sliced at 400 μm thickness using a vibrating slicer ( VT1200S , Leica). After a recovery incubation at room temperature for 2 h (Mathis et al, 2011; Ting et al, 2014) in a solution containing 92 mM NaCl, 2.5 mM KCl, 1.25 mM NaH 2 PO 4 , 30 mM NaHCO 3 , 20 mM HEPES, 25 mM glucose, 2 mM thiourea, 5 mM Na‐ascorbate, 3 mM Na‐pyruvate, 2 mM CaCl 2 , 2 mM MgSO 4 , and 3 mM N‐Acetyl‐ l ‐cysteine, with pH and osmolality set to 7.3–7.4 and 300–310 mOsm, respectively, and saturated with a gas mixture of 5% CO 2 + 95% O 2 with persistent blowing, the slice was transferred to a recording chamber and continuously perfused with aCSF for recording. The stimulation electrode (concentric bipolar tungsten electrode) and recording pipette were placed in the Schaffer collateral commissure fibers and stratum radiatum of the hippocampal CA1 region, respectively.…”

“…The freshly separated hippocampi were sliced at 400 μm thickness using a vibrating slicer (VT1200S, Leica). After a recovery incubation at room temperature for 2 h (Mathis et al, 2011;Ting et al, 2014) to the stimulus intensity. The PPF was induced using double-pulse stimulation at intervals of 100 ms every 20 s for 5 min at an intensity of 40-50% of the maximum fEPSP amplitude.…”

Effect of sacubitril/valsartan on cognitive impairment in colchicine‐induced Alzheimer's model in rats

“…The hippocampi and prefrontal cortices were dissected and (10% w/v) of each tissue was homogenized separately at 4°C in PBS (pH = 7.4) containing cocktail of protease inhibitor to protect the dissected brain components from autoxidation. After centrifuging the homogenates for 15 min at 3000 rpm, aliquots of supernatant were kept at −80°C for further biochemical testing [31]. The Lowry technique was used to determine the protein content in samples [32].…”

High uric acid induced hippocampal mitochondrial dysfunction and cognitive impairment involving intramitochondrial NF-κB inhibitor α/nuclear factor-κB pathway

“…The abnormal accumulation of UA in serum (>6.8-7 mg/dl) is defined as hyperuricemia, which is well known to cause gout [5]. The effect of UA on cognitive ability is still uncertain because UA can work as an antioxidant and inflammation inducer in the brain [6]. Hyperuricemia has been reported as an independent detrimental factor for cognitive dysfunction [7,8].…”

“…A recent study has shown that hippocampal nuclear factor-κB (NF-κB) becomes activated under hyperuricemic stress to impair cognitive ability [6]. In addition, excess UA has been validated to trigger inflammatory responses in multiple tissues, such as the liver, kidney, hypothalamus and hippocampus, via the intramitochondrial NF-κB inhibitor α (IκBα)/NF-κB pathway [6,[10][11][12]. More importantly, mitochondria contain the major components of the NF-κB pathway, including IκBα and NF-κB [13].…”