cognitive phenotype
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2021 ◽  
Author(s):  
◽  
Saskia Rutherford-Ymker

<p>The underpinning hypothesis of this study is that the environmental insults implicated in schizophrenia cause epigenetic changes that trigger deleterious gene expression, resulting in deviations from normal neurodevelopment. The behavioural abnormalities in schizophrenia can be grouped into the three common classes of symptoms: positive, negative, and cognitive. Cognitive symptoms are symptoms that impair cognitive processing and have detrimental effects on individuals with schizophrenia. Maternal immune activation refers to a rat model that stimulates a maternal immune system with an infection or infectious-like stimulus resulting in adverse phenotypes. A cognitive phenotype, maternal immune activation (MIA) model of schizophrenia was employed to use epigenetic markers to discover what deleterious genes drive the cognitive deficits phenotype.  Previous work has discerned many changes in gene expression that are implicated in schizophrenia. A hypothesis-driven approach was utilized to determine whether previously studied candidate genes are relevant in the cognitive symptoms of schizophrenia in this cognitive-phenotype model. It was found that prenatal treatment of lipopolysaccharide (LPS) (which is the major outer membrane component of gram-negative bacteria and mimics bacterial infection) on prenatal day 10 and 11 led to changes in mRNA levels in the prefrontal cortex of adolescent rats. Typically, an increase in the amount of transcript in the LPS condition compared to the saline condition, or a greater variability in the amount of transcript between replicates in the LPS condition than the saline condition, was observed. Statistical analysis revealed that these changes did not met statistical significance.  To build towards a whole genome DNA methylation analysis, two discrete approaches were used. The first utilized bisulfite modification and investigated changes in candidate genes as a precursor to genome-wide BS-sequencing. DNA methylation was measured across CpG rich regions and an absence of DNA methylation was detected in these regions in both the LPS and saline conditions in the candidate genes.   The second approach utilized a long-read sequencing platform to establish the feasibility of a bisulfite conversion-free method for whole-genome DNA methylation approach within our lab. Through the establishment of this method factors that affect the reliability, quality, and accuracy of the final sequencing product were explored. Many of which were in the downstream-from-sequencing, data analysis component of the process. Discoveries were also made regarding how much data would be needed to make direct DNA methylation detection feasible.   The data presented here demonstrated that the cognitive-phenotype MIA model had altered gene expression correlating with previously measured behavioural cognitive deficits in the prefrontal cortex in genes that were known to be associated with schizophrenia. To extend this further, a whole genome approach would be needed to discover novel drivers of the phenotype. In the current study, headway was made towards the development and establishment of a whole genome DNA methylation detection method to further this continued aim.</p>


2021 ◽  
Author(s):  
◽  
Saskia Rutherford-Ymker

<p>The underpinning hypothesis of this study is that the environmental insults implicated in schizophrenia cause epigenetic changes that trigger deleterious gene expression, resulting in deviations from normal neurodevelopment. The behavioural abnormalities in schizophrenia can be grouped into the three common classes of symptoms: positive, negative, and cognitive. Cognitive symptoms are symptoms that impair cognitive processing and have detrimental effects on individuals with schizophrenia. Maternal immune activation refers to a rat model that stimulates a maternal immune system with an infection or infectious-like stimulus resulting in adverse phenotypes. A cognitive phenotype, maternal immune activation (MIA) model of schizophrenia was employed to use epigenetic markers to discover what deleterious genes drive the cognitive deficits phenotype.  Previous work has discerned many changes in gene expression that are implicated in schizophrenia. A hypothesis-driven approach was utilized to determine whether previously studied candidate genes are relevant in the cognitive symptoms of schizophrenia in this cognitive-phenotype model. It was found that prenatal treatment of lipopolysaccharide (LPS) (which is the major outer membrane component of gram-negative bacteria and mimics bacterial infection) on prenatal day 10 and 11 led to changes in mRNA levels in the prefrontal cortex of adolescent rats. Typically, an increase in the amount of transcript in the LPS condition compared to the saline condition, or a greater variability in the amount of transcript between replicates in the LPS condition than the saline condition, was observed. Statistical analysis revealed that these changes did not met statistical significance.  To build towards a whole genome DNA methylation analysis, two discrete approaches were used. The first utilized bisulfite modification and investigated changes in candidate genes as a precursor to genome-wide BS-sequencing. DNA methylation was measured across CpG rich regions and an absence of DNA methylation was detected in these regions in both the LPS and saline conditions in the candidate genes.   The second approach utilized a long-read sequencing platform to establish the feasibility of a bisulfite conversion-free method for whole-genome DNA methylation approach within our lab. Through the establishment of this method factors that affect the reliability, quality, and accuracy of the final sequencing product were explored. Many of which were in the downstream-from-sequencing, data analysis component of the process. Discoveries were also made regarding how much data would be needed to make direct DNA methylation detection feasible.   The data presented here demonstrated that the cognitive-phenotype MIA model had altered gene expression correlating with previously measured behavioural cognitive deficits in the prefrontal cortex in genes that were known to be associated with schizophrenia. To extend this further, a whole genome approach would be needed to discover novel drivers of the phenotype. In the current study, headway was made towards the development and establishment of a whole genome DNA methylation detection method to further this continued aim.</p>


Author(s):  
Florian Cherik ◽  
Mathis Lepage ◽  
Ganaelle Remerand ◽  
Christine Francannet ◽  
Amélie Delabaere ◽  
...  

Author(s):  
Cayley Swinton ◽  
Erin Swinton ◽  
Iain Phillips ◽  
Ken Lukowiak

A heat stressor (1h at 30o C) in Lymnaea stagnalis before operant conditioning training of aerial respiration is sufficient to enhance long-term memory (LTM) formation in average cognitive-ability, laboratory-reared, inbred snails. However, in freshly collected outbred snails the same heat stressor blocks LTM formation in smart cognitive phenotype but not in average cognitive phenotype strains. Here we hypothesize that: 1) preventing the stress associated with the heat stressor before training allows LTM to form in the smart phenotype strains ; and 2) alleviating the stress before a memory recall session allows a formed LTM to be recalled in the smart phenotype strains. We found that an injection of propranolol, which mitigates the stressor, before snails experience the heat stressor enabled two strains of the smart phenotype snails to form LTM formation, consistent with our first hypothesis. However, the injection of propranolol before a memory test session, did not alleviate a memory recall block in the smart phenotype snails. Thus, our second hypothesis was not supported. Thus, smart cognitive phenotype snails encountering a heat stressor have an inability to form LTM, but this inability can be overcome by the pre-injection of propranolol.


Author(s):  
Jannis Liedtke ◽  
Lutz Fromhage

Both cognitive abilities and dispersal tendencies can vary strongly between individuals. Since cognitive abilities may help dealing with unknown circumstances it is conceivable that dispersers may rely more heavily on learning abilities than residents. However, cognitive abilities are costly and leaving a familiar place might result in losing the advantage of having learned to deal with local conditions. Thus, individuals which invested in learning to cope with local conditions may be more reluctant to leave their natal place. In order to disentangle the complex relationship between dispersal and learning abilities we implemented individual-based simulations. By allowing for developmental plasticity, individuals could either develop a ‘resident´ or ‘dispersal´ cognitive phenotype. In line with our expectations, the correlation between learning abilities and dispersal could take any direction, depending how much time individuals had to recoup their investment in cognition. Both, longevity and the timing of dispersal within lifecycles determine the time individuals have to recoup that investment and thus crucially influence this correlation. We therefore suggest that species´ life-history will strongly impact the expected cognitive abilities of dispersers, relative to their resident conspecifics, and that cognitive abilities might be an integral part of dispersal syndromes.


2020 ◽  
Vol 16 (S6) ◽  
Author(s):  
Philip W. Tipton ◽  
Nazli G. Bulbul ◽  
Julia E. Crook ◽  
Ryan J. Uitti ◽  
Zbigniew Wszolek ◽  
...  

2020 ◽  
Vol 60 (4) ◽  
pp. 925-928
Author(s):  
Sabrina S Burmeister ◽  
Yuxiang Liu

Synopsis A long-standing question in animal behavior is what are the patterns and processes that shape the evolution of cognition? One effective way to address this question is to study cognitive abilities in a broad spectrum of animals. While comparative psychologists have traditionally focused on a narrow range of organisms, today they may work with any number of species, from frogs to birds or bees. This broader range of study species has greatly enriched our understanding of the diversity of cognitive processes among animals. Yet, this diversity has highlighted the fundamental challenge of comparing cognitive processes across animals. An analysis of the neural and molecular mechanisms of cognition may be necessary to solve this problem. The goal of our symposium was to bring together speakers studying a range of species to gain a broadly integrative perspective on cognition while at the same time considering the potentially important role of neurobiology and genomics in addressing the difficult problem of comparing cognition across species. For example, work by MaBouDi et al. indicates that neural constraints on computing power may impact the cognitive processes underlying numerical discrimination in bees. A presentation by Lara LaDage demonstrated how neurobiology can be used to better understand cognition and its evolution in reptiles while Edwards et al. identify the cerebellum as potentially important in the performance of the complex process of nest building. We see that molecular approaches highlight the contributions of the prefrontal cortex and hippocampus to cognitive phenotype across vertebrates while, at the same time, identifying the genes and cellular processes that may contribute to evolution of cognition. The potentially important role of neurogenesis and synaptic plasticity emerge clearly from such studies. Still unanswered is the question of whether molecular tools will contribute to our ability to discriminate convergent/parallel evolution from homology in the evolution of cognitive phenotype.


2020 ◽  
Vol 52 (7) ◽  
pp. 3828-3845 ◽  
Author(s):  
Kristine M. Ulrichsen ◽  
Dag Alnæs ◽  
Knut K. Kolskår ◽  
Geneviève Richard ◽  
Anne‐Marthe Sanders ◽  
...  

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