Crocin attenuates the granular cells damages on the dentate gyrus and pyramidal neurons in the CA3 regions of the hippocampus and frontal cortex in the rat model of Alzheimer's disease

2020 ◽  
pp. 101837 ◽  
Author(s):  
Mohammadmehdi Hadipour ◽  
Gholam Hossein Meftahi ◽  
Mohammad Reza Afarinesh ◽  
Gila Pirzad Jahromi ◽  
Boshra Hatef
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Dentate Gyrus ◽  
Frontal Cortex ◽  
Rat Model ◽  
Pyramidal Neurons ◽  
Granular Cells ◽  
Model Of Alzheimer’S Disease

scholarly journals Hippocampal hyperactivity in a rat model of Alzheimer’s disease

2020 ◽  
Author(s):  
Liudmila Sosulina ◽  
Manuel Mittag ◽  
Hans-Rüdiger Geis ◽  
Kerstin Hoffmann ◽  
Igor Klyubin ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rat Model ◽  
Pyramidal Neurons ◽  
Brain Slices ◽  
Disease Stage ◽  
Intrinsic Excitability ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons ◽  
Model Of Alzheimer’S Disease

AbstractNeuronal network dysfunction is a hallmark of Alzheimer’s disease (AD). However, the underlying pathomechanisms remain unknown. We analyzed the hippocampal micronetwork in a rat model of AD at an early disease stage at the beginning of extracellular amyloid beta (Aβ) deposition. We established two-photon Ca2+-imaging in vivo in the hippocampus of rats and found hyperactivity of CA1 neurons. Patch-clamp recordings in brain slices in vitro revealed changes in the passive properties and intrinsic excitability of CA1 pyramidal neurons. Furthermore, we observed increased neuronal input resistance and prolonged action potential width in CA1 pyramidal neurons. Surprisingly, all parameters measured to quantify synaptic inhibition and excitation onto CA1 pyramidal neurons were intact suggesting a cell immanent deficit. Our data support the view that altered intrinsic excitability of CA1 neurons may precede inhibitory dysfunction at an early stage of disease progression.

scholarly journals Neuronal and Astrocytic Metabolism in a Transgenic Rat Model of Alzheimer's Disease

2014 ◽  
Vol 34 (5) ◽  
pp. 906-914 ◽  
Author(s):  
Linn Hege Nilsen ◽  
Menno P Witter ◽  
Ursula Sonnewald
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Frontal Cortex ◽  
Rat Model ◽  
Hippocampal Formation ◽  
Tricarboxylic Acid Cycle ◽  
Amyloid Β ◽  
Transgenic Rat ◽  
Resonance Spectroscopy ◽  
Model Of Alzheimer’S Disease

Regional hypometabolism of glucose in the brain is a hallmark of Alzheimer's disease (AD). However, little is known about the specific alterations of neuronal and astrocytic metabolism involved in homeostasis of glutamate and GABA in AD. Here, we investigated the effects of amyloid β (Aβ) pathology on neuronal and astrocytic metabolism and glial-neuronal interactions in amino acid neurotransmitter homeostasis in the transgenic McGill-R-Thyl-APP rat model of AD compared with healthy controls at age 15 months. Rats were injected with [1-13C]glucose and [1,2-13C]acetate, and extracts of the hippocampal formation as well as several cortical regions were analyzed using 1H- and 13C nuclear magnetic resonance spectroscopy and high-performance liquid chromatography. Reduced tricarboxylic acid cycle turnover was evident for glutamatergic and GABAergic neurons in hippocampal formation and frontal cortex, and for astrocytes in frontal cortex. Pyruvate carboxylation, which is necessary for de novo synthesis of amino acids, was decreased and affected the level of glutamine in hippocampal formation and those of glutamate, glutamine, GABA, and aspartate in the retrosplenial/cingulate cortex. Metabolic alterations were also detected in the entorhinal cortex. Overall, perturbations in energy- and neurotransmitter homeostasis, mitochondrial astrocytic and neuronal metabolism, and aspects of the glutamate-glutamine cycle were found in McGill-R-Thy1-APP rats.

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