Faculty Opinions recommendation of Coding of social novelty in the hippocampal CA2 region and its disruption and rescue in a 22q11.2 microdeletion mouse model.

2021 ◽  
Author(s):  
Lily Jan
Keyword(s):  
Mouse Model ◽  
22Q11.2 Microdeletion

Dependency of prepulse inhibition deficits on baseline startle reactivity in a mouse model of the human 22q11.2 microdeletion syndrome

2018 ◽  
Vol 18 (4) ◽  
pp. e12523 ◽  
Author(s):  
Joseph Scarborough ◽  
Flavia Mueller ◽  
Ulrike Weber‐Stadlbauer ◽  
Juliet Richetto ◽  
Urs Meyer
Keyword(s):  
Mouse Model ◽  
Prepulse Inhibition ◽  
Microdeletion Syndrome ◽  
22Q11.2 Microdeletion

scholarly journals Neuroanatomical phenotypes in a mouse model of the 22q11.2 microdeletion

2013 ◽  
Vol 19 (1) ◽  
pp. 99-107 ◽  
Author(s):  
J Ellegood ◽  
S Markx ◽  
J P Lerch ◽  
P E Steadman ◽  
C Genç ◽  
...  
Keyword(s):  
Mouse Model ◽  
22Q11.2 Microdeletion

scholarly journals Coding of social novelty in the hippocampal CA2 region and its disruption and rescue in a mouse model of schizophrenia

2019 ◽  
Author(s):  
Macayla L. Donegan ◽  
Fabio Stefanini ◽  
Torcato Meira ◽  
Joshua A. Gordon ◽  
Stefano Fusi ◽  
...  
Keyword(s):  
Mouse Model ◽  
Social Interactions ◽  
Pyramidal Neurons ◽  
Social Memory ◽  
Spatial Location ◽  
Memory Deficits ◽  
Spatial Coding ◽  
Social Stimuli ◽  
The Social ◽  
22Q11.2 Microdeletion

AbstractThe hippocampal CA2 region is essential for social memory and has been implicated in neuropsychiatric disorders. However, little is known about how CA2 neural activity encodes social interactions and how this coding is altered in disease. We recorded from CA2 pyramidal neurons as mice engaged in social interactions and found that while CA2 failed to stably represent spatial location, CA2 activity encoded contextual changes and novel social stimuli. In the Df(16)A+/- mouse model of the human 22q11.2 microdeletion, a major schizophrenia risk factor, CA2 activity showed a surprising increase in spatial coding while failing to encode social novelty, consistent with the social memory deficit in these mice. Previous work has shown that CA2 pyramidal neurons are hyperpolarized in Df(16)A+/- mice, likely as a result of upregulation of TREK-1 K+ current. We found that administration of a TREK-1 antagonist rescued the social memory deficits and restored normal CA2 coding properties in Df(16)A+/- mice, supporting a crucial role for CA2 in the encoding of novel social stimuli and social dysfunction.

scholarly journals Continuous performance test impairment in a 22q11.2 microdeletion mouse model: improvement by amphetamine

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Simon R. O. Nilsson ◽  
Christopher J. Heath ◽  
Samir Takillah ◽  
Steve Didienne ◽  
Kim Fejgin ◽  
...  
Keyword(s):  
Mouse Model ◽  
Performance Test ◽  
Continuous Performance Test ◽  
Continuous Performance ◽  
22Q11.2 Microdeletion ◽  
Model Improvement

scholarly journals Assessing the Cognitive Translational Potential of a Mouse Model of the 22q11.2 Microdeletion Syndrome

2016 ◽  
Vol 26 (10) ◽  
pp. 3991-4003 ◽  
Author(s):  
Simon RO. Nilsson ◽  
Kim Fejgin ◽  
Francois Gastambide ◽  
Miriam A. Vogt ◽  
Brianne A. Kent ◽  
...  
Keyword(s):  
Mouse Model ◽  
Microdeletion Syndrome ◽  
22Q11.2 Microdeletion

scholarly journals Cognition- and circuit-based dysfunction in a mouse model of 22q11.2 microdeletion syndrome: effects of stress

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Anushree Tripathi ◽  
Michael Spedding ◽  
Esther Schenker ◽  
Michael Didriksen ◽  
Arnaud Cressant ◽  
...  
Keyword(s):  
Mouse Model ◽  
Microdeletion Syndrome ◽  
22Q11.2 Microdeletion ◽  
Effects Of Stress

scholarly journals Evidence for altered hippocampal function in a mouse model of the human 22q11.2 microdeletion

2011 ◽  
Vol 47 (4) ◽  
pp. 293-305 ◽  
Author(s):  
Liam J. Drew ◽  
Kimberly L. Stark ◽  
Karine Fénelon ◽  
Maria Karayiorgou ◽  
Amy B. MacDermott ◽  
...  
Keyword(s):  
Mouse Model ◽  
Hippocampal Function ◽  
22Q11.2 Microdeletion

scholarly journals Coding of social novelty in the hippocampal CA2 region and its disruption and rescue in a 22q11.2 microdeletion mouse model

2020 ◽  
Vol 23 (11) ◽  
pp. 1365-1375 ◽  
Author(s):  
Macayla L. Donegan ◽  
Fabio Stefanini ◽  
Torcato Meira ◽  
Joshua A. Gordon ◽  
Stefano Fusi ◽  
...  
Keyword(s):  
Mouse Model ◽  
22Q11.2 Microdeletion

Regenerating myofibers in tibialis anterior muscles of young ‘MDX’ mice

1987 ◽  
Vol 45 ◽  
pp. 726-727
Author(s):  
H. D. Geissinge ◽  
L.D. Rhodes
Keyword(s):  
Muscular Dystrophy ◽  
Mouse Model ◽  
Tibialis Anterior ◽  
Physiological Activity ◽  
Mdx Mice ◽  
Mode Of Inheritance

A recently discovered mouse model (‘mdx’) for muscular dystrophy in man may be of considerable interest, since the disease in ‘mdx’ mice is inherited by the same mode of inheritance (X-linked) as the human Duchenne (DMD) muscular dystrophy. Unlike DMD, which results in a situation in which the continual muscle destruction cannot keep up with abortive regenerative attempts of the musculature, and the sufferers of the disease die early, the disease in ‘mdx’ mice appears to be transient, and the mice do not die as a result of it. In fact, it has been reported that the severely damaged Tibialis anterior (TA) muscles of ‘mdx’ mice seem to display exceptionally good regenerative powers at 4-6 weeks, so much so, that these muscles are able to regenerate spontaneously up to their previous levels of physiological activity.

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