Spatial learning and memory function-related gene expression in the hippocampus of mouse exposed to nanoparticle-rich diesel exhaust

2008 ◽  
Vol 29 (6) ◽  
pp. 940-947 ◽  
Author(s):  
Tin-Tin Win-Shwe ◽  
Shoji Yamamoto ◽  
Yuji Fujitani ◽  
Seishiro Hirano ◽  
Hidekazu Fujimaki
Keyword(s):  
Gene Expression ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Diesel Exhaust ◽  
Memory Function ◽  
Spatial Learning And Memory ◽  
Related Gene

Maternal and postweaning high-fat diets disturb hippocampal gene expression, learning, and memory function

2014 ◽  
Vol 306 (8) ◽  
pp. R527-R537 ◽  
Author(s):  
Kathleen C. Page ◽  
Elizabeth K. Jones ◽  
Endla K. Anday
Keyword(s):  
Gene Expression ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Memory Function ◽  
Saturated Fat ◽  
Spatial Learning And Memory ◽  
Adult Males ◽  
High Fat ◽  
High Fat Diets ◽  
Fat Diets

We tested the hypothesis that excess saturated fat consumption during pregnancy, lactation, and/or postweaning alters the expression of genes mediating hippocampal synaptic efficacy and impairs spatial learning and memory in adulthood. Dams were fed control chow or a diet high in saturated fat before mating, during pregnancy, and into lactation. Offspring were weaned to either standard chow or a diet high in saturated fat. The Morris Water Maze was used to evaluate spatial learning and memory. Open field testing was used to evaluate motor activity. Hippocampal gene expression in adult males was measured using RT-PCR and ELISA. Offspring from high fat-fed dams took longer, swam farther, and faster to try and find the hidden platform during the 5-day learning period. Control offspring consuming standard chow spent the most time in memory quadrant during the probe test. Offspring from high fat-fed dams consuming excess saturated fat spent the least. The levels of mRNA and protein for brain-derived neurotrophic factor and activity-regulated cytoskeletal-associated protein were significantly decreased by maternal diet effects. Nerve growth factor mRNA and protein levels were significantly reduced in response to both maternal and postweaning high-fat diets. Expression levels for the N-methyl-d-aspartate receptor (NMDA) receptor subunit NR2B as well as synaptophysin were significantly decreased in response to both maternal and postweaning diets. Synaptotagmin was significantly increased in offspring from high fat-fed dams. These data support the hypothesis that exposure to excess saturated fat during hippocampal development is associated with complex patterns of gene expression and deficits in learning and memory.

scholarly journals Milk Exosomes Cross the Blood-Brain Barrier in Murine Cerebral Cortex Endothelial Cells and Promote Dendritic Complexity in the Hippocampus and Brain Function in C57BL/6J Mice

2021 ◽  
Author(s):  
Fang Zhou ◽  
Pearl Ebea ◽  
Ezra Mutai ◽  
Sonal Sukreet ◽  
Shya Navazesh ◽  
...  
Keyword(s):  
Gene Expression ◽  
Endothelial Cells ◽  
Brain Development ◽  
Learning And Memory ◽  
Kainic Acid ◽  
Spatial Learning ◽  
Granule Cells ◽  
Spatial Learning And Memory ◽  
Adult Mice ◽  
Dendritic Complexity

Background: Human milk contains large amounts of exosomes (MEs) and their regulatory microRNA cargos, whereas infant formulas contain only trace amounts of MEs and microRNAs. Breastfeeding has been implicated in optimal brain development but experimental evidence linking ME intake with brain development is limited. Objectives: We assessed the transport of MEs across the blood-brain barrier (BBB) and ME accumulation in distinct regions of the brain in brain endothelial cells and suckling mice. We further assessed BME-dependent gene expression profiles and effects on the dendritic complexity of hippocampal granule cells and phenotypes of BME depletion in neonate, juvenile and adult mice. Methods: The transfer of MEs across the BBB was assessed by using bovine MEs labeled with FM4-64 or loaded with IRDye-labeled miR-34a in murine brain endothelial bEnd.3 cell monolayers and dual chamber systems, and in wild-type newborn pups fostered to exosome and cargo tracking (ECT) dams that express MEs endogenously labeled with a CD63-eGFP fusion protein for subsequent analysis by serial two-photon tomography and staining with anti-eGFP antibodies. Effects of MEs on gene expression and dendritic architecture of granule cells was analyzed in hippocampi from juvenile mice fed exosome and RNA-depleted (ERD) and exosome and RNA-sufficient (ERS) diets by using RNA-sequencing analysis and Golgi-Cox staining followed by integrated neuronal tracing and morphological analysis of neuronal dendrites, respectively. Spatial learning and severity of kainic acid-induced seizures were assessed in mice fed ERD and ERS diets. Results: bEnd.3 cells internalized MEs by using a saturable transport mechanism and secreted miR-34a across the basal membrane. MEs penetrated the entire brain in fostering experiments; major regions of accumulation included the hippocampus, cortex and cerebellum. Two hundred ninety-five genes were differentially expressed in hippocampi from male mice fed ERD and ERS diets; high-confidence gene networks included pathways implicated in axon guidance and calcium signaling. Only one gene was differentially expressed in females fed the experimental diets. Juvenile pups fed the ERD diet had reduced dendritic complexity of dentate granule cells in the hippocampus, scored nine-fold lower in the Barnes maze test of spatial learning and memory (P < 0.01), and the severity of seizures was 5-fold higher following kainic acid administration in adult mice fed the ERD diet compared to mice fed the ERS diet (P < 0.01). Conclusions: MEs cross the BBB and contribute toward optimal neuronal development, spatial learning and memory, and resistance to kainic acid-induced seizures in mice.

scholarly journals Reelin Improves Cognition and Extends the Lifespan of Mutant Ndel1 Mice with Postnatal CA1 Hippocampus Deterioration

2020 ◽  
Vol 30 (9) ◽  
pp. 4964-4978 ◽  
Author(s):  
Ivana Kiroski ◽  
Yulan Jiang ◽  
Cezar Gavrilovici ◽  
Fan Gao ◽  
Sukyoung Lee ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Pyramidal Neurons ◽  
Neurological Diseases ◽  
Memory Function ◽  
Neuronal Cell ◽  
Adult Brain ◽  
Conditional Knockout ◽  
Spatial Learning And Memory ◽  
Ca1 Pyramidal Neurons

Abstract The glycoprotein Reelin maintains neuronal positioning and regulates neuronal plasticity in the adult brain. Reelin deficiency has been associated with neurological diseases. We recently showed that Reelin is depleted in mice with a targeted disruption of the Ndel1 gene in forebrain postnatal excitatory neurons (Ndel1 conditional knockout (CKO)). Ndel1 CKO mice exhibit fragmented microtubules in CA1 pyramidal neurons, profound deterioration of the CA1 hippocampus and a shortened lifespan (~10 weeks). Here we report that Ndel1 CKO mice (of both sexes) experience spatial learning and memory deficits that are associated with deregulation of neuronal cell adhesion, plasticity and neurotransmission genes, as assessed by genome-wide transcriptome analysis of the hippocampus. Importantly, a single injection of Reelin protein in the hippocampus of Ndel1 CKO mice improves spatial learning and memory function and this is correlated with reduced intrinsic hyperexcitability of CA1 pyramidal neurons, and normalized gene deregulation in the hippocampus. Strikingly, when treated with Reelin, Ndel1 CKO animals that die from an epileptic phenotype, live twice as long as nontreated, or vehicle-treated CKO animals. Thus, Reelin confers striking beneficial effects in the CA1 hippocampus, and at both behavioral and organismal levels.

scholarly journals The Effect of D-Cycloserine on Spatial Learning Performance and Memory Function-Related Gene Expression in Mice Following Toluene Exposure

2010 ◽  
Vol 32 (2) ◽  
pp. 127-140 ◽  
Author(s):  
Tin-Tin WIN-SHWE ◽  
Shiho KAGEYAMA ◽  
Shinji TSUKAHARA ◽  
Daisuke NAKAJIMA ◽  
Hidekazu FUJIMAKI
Keyword(s):  
Gene Expression ◽  
Spatial Learning ◽  
Memory Function ◽  
Learning Performance ◽  
Related Gene ◽  
Toluene Exposure

scholarly journals Proinflammatory Factors Mediate Paclitaxel-Induced Impairment of Learning and Memory

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Zhao Li ◽  
Shuang Zhao ◽  
Hai-Lin Zhang ◽  
Peng Liu ◽  
Fei-Fei Liu ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Neuronal Apoptosis ◽  
Memory Function ◽  
Interleukin 1 ◽  
Spatial Learning And Memory ◽  
Synthesis Inhibitor ◽  
Expression Levels ◽  
Proinflammatory Factor ◽  
Paclitaxel Treatment

The chemotherapeutic agent paclitaxel is widely used for cancer treatment. Paclitaxel treatment impairs learning and memory function, a side effect that reduces the quality of life of cancer survivors. However, the neural mechanisms underlying paclitaxel-induced impairment of learning and memory remain unclear. Paclitaxel treatment leads to proinflammatory factor release and neuronal apoptosis. Thus, we hypothesized that paclitaxel impairs learning and memory function through proinflammatory factor-induced neuronal apoptosis. Neuronal apoptosis was assessed by TUNEL assay in the hippocampus. Protein expression levels of tumor necrosis factor-α(TNF-α) and interleukin-1β(IL-1β) in the hippocampus tissue were analyzed by Western blot assay. Spatial learning and memory function were determined by using the Morris water maze (MWM) test. Paclitaxel treatment significantly increased the escape latencies and decreased the number of crossing in the MWM test. Furthermore, paclitaxel significantly increased the number of TUNEL-positive neurons in the hippocampus. Also, paclitaxel treatment increased the expression levels of TNF-αand IL-1βin the hippocampus tissue. In addition, the TNF-αsynthesis inhibitor thalidomide significantly attenuated the number of paclitaxel-induced TUNEL-positive neurons in the hippocampus and restored the impaired spatial learning and memory function in paclitaxel-treated rats. These data suggest that TNF-αis critically involved in the paclitaxel-induced impairment of learning and memory function.

scholarly journals Endocrine, liver-derived IGF-I is of importance for spatial learning and memory in old mice

2006 ◽  
Vol 189 (3) ◽  
pp. 617-627 ◽  
Author(s):  
J Svensson ◽  
M Diez ◽  
J Engel ◽  
C Wass ◽  
Å Tivesten ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Metabotropic Glutamate Receptor ◽  
Memory Function ◽  
Morris Water Maze Test ◽  
Spatial Learning And Memory ◽  
Mrna Levels ◽  
Age Related ◽  
Igf I ◽  
Old Mice

IGF-I is a neuroprotective hormone, and neurodegenerative disorders, including Alzheimer’s disease, have been associated with decreased serum IGF-I concentration. In this study, IGF-I production was inactivated in the liver of adult mice (LI-IGF-I−/−), resulting in an approximately 80–85% reduction of circulating IGF-I concentrations. In young (6-month-old) mice there was no difference between the LI-IGF-I−/− and the control mice in spatial learning and memory as measured using the Morris water maze test. In old (aged 15 and 18 months) LI-IGF-I−/− mice, however, the acquisition of the spatial task was slower than in the controls. Furthermore, impaired spatial working as well as reference memory was observed in the old LI-IGF−/− mice. Histochemical analyses revealed an increase in dynorphin and enkephalin immunoreactivities but decreased mRNA levels in the hippocampus of old LI-IGF-I−/− mice. These mice also displayed astrocytosis and increased metabotropic glutamate receptor 7a-immunoreactivity. These neurochemical disturbances suggest synaptic dysfunction and early neurodegeneration in old LI-IGF-I−/− mice. The decline in serum IGF-I with increasing age may therefore be important for the age-related decline in memory function.

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