Increased vulnerability of hippocampal CA1 neurons to hypoperfusion in ataxia and male sterility (AMS) mouse

Liang, Xueyun; Nagai, Atsushi; Sheikh, Abdullah Md.; Wang, Hui; Mitaki, Shingo; Araki, Asuka; Maruyama, Riruke; Harada, Takayuki

doi:10.1016/j.brainres.2012.11.046

Cited by 9 publications

(10 citation statements)

References 30 publications

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“…The special vulnerability of this region to various neuropathological conditions (epilepsy, depression, encephalitis, stroke, limbic encephalitis, hypoglycaemic encephalopathy, multiple sclerosis, transient global amnesia, Alzheimer disease, etc.) is well known (Liang et al, 2013;Medvedeva, Ji, Yin, & Weiss, 2017). The basis of such susceptibility is still obscure but may include genetically determined glutamate-dependent and calcium-mediated mechanisms of neuronal excitability and oxidative stress (Bartsch et al, 2015).…”

Section: Discussionmentioning

confidence: 99%

Behavioural and brain ultrastructural changes following the systemic administration of propionic acid in adolescent male rats. Further development of a rodent model of autism

Lobzhanidze

Japaridze²,

Lordkipanidze

et al. 2020

Intl J of Devlp Neuroscience

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Short chain fatty acids, produced as gut microbiome metabolites but also present in the diet, exert broad effects in host physiology. Propionic acid (PPA), along with butyrate and acetate, plays a growing role in health, but also in neurological conditions. Increased PPA exposure in humans, animal models and cell lines elicit diverse behavioural and biochemical changes consistent with organic acidurias, mitochondrial disorders and autism spectrum disorders (ASD). ASD is considered a disorder of synaptic dysfunction and cell signalling, but also neuroinflammatory and neurometabolic components. We examined behaviour (Morris water and radial arm mazes) and the ultrastructure of the hippocampus and medial prefrontal cortex (electron microscopy) following a single intraperitoneal (i.p.) injection of PPA (175 mg/kg) in male adolescent rats. PPA treatment showed altered social and locomotor behaviour without changes in learning and memory. Both transient and enduring ultrastructural alterations in synapses, astro‐ and microglia were detected in the CA1 hippocampal area. Electron microscopic analysis showed the PPA treatment significantly decreased the total number of synaptic vesicles, presynaptic mitochondria and synapses with a symmetric active zone. Thus, brief systemic administration of this dietary and enteric short chain fatty acid produced behavioural and dynamic brain ultrastructural changes, providing further validation of the PPA model of ASD.

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Section: Discussionmentioning

confidence: 99%

Behavioural and brain ultrastructural changes following the systemic administration of propionic acid in adolescent male rats. Further development of a rodent model of autism

Lobzhanidze

Japaridze²,

Lordkipanidze

et al. 2020

Intl J of Devlp Neuroscience

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“…Although differences in the brain vulnerability to ischemia are observed in most strains of BCCAO models, a similar pattern of selective hippocampal CA1 neuronal loss has been found [10,11,32]. The severity of hippocampal neuronal loss in the BCCAO models may be different in terms of animals (such as rat, mouse and gerbil) [9,32], time of occlusion [12,33], etc. Furthermore, significant cell loss of hippocampal GABAergic interneurons has been reported in the neurodegenerative diseases as well, such as AD and aging [34,35].…”

Section: Discussionmentioning

confidence: 85%

“…Figures 2 and 3 illustrate the significantly decreased GABAergic expression in the hippocampal CA1 subarea in rats subjected to BCCAO. Immunofluorescence experiments were performed on Day 33 to estimate the numbers of the GABAergic interneurons (including PV-, NPY-and SOM-positive neurons) of the two groups (Figure 2A-B). These experiments revealed that the population of PV-and NPYpositive neurons in the CA1 region decreased in the BCCAO group compared to the sham group (*P=0.0233<0.05 for PV; **P=0.0024<0.01 for NPY), but the SOM-positive neurons in the BCCAO group showed no significant difference compared to the sham group (*P=0.4140>0.05).…”

Section: Discussionmentioning

confidence: 99%

“…Rats (sham group: n=6; BCCAO group: n=8) were sacrificed to observe the altered GABAergic cells on Day 33 after MWM test. Rats were anesthetized using 300 mg/kg chloral hydrate and perfused with 0.9% phosphate-buffered saline (PBS, pH 7.3) followed by 4% paraformaldehyde.…”

Section: Immunohistochemistry and Cell Countingmentioning

confidence: 99%

“…Cell proteins were extracted on Day 33 from the hippocampal CA1 area of rats (sham group: n=6; BCCAO group, n=8) for immunoblotting analysis using the BioRad protein assay kit (Hercules, DE, USA) and measured using micro-BCA protein assay (Pierce, UT, USA). Protein samples were fractionated with 10 % SDS-PAGE gel, transferred to 0.45-lm PVDF membranes, and stained with Ponceau red to confirm equal loading.…”

Section: Western Blottingmentioning

confidence: 99%

See 2 more Smart Citations

Parvalbumin and Neuropeptide Y Neuronal Loss in the Hippocampal CA1 Subarea is Associated with Cognitive Deficits in a Rat Model of Chronic Cerebral Hypoperfusion

Hei¹,

Wei²,

Yi³

et al. 2018

Neuropsychiatry

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BackgroundPermanent bilateral common carotid artery occlusion (BCCAO) produces a chronic cerebral hypoperfusion (CCH) state, which may cause cognitive impairments in aging, Alzheimer's disease and vascular dementia. Recent studies have noticed the crucial role of gamma amino butyric acid (GABA)ergic system in regulation of cognitive ability in a rat model of CCH, but the pathological processes of hippocampal GABAergic interneurons in CCH has not been systematically investigated so far. Here we investigated the altered amounts of GABAergic interneurons, namely parvalbumin (PV)-, neuropeptide Y (NPY)-and somatostatin (SOM)-positive cells and their possible relationship with cognitive deficits. Methods 55 male Sprague Dawley (SD) rats were randomly divided into BCCAO group (n=33, treated with permanent BCCAO) and sham group (n=22, same operation without ligation). Four weeks later, Morris Water Maze was used to analyze the cognitive deficits, and immunohistochemistry or western blotting was employed to investigate the GABAergic expression in the hippocampus of the rat model.

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Reversible recovery of neuronal structures depends on the degree of neuronal damage after global cerebral ischemia in mice

Zhu

Wang

et al. 2017

Experimental Neurology

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Increased vulnerability of hippocampal CA1 neurons to hypoperfusion in ataxia and male sterility (AMS) mouse

Cited by 9 publications

References 30 publications

Behavioural and brain ultrastructural changes following the systemic administration of propionic acid in adolescent male rats. Further development of a rodent model of autism

Behavioural and brain ultrastructural changes following the systemic administration of propionic acid in adolescent male rats. Further development of a rodent model of autism

Parvalbumin and Neuropeptide Y Neuronal Loss in the Hippocampal CA1 Subarea is Associated with Cognitive Deficits in a Rat Model of Chronic Cerebral Hypoperfusion

Reversible recovery of neuronal structures depends on the degree of neuronal damage after global cerebral ischemia in mice

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