Abstract:We characterized the transcriptional response accompanying maintenance of long-term sensitization (LTS) memory in the pleural ganglia of using microarray ( = 8) and qPCR ( = 11 additional samples). We found that 24 h after memory induction there is strong regulation of 1198 transcripts (748 up and 450 down) in a pattern that is almost completely distinct from what is observed during memory encoding (1 h after training). There is widespread up-regulation of transcripts related to all levels of protein productio… Show more
“…Furthermore, in these studies, neuronal genes like neurotransmitter receptor subunits or vesicle fusion proteins are found, consistent with CREB's role in the neuronal processes . Moreover, CREB's reported role in development is recapitulated by hits such as CDKs (involved in cell‐cycle regulation) or hox genes.…”
Section: Main Textsupporting
confidence: 73%
“…A variety of stimuli have been used to activate the CREB signaling pathway, for example, forskolin treatment, which activates cAMP‐signaling, constitutive active CREB, electrostimulation, or conditioning training . Similar approaches have also been used in Drosophila , Aplysia , and C. elegans . In Drosophila , selected cells involved in learning and memory were picked either by patch clamp or tagged nuclei (INTACT) to obtain cell‐type‐specific transcriptomic profiles.…”
Consolidation of long‐term memory is a highly and precisely regulated multistep process. The transcription regulator cAMP response element‐binding protein (CREB) plays a key role in initiating memory consolidation. With time processing, first the cofactors are changed and, secondly, CREB gets dispensable. This ultimately changes the expressed gene program to genes required to maintain the memory. Regulation of memory consolidation also requires epigenetic mechanisms and control at the RNA level. At the neuronal circuit level, oscillation in the activity of CREB and downstream factor define engram cells. Together the combination of all regulation mechanisms allows correct memory processing while keeping the process dynamic and flexible to adjust to different contexts. Also see the video abstract here https://youtu.be/BhSCSmorpEc.
“…Furthermore, in these studies, neuronal genes like neurotransmitter receptor subunits or vesicle fusion proteins are found, consistent with CREB's role in the neuronal processes . Moreover, CREB's reported role in development is recapitulated by hits such as CDKs (involved in cell‐cycle regulation) or hox genes.…”
Section: Main Textsupporting
confidence: 73%
“…A variety of stimuli have been used to activate the CREB signaling pathway, for example, forskolin treatment, which activates cAMP‐signaling, constitutive active CREB, electrostimulation, or conditioning training . Similar approaches have also been used in Drosophila , Aplysia , and C. elegans . In Drosophila , selected cells involved in learning and memory were picked either by patch clamp or tagged nuclei (INTACT) to obtain cell‐type‐specific transcriptomic profiles.…”
Consolidation of long‐term memory is a highly and precisely regulated multistep process. The transcription regulator cAMP response element‐binding protein (CREB) plays a key role in initiating memory consolidation. With time processing, first the cofactors are changed and, secondly, CREB gets dispensable. This ultimately changes the expressed gene program to genes required to maintain the memory. Regulation of memory consolidation also requires epigenetic mechanisms and control at the RNA level. At the neuronal circuit level, oscillation in the activity of CREB and downstream factor define engram cells. Together the combination of all regulation mechanisms allows correct memory processing while keeping the process dynamic and flexible to adjust to different contexts. Also see the video abstract here https://youtu.be/BhSCSmorpEc.
“…The effect size for a t-test is the difference between the two means. Example from Conte et al (2017): Reflexes responses were 8.9s before training and 16.5s after training, an average increase of 7.5s 95% CI [6.8,8.2]. 2x2 Interaction in a Factorial ANOVA.…”
Section: Effect Sizes Can Be Expressed In Standardized Unitsmentioning
confidence: 99%
“…We now obtain effect sizes of around 2.6 standard deviations. With much larger effect sizes we now use fewer animals (8-12/experiment) to obtain much more consistent results (Conte et al 2017;Perez et al 2018).…”
Section: Effect Sizes Can Be Expressed In Standardized Unitsmentioning
This paper has now been published in the Journal of Undergraduate Neuroscience Eduction: http://www.funjournal.org/wp-content/uploads/2018/04/june-16-e21.pdf?x91298. See also, this record on PubMed and PubMedCentral: https://www.ncbi.nlm.nih.gov/pubmed/30057503. An ongoing reform in statistical practice is to report and interpret effect sizes. This paper provides a short tutorial on effect sizes and some tips on how to help your students think in terms of effect sizes when analyzing data. An effect size is just a quantitative answer to a research question. Effect sizes should always be accompanied by a confidence interval or some other means of expressing uncertainty in generalizing from the sample to the population. Effect sizes are best interpreted in raw scores, but can also be expressed in standardized terms; several popular standardized effect score measures are explained and compared. Training your students to reporting and interpreting effect sizes can help them be better scientists: it will help them think critically about the practical significance of their results, makes uncertainty salient, foster better planning for subsequent experiments, encourage meta-analytic thinking, and can help focus their efforts on optimizing measurement. You can help your students start to think in effect sizes by giving them tools to visualize and translate between different effect size measures, and by tasking them to build a ‘library’ of effect sizes in a research field of interest.
This is a pre-print of a paper now published in Neurobiology of Learning and Memory: https://doi.org/10.1016/j.nlm.2018.09.007 Most long-term memories are forgotten, becoming progressively less likely to be recalled. Still, some memory fragments may persist beyond forgetting, as savings memory (easier relearning) can persist long after recall has become impossible. What happens to a memory trace during forgetting that makes it inaccessible for recall and yet still effective to spark easier re-learning? We are addressing this question by tracking the transcriptional changes that accompany learning and then forgetting of a long-term sensitization memory in the tail-elicited siphon withdrawal reflex of Aplysia californica. First, we tracked savings memory. We found that even though recall of sensitization fades completely within 1 week of training, savings memory is still robustly expressed at 2 weeks post training. Next, we tracked the time-course of regulation of 11 transcripts we previously identified as potentially being regulated beyond the decay of recall. Remarkably, 3 transcripts still show strong regulation of expression 2 weeks after training and an additional 4 are regulated for at least 1 week. These long-lasting changes in gene expression always began early in the memory process, within 1 day of training. We present a synthesis of our results tracking gene expression changes accompanying sensitization and provide a testable model of how sensitization memory is forgotten.
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