scholarly journals Immunohistochemical Visualization of Hippocampal Neuron Activity After Spatial Learning in a Mouse Model of Neurodevelopmental Disorders

10.3791/52919 ◽  
2015 ◽  
Author(s):  
Giovanni Provenzano ◽  
Luca Pangrazzi ◽  
Andrea Poli ◽  
Nicoletta Berardi ◽  
Yuri Bozzi
Keyword(s):  
Mouse Model ◽  
Spatial Learning ◽  
Neurodevelopmental Disorders ◽  
Hippocampal Neuron ◽  
Neuron Activity

Preeclampsia and Risk for Neurodevelopmental Disorders: Mouse Model Insights Into IL17 and Placental Function

2021 ◽  
Vol 89 (9) ◽  
pp. S65-S66
Author(s):  
Banu Gumusoglu ◽  
Akanksha Chilukuri ◽  
Sabrina Scroggins ◽  
Benjamin Hing ◽  
Jessica DeWitt ◽  
...  
Keyword(s):  
Mouse Model ◽  
Neurodevelopmental Disorders ◽  
Placental Function

P1-049: Chronic Memantine administration reduces APP expression, normalizes glutamatergic synapse density, and improves spatial learning in the Ts65Dn mouse model for down syndrome

2008 ◽  
Vol 4 ◽  
pp. T220-T220
Author(s):  
Carmen Martı́nez-Cué ◽  
Noemı́ Rueda ◽  
Marı́a Llorens-Martı́n ◽  
Jesús Flórez ◽  
Elsa Valdizán ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Mouse Model ◽  
Spatial Learning ◽  
Glutamatergic Synapse ◽  
Ts65dn Mouse ◽  
Synapse Density

scholarly journals The effects of low doses of proton, iron or silicon radiation on spatial learning in a mouse model of Alzheimer's disease

2014 ◽  
Vol 55 (suppl 1) ◽  
pp. i95-i96 ◽  
Author(s):  
J. A. Bellone ◽  
R. E. Hartman ◽  
R. Vlkolinsky
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Spatial Learning ◽  
Low Doses ◽  
Model Of Alzheimer’S Disease

scholarly journals Hippocampal Neuron Loss Exceeds Amyloid Plaque Load in a Transgenic Mouse Model of Alzheimer's Disease

2004 ◽  
Vol 164 (4) ◽  
pp. 1495-1502 ◽  
Author(s):  
Christoph Schmitz ◽  
Bart P.F. Rutten ◽  
Andrea Pielen ◽  
Stephanie Schäfer ◽  
Oliver Wirths ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Transgenic Mouse ◽  
Hippocampal Neuron ◽  
Amyloid Plaque ◽  
Transgenic Mouse Model ◽  
Neuron Loss ◽  
Model Of Alzheimer’S Disease ◽  
Plaque Load

scholarly journals Impairments in sensory-motor gating and information processing in a mouse model of Ehmt1 haploinsufficiency

2020 ◽  
Vol 4 ◽  
pp. 239821282092864
Author(s):  
Brittany A Davis ◽  
François David ◽  
Ciara O’Regan ◽  
Manal A Adam ◽  
Adrian J Harwood ◽  
...  
Keyword(s):  
Information Processing ◽  
Mouse Model ◽  
Neurodevelopmental Disorders ◽  
Auditory Evoked Potentials ◽  
Autism Spectrum ◽  
Oscillatory Activity ◽  
Kleefstra Syndrome ◽  
Sensory Motor ◽  
Processing Deficits ◽  
Information Processing Deficits

Regulators of chromatin dynamics and transcription are increasingly implicated in the aetiology of neurodevelopmental disorders. Haploinsufficiency of EHMT1, encoding a histone methyltransferase, is associated with several neurodevelopmental disorders, including Kleefstra syndrome, developmental delay and autism spectrum disorder. Using a mouse model of Ehmt1 haploinsufficiency ( Ehmt1D6Cre/+), we examined a number of brain and behavioural endophenotypes of relevance to neurodevelopmental disorders. Specifically, we show that Ehmt1D6Cre/+ mice have deficits in information processing, evidenced by abnormal sensory-motor gating, a complete absence of object recognition memory, and a reduced magnitude of auditory evoked potentials in both paired-pulse inhibition and mismatch negativity. The electrophysiological experiments show that differences in magnitude response to auditory stimulus were associated with marked reductions in total and evoked beta- and gamma-band oscillatory activity, as well as significant reductions in phase synchronisation. The pattern of electrophysiological deficits in Ehmt1D6Cre/+ matches those seen in control mice following administration of the selective NMDA-R antagonist, ketamine. This, coupled with reduction of Grin1 mRNA expression in Ehmt1D6Cre/+ hippocampus, suggests that Ehmt1 haploinsufficiency may lead to disruption in NMDA-R. Taken together, these data indicate that reduced Ehmt1 dosage during forebrain development leads to abnormal circuitry formation, which in turn results in profound information processing deficits. Such information processing deficits are likely paramount to our understanding of the cognitive and neurological dysfunctions shared across the neurodevelopmental disorders associated with EHMT1 haploinsufficiency.

scholarly journals Inhibitory Neuron Activity Contributions to Hemodynamic Responses and Metabolic Load Examined Using an Inhibitory Optogenetic Mouse Model

2018 ◽  
Vol 28 (11) ◽  
pp. 4105-4119 ◽  
Author(s):  
Alberto L Vazquez ◽  
Mitsuhiro Fukuda ◽  
Seong-Gi Kim
Keyword(s):  
Mouse Model ◽  
Inhibitory Neuron ◽  
Neuron Activity ◽  
Hemodynamic Responses ◽  
Metabolic Load
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