scholarly journals Automatic analysis of altered gait in arylsulphatase A-deficient mice in the open field

2009 ◽  
Vol 41 (3) ◽  
pp. 787-794 ◽  
Author(s):  
Toon Leroy ◽  
Stijn Stroobants ◽  
Jean-Marie Aerts ◽  
Rudi D’Hooge ◽  
Daniel Berckmans
Keyword(s):  
Open Field ◽  
Automatic Analysis ◽  
Arylsulphatase A ◽  
Deficient Mice

P.716 Negr1-deficient mice display anxiolytic effect in the open field but their sensitivity to amphetamine is not altered

2019 ◽  
Vol 29 ◽  
pp. S484
Author(s):  
M. Kaare ◽  
A. Bregin ◽  
K. Singh ◽  
M. Yayaram ◽  
J. Innos ◽  
...  
Keyword(s):  
Open Field ◽  
Anxiolytic Effect ◽  
Deficient Mice

Connexin30-deficient mice show increased emotionality and decreased rearing activity in the open-field along with neurochemical changes

2003 ◽  
Vol 18 (3) ◽  
pp. 629-638 ◽  
Author(s):  
E. Dere ◽  
M. A. De Souza-Silva ◽  
C. Frisch ◽  
B. Teubner ◽  
G. Sohl ◽  
...  
Keyword(s):  
Open Field ◽  
Neurochemical Changes ◽  
Deficient Mice

scholarly journals Sema4D/CD100 Deficiency Leads to Superior Performance in Mouse Motor Behavior

2009 ◽  
Vol 36 (03) ◽  
pp. 349-355 ◽  
Author(s):  
Kazunori Yukawa ◽  
Tetsuji Tanaka ◽  
Noriko Takeuchi ◽  
Hiroyuki Iso ◽  
Li Li ◽  
...  
Keyword(s):  
Open Field ◽  
Water Maze ◽  
Motor Behavior ◽  
Superior Performance ◽  
Adhesive Tape ◽  
Wild Type ◽  
Maze Task ◽  
Embryonic Mouse ◽  
Water Maze Task ◽  
Deficient Mice

Background:Sema4D/CD100 is a type of class 4 semaphorin, exhibiting crucial rôles in growth cone guidance in developing neurons. Sema4D is widely expressed throughout the central nervous system in embryonic mouse brain, and is selectively localized to oligodendrocytes and myelin in the postnatal brain. However, direct evidence of the actual involvement of Sema4D in the neuronal network development crucial for neurobehavioral performance is still lacking. The present study therefore examined whether Sema4D deficiency leads to abnormal behavioral development.Methods:Both wild-type and Sema4D-deficient mice were subjected to behavioral analyses including open-field, adhesive tape removal, rotarod tests and a water maze task.Results:Open-field tests revealed increased locomotor activity in Sema4D-deficient mice with less percentage of time spent in the center of the field. In both the adhesive tape removal and rotarod tests, which examine motor coordination and balance, Sema4D-deficient mice showed significantly superior performance, suggesting facilitated motor behavior. Both Sema4D-deficient and wild-type mice successfully learnt the water maze task, locating a hidden escape platform, and also showed precise memory for the platform position in probe tests. However, the swimming speed of Sema4D-deficient mice was significantly faster than that of wild-type mice, providing further evidence of their accelerated motor behavior.Conclusion:Our mouse behavioral analyses revealed enhanced motor activity in Sema4D-deficient mice, suggesting the crucial involvement of Sema4D in the neurodevelopmental processes of the central structures mediating motor behavior in mice.

scholarly journals ACAD10 protein expression and Neurobehavioral assessment of Acad10-deficient mice

PLoS ONE ◽  
2020 ◽  
Vol 15 (12) ◽  
pp. e0242445
Author(s):  
Kaitlyn Bloom ◽  
Anuradha Karunanidhi ◽  
Kimimasa Tobita ◽  
Charles Hoppel ◽  
Edda Thiels ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Open Field ◽  
Motor Impairment ◽  
Field Testing ◽  
Acid Oxidation ◽  
Mouse Behavior ◽  
Mitochondrial Energy Metabolism ◽  
Peripheral Insulin Resistance ◽  
Deficient Mice

Acyl-CoA dehydrogenase 10 (Acad10)-deficient mice develop impaired glucose tolerance, peripheral insulin resistance, and abnormal weight gain. In addition, they exhibit biochemical features of deficiencies of fatty acid oxidation, such as accumulation of metabolites consistent with abnormal mitochondrial energy metabolism and fasting induced rhabdomyolysis. ACAD10 has significant expression in mouse brain, unlike other acyl-CoA dehydrogenases (ACADs) involved in fatty acid oxidation. The presence of ACAD10 in human tissues was determined using immunohistochemical staining. To characterize the effect of ACAD10 deficiency on the brain, micro-MRI and neurobehavioral evaluations were performed. Acad10-deficient mouse behavior was examined using open field testing and DigiGait analysis for changes in general activity as well as indices of gait, respectively. ACAD10 protein was shown to colocalize to mitochondria and peroxisomes in lung, muscle, kidney, and pancreas human tissue. Acad10-deficient mice demonstrated subtle behavioral abnormalities, which included reduced activity and increased time in the arena perimeter in the open field test. Mutant animals exhibited brake and propulsion metrics similar to those of control animals, which indicates normal balance, stability of gait, and the absence of significant motor impairment. The lack of evidence for motor impairment combined with avoidance of the center of an open field arena and reduced vertical and horizontal exploration are consistent with a phenotype characterized by elevated anxiety. These results implicate ACAD10 function in normal mouse behavior, which suggests a novel role for ACAD10 in brain metabolism.

scholarly journals 4333 The role of the L-type calcium channel, Cav1.3, in motor and associative learning

2020 ◽  
Vol 4 (s1) ◽  
pp. 19-20
Author(s):  
Aislinn Joanmarie Williams ◽  
Marisol Lauffer ◽  
Hsiang Wen ◽  
Bryn Myers
Keyword(s):  
Motor Learning ◽  
Associative Learning ◽  
Fear Conditioning ◽  
Open Field ◽  
Genetic Background ◽  
Forced Swim Test ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
Increased Risk ◽  
Deficient Mice

OBJECTIVES/GOALS: Genetic variation in L-type voltage-gated calcium channels, including CaV1.3, is associated with increased risk for psychiatric disorders including bipolar disorder and schizophrenia. Additionally, rare mutations in CaV1.3 have been linked to epilepsy, developmental delay, and autism. Deletion of CaV1.3 in mice is associated with impaired consolidation of contextual fear conditioning. Some studies have also observed affective behavior deficits in CaV1.3-deficient mice, but other studies have not found affective phenotypes, perhaps due to differences in genetic backgrounds, sex ratios, or task protocols. CaV1.3 is important for slow afterhyperpolarization in hippocampal and amygdala neurons, which prevents excessive firing in response to sustained excitatory input, and CaV1.3-deficient amygdala neurons exhibit hyperexcitability and impaired LTP. CaV1.3 is also expressed in the cerebellum, but its functional role there is not well understood. Given its importance in shaping neuronal activity in the hippocampus and amygdala, we hypothesized that loss of CaV1.3 would cause abnormalities in motor learning as well as affective and cognitive behaviors. METHODS/STUDY POPULATION: Wild-type (WT), haploinsufficient (Hap), and knockout (KO) mice were maintained on a congenic C57BL/6NTac genetic background and were subjected to behavioral tasks including open field, rotarod, ErasmusLadder, elevated zero maze, forced swim test, and tail suspension test. Data were analyzed with sexes combined and with sexes separated to assess for sex as a biological variable. Studies were analyzed by one-way ANOVA, two-way ANOVA, or generalized linear mixed model, where appropriate. RESULTS/ANTICIPATED RESULTS: CaV1.3 KO was associated with impaired motor learning in the rotarod task (p < 0.05), as well as impaired associative learning in the ErasmusLadder task (p < 0.01), despite intact locomotor function on both tasks. When examined by sex, the rotarod phenotypes were driven by motor learning impairments in males (both Hap and KO, p < 0.05 and p < 0.01, respectively), whereas the ErasmusLadder associative learning phenotypes were present in both sexes only in the KO condition, consistent with previously reported impairments in CaV1.3-deficient mice in consolidation of contextual fear conditioning. Although KO mice learned the motor aspects of the ErasmusLadder task, they learned more slowly. They also failed to learn start cues, which requires intact associative learning. No differences were observed in overall exploration or locomotor activity in open field or elevated zero maze. Analyses from affective tasks are ongoing. DISCUSSION/SIGNIFICANCE OF IMPACT: These preliminary studies provide new evidence that CaV1.3 is important for the function of neural circuits involved in motor learning, and concur with previous data showing its involvement in associative learning. Our data differ slightly from previous studies of CaV1.3 in motor learning, which could be attributable to differences in task protocols and/or genetic background. These results highlight the importance of CaV1.3 in a variety of behaviors, which may help explain why variation in CaV1.3 expression and function has pleiotropic effects in humans.

scholarly journals Obesity Impairs Mobility and Adult Hippocampal Neurogenesis

2019 ◽  
Vol 13 ◽  
pp. 117906951988358 ◽  
Author(s):  
Alexander Bracke ◽  
Grazyna Domanska ◽  
Katharina Bracke ◽  
Steffen Harzsch ◽  
Jens van den Brandt ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Open Field ◽  
Dendritic Spine ◽  
Water Maze ◽  
Brain Volume ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Obese Mice ◽  
Phosphohistone H3 ◽  
Deficient Mice

Currently, it is controversially discussed whether a relationship between obesity and cognition exists. We here analyzed a mouse model of obesity (leptin-deficient mice) to study the effects of obesity on the morphology of the hippocampus (a brain structure involved in mechanisms related to learning and memory) and on behavior. Mice aged 4 to 6 months were analyzed. At this age, the obese mice have nearly double the body weight as controls, but display smaller brains (brain volume is about 10% smaller) as control animals of the same age. Adult hippocampal neurogenesis, a process that is linked to learning and memory, might be disturbed in the obese mice and contribute to the smaller brain volume. Adult hippocampal neurogenesis was examined using specific markers for cell proliferation (phosphohistone H3), neuronal differentiation (doublecortin), and apoptosis (caspase 3). The number of phosphohistone H3 and doublecortin-positive cells was markedly reduced in leptin-deficient mice, but not the number of apoptotic cells, indicating that adult hippocampal neurogenesis on the level of cell proliferation was affected. In addition, dendritic spine densities of pyramidal neurons in the hippocampal area CA1 were analyzed using Golgi impregnation. However, no significant change in dendritic spine densities was noted in the obese mice. Moreover, the performance of the mice was analyzed in the open field as well as in the Morris water maze. In the open field test, obese mice showed reduced locomotor activity, but in the Morris water maze they showed similar performance compared with control animals.

Delay of myelin formation in arylsulphatase A-deficient mice

2005 ◽  
Vol 21 (3) ◽  
pp. 711-720 ◽  
Author(s):  
Afshin Yaghootfam ◽  
Volkmar Gieselmann ◽  
Matthias Eckhardt
Keyword(s):  
Myelin Formation ◽  
Arylsulphatase A ◽  
Deficient Mice

Comparison of localization of metallothionein in tissues of metallothionein-deficient mice

1995 ◽  
Vol 53 ◽  
pp. 1042-1043
Author(s):  
H. Nishimura ◽  
R Nishimura ◽  
D.L. Adelson ◽  
A.E. Michaelska ◽  
K.H.A. Choo ◽  
...  
Keyword(s):  
Metal Binding ◽  
Immunohistochemical Staining ◽  
Squamous Epithelium ◽  
Rabbit Antiserum ◽  
Slight Modification ◽  
Positive Control ◽  
Heavy Metal Binding ◽  
Critical Organ ◽  
Metal Binding Protein ◽  
Deficient Mice

Metallothionein (MT), a cysteine-rich heavy metal binding protein, has several isoforms designated from I to IV. Its major isoforms, I and II, can be induced by heavy metals like cadmium (Cd) and, are present in various organs of man and animals. Rodent testes are a critical organ to Cd and it is still a controversial matter whether MT exists in the testis although it is clear that MT is not induced by Cd in this tissue. MT-IV mRNA was found to localize within tongue squamous epithelium. Whether MT-III is present mainly glial cells or neurons has become a debatable topic. In the present study, we have utilized MT-I and II gene targeted mice and compared MT localization in various tissues from both MT-deficient mice and C57Black/6J mice (C57BL) which were used as an MT-positive control. For MT immunostaining, we have used rabbit antiserum against rat MT-I known to cross-react with mammalian MT-I and II and human MT-III. Immunohistochemical staining was conducted by the method described in the previous paper with a slight modification after the tissues were fixed in HistoChoice and embedded in paraffin.

Alterations during Positive Selection in the Thymus of nackt CD4-Deficient Mice

2000 ◽  
Vol 52 (6) ◽  
pp. 555-562 ◽  
Author(s):  
I. Nepomnaschy ◽  
G. Lombardi ◽  
P. Bekinschtein ◽  
P. Berguer ◽  
V. Francisco ◽  
...  
Keyword(s):  
Positive Selection ◽  
Deficient Mice
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