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J. David Sweatt - One of the best experts on this subject based on the ideXlab platform.
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DNA methylation and Memory Formation
Nature neuroscience, 2010Co-Authors: Jeremy J. Day, J. David SweattAbstract:Memory Formation and storage require long-lasting changes in Memory-related neuronal circuits. Recent evidence indicates that DNA methylation may serve as a contributing mechanism in Memory Formation and storage. These emerging findings suggest a role for an epigenetic mechanism in learning and long-term Memory maintenance and raise apparent conundrums and questions. For example, it is unclear how DNA methylation might be reversed during the Formation of a Memory, how changes in DNA methylation alter neuronal function to promote Memory Formation, and how DNA methylation patterns differ between neuronal structures to enable both consolidation and storage of memories. Here we evaluate the existing evidence supporting a role for DNA methylation in Memory, discuss how DNA methylation may affect genetic and neuronal function to contribute to behavior, propose several future directions for the emerging subfield of neuroepigenetics, and begin to address some of the broader implications of this work.
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Regulation of chromatin structure in Memory Formation.
Current opinion in neurobiology, 2009Co-Authors: Tania L. Roth, J. David SweattAbstract:This brief review focuses on the role of epigenetic mechanisms in plasticity and Memory Formation, and their identification as targets of activity-dependent regulation in neurons. Epigenetic modifications of chromatin, namely post-translational modifications of nuclear proteins and covalent modification of DNA, result in potent regulation of gene readout. Recent data have demonstrated that epigenetic mechanisms play a significant role in regulating synaptic plasticity and Memory. In this review, we focus on this theme, describing some basic background concerning epigenetic molecular mechanisms, and describing recent results concerning plasticity and Memory Formation. As an understanding of these novel mechanisms of transcriptional regulation promises to invigorate many areas of investigation, we end by speculating upon some of the open questions ripe for discovery.
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Altered protein synthesis is a trigger for long-term Memory Formation.
Neurobiology of learning and memory, 2007Co-Authors: Eric Klann, J. David SweattAbstract:There is ongoing debate concerning whether new protein synthesis is necessary for, or even contributes to, Memory Formation and storage. This review summarizes a contemporary model proposing a role for altered protein synthesis in Memory Formation and its subsequent stabilization. One defining aspect of the model is that altered protein synthesis serves as a trigger for Memory consolidation. Thus, we propose that specific alterations in the pattern of neuronal protein translation serve as an initial event in long-term Memory Formation. These specific alterations in protein readout result in the Formation of a protein complex that then serves as a nidus for subsequent perpetuating reinforcement by a positive feedback mechanism. The model proposes this scenario as a minimal but requisite component for long-term Memory Formation. Our description specifies three aspects of prevailing scenarios for the role of altered protein synthesis in Memory that we feel will help clarify what, precisely, is typically proposed as the role for protein translation in Memory Formation. First, that a relatively short initial time window exists wherein specific alterations in the pattern of proteins translated (not overall protein synthesis) is involved in initializing the engram. Second, that a self-perpetuating positive feedback mechanism maintains the altered pattern of protein expression (synthesis or recruitment) locally. Third, that other than the Formation and subsequent perpetuation of the unique initializing proteins, ongoing constitutive protein synthesis is all that is minimally necessary for Formation and maintenance of the engram. We feel that a clear delineation of these three principles will assist in interpreting the available experimental data, and propose that the available data are consistent with a role for protein synthesis in Memory.
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Covalent Modification of DNA Regulates Memory Formation
Neuron, 2007Co-Authors: Courtney A Miller, J. David SweattAbstract:Summary DNA methylation is a covalent chemical modification of DNA catalyzed by DNA methyltransferases (DNMTs). DNA methylation is associated with transcriptional silencing and has been studied extensively as a lifelong molecular inFormation storage mechanism put in place during development. Here we report that DNMT gene expression is upregulated in the adult rat hippocampus following contextual fear conditioning and that DNMT inhibition blocks Memory Formation. In addition, fear conditioning is associated with rapid methylation and transcriptional silencing of the Memory suppressor gene PP1 and de methylation and transcriptional activation of the synaptic plasticity gene reelin , indicating both methyltransferase and demethylase activity during consolidation. DNMT inhibition prevents the PP1 methylation increase, resulting in aberrant transcription of the gene during the Memory-consolidation period. These results demonstrate that DNA methylation is dynamically regulated in the adult nervous system and that this cellular mechanism is a crucial step in Memory Formation.
Guillén Fernández - One of the best experts on this subject based on the ideXlab platform.
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Intermediate Levels of Hippocampal Activity Appear Optimal for Associative Memory Formation
PloS one, 2010Co-Authors: Xiao Liu, Shaozheng Qin, Mark Rijpkema, Jing Luo, Guillén FernándezAbstract:Background: It is well established that hippocampal activity is positively related to effective associative Memory Formation. However, in biological systems often optimal levels of activity are contrasted by both sub-and supra-optimal levels. Suboptimal levels of hippocampal activity are commonly attributed to unsuccessful Memory Formation, whereas the supraoptimal levels of hippocampal activity related to unsuccessful Memory Formation have been rarely studied. It is still unclear under what circumstances such supra-optimal levels of hippocampal activity occur. To clarify this issue, we aimed at creating a condition, in which supra-optimal hippocampal activity is associated with encoding failure. We assumed that such supra-optimal activity occurs when task-relevant inFormation is embedded in task-irrelevant, distracting inFormation, which can be considered as noise.
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Stressed Memories: How Acute Stress Affects Memory Formation in Humans
The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009Co-Authors: Marloes J. A. G. Henckens, Erno J. Hermans, Marian Joëls, Guillén FernándezAbstract:Stressful, aversive events are extremely well remembered. Such a declarative Memory enhancement is evidently beneficial for survival, but the same mechanism may become maladaptive and culminate in mental diseases such as posttraumatic stress disorder (PTSD). Stress hormones are known to enhance postlearning consolidation of aversive memories but are also thought to have immediate effects on attentional, sensory, and mnemonic processes at Memory Formation. Despite their significance for our understanding of the etiology of stress-related mental disorders, effects of acute stress at Memory Formation, and their brain correlates at the system scale, remain elusive. Using an integrated experimental approach, we probed the neural correlates of Memory Formation while participants underwent a controlled stress induction procedure in a crossover design. Physiological (cortisol level, heart rate, and pupil dilation) and subjective measures confirmed acute stress. Remarkably, reduced hippocampal activation during encoding predicted stress-enhanced Memory performance, both within and between participants. Stress, moreover, amplified early visual and inferior temporal responses, suggesting that hypervigilant processing goes along with enhanced inferior temporal inFormation reduction to relay a higher proportion of task-relevant inFormation to the hippocampus. Thus, acute stress affects neural correlates of Memory Formation in an unexpected manner, the understanding of which may elucidate mechanisms underlying psychological trauma etiology.
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Memory Formation by neuronal synchronization.
Brain research reviews, 2006Co-Authors: Nikolai Axmacher, Guillén Fernández, Christian E Elger, Florian Mormann, Juergen FellAbstract:Cognitive functions not only depend on the localization of neural activity, but also on the precise temporal pattern of activity in neural assemblies. Synchronization of action potential discharges provides a link between large-scale EEG recordings and cellular plasticity mechanisms. Here, we focus on the role of neuronal synchronization in different frequency domains for the subsequent stages of Memory Formation. Recent EEG studies suggest that synchronized neural activity in the gamma frequency range (around 30-100 Hz) plays a functional role for the Formation of declarative long-term memories in humans. On the cellular level, gamma synchronization between hippocampal and parahippocampal regions may induce LTP in the CA3 region of the hippocampus. In order to encode spatial locations or sequences of multiple items and to guarantee a defined temporal order of Memory processing, synchronization in the gamma frequency range has to be accompanied by a stimulus-locked phase reset of ongoing theta oscillations. Simultaneous gamma- and theta-dependent plasticity leads to complex learning rules required for realistic declarative Memory Formation. Subsequently, consolidation of declarative memories may occur via replay of newly acquired patterns in so-called sharp wave-ripple complexes, predominantly during slow-wave sleep. These irregular bursts induce longer lasting forms of synaptic plasticity in output regions of the hippocampus and in the neocortex. In summary, synchronization of neural assemblies in different frequency ranges induces specific forms of cellular plasticity during subsequent stages of Memory Formation.
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Rhinal-hippocampal connectivity determines Memory Formation during sleep.
Brain : a journal of neurology, 2005Co-Authors: Juergen Fell, Guillén Fernández, Carlo Schaller, Christian E Elger, Martin T Lutz, Edgar Kockelmann, Wieland Burr, Christoph HelmstaedterAbstract:Compared with waking state attention, volition and semantic processing play a minor role during sleep. Thus, investigating declarative Memory Formation during sleep may allow us to isolate mnemonic core processes. The most feasible approach to Memory Formation during sleep is the analysis of dream memories. Lesion and imaging studies have demonstrated that encoding of declarative memories, i.e. consciously accessible events and facts, depends on operations within the rhinal cortex and the hippocampus, two substructures of the medial temporal lobe. Successful Memory Formation is accompanied by a transient rhinal-hippocampal interaction. Consequently, the ability to memorize dreams may be related to mediotemporal connectivity. Therefore, we recorded EEG during sleep from rhinal and hippocampal depth electrodes implanted in 12 epilepsy patients (eight women, mean age 41.1 +/- 6.4 years). They were awakened during rapid eye movement sleep (REM) and asked to recall their dream. Via coherence analyses we show that rhinal-hippocampal connectivity values are approximately twice as large for patients with good dream recall versus those patients with poor recall. This suggests that rhinal-hippocampal connectivity is a key factor in determining declarative Memory Formation.
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rhinal hippocampal theta coherence during declarative Memory Formation interaction with gamma synchronization
European Journal of Neuroscience, 2003Co-Authors: Juergen Fell, Peter Klaver, Hakim Elfadil, Carlo Schaller, Christian E Elger, Guillén FernándezAbstract:The hippocampus and the rhinal cortex, two substructures of the medial temporal lobe, together play a crucial role in human declarative Memory Formation. To investigate in detail the mechanism connecting these two structures transiently during Memory Formation we recorded depth EEG in epilepsy patients from within the hippocampus and the rhinal cortex. During this recording, patients performed a single-trial word list-learning paradigm with a free recall Memory test following a distraction task. Rhinal-hippocampal EEG coherence and spectral power at both locations in the time interval up to 2 s after onset of word presentation were analysed in the frequency range 1-19 Hz. Successful as opposed to unsuccessful Memory Formation was associated with a general rhinal-hippocampal coherence enhancement, but without alterations in spectral power. Coherence increases in the theta range were correlated with the previously reported Memory-related changes in rhinal-hippocampal gamma phase synchronization. This correlation may suggest an interaction of the two mechanisms during declarative Memory Formation. While theta coherence might be associated with slowly modulated coupling related to an encoding state, rhinal-hippocampal gamma synchronization may be more closely related to actual Memory processes by enabling fast coupling and decoupling of the two structures.
Christian E Elger - One of the best experts on this subject based on the ideXlab platform.
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Phase-locking within human mediotemporal lobe predicts Memory Formation.
NeuroImage, 2008Co-Authors: Jürgen Fell, Nikolai Axmacher, Eva Ludowig, Timm Rosburg, Christian E ElgerAbstract:Lesion and imaging studies have demonstrated that encoding of declarative memories, i.e. consciously accessible events and facts, is supported by processes within the rhinal cortex and the hippocampus, two substructures of the mediotemporal lobe (MTL). Successful Memory Formation has, for instance, been shown to be accompanied by the rhinal N400 component, followed by a hippocampal positivity, as well as by transient rhinal-hippocampal phase synchronization. However, it has been an open question, which mediotemporal electroencephalogram (EEG) measures predict Memory Formation most accurately. Therefore, we analyzed and compared the association of different mediotemporal EEG measures with successful Memory Formation. EEG characteristics were extracted from intracranial rhinal and hippocampal depth recordings in 31 epilepsy patients performing a continuous word recognition paradigm. Classical event-related potential measures, rhinal-hippocampal synchronization, as well as inter-trial phase-locking and power changes within rhinal cortex and hippocampus were evaluated. We found that inter-trial phase-locking is superior to other EEG measures in predicting subsequent Memory. This means that Memory Formation is related to the precise timing of EEG phases within the MTL with respect to stimulus onset. In particular, early rhinal and hippocampal phase-locking in the alpha/beta range reaching its maximum already between 100 and 300 ms after stimulus onset appears to be a precursor of successful Memory Formation. Our data suggest that early mediotemporal phase adjustments constitute a relevant mechanism underlying declarative Memory encoding.
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Memory Formation by refinement of neural representations: the inhibition hypothesis.
Behavioural brain research, 2007Co-Authors: Nikolai Axmacher, Christian E Elger, Juergen FellAbstract:There is no reasonable doubt that the hippocampus plays an important role in Memory processing. A virtually uncountable number of studies in animals and humans have revealed changes in neural activity in this structure during Memory Formation [Squire LR. Memory and the hippocampus: a synthesis from findings with rats, monkeys, and humans. Psychol Rev 1992;99:195-231; Squire LR, Stark CE, Clark RE. The medial temporal lobe. Annu Rev Neurosci 2004;27:279-306], and hippocampal damage reliably leads to impairments in a large number of Memory tests. However, while several correlates of successful Memory Formation have been found in the hippocampus, it is still an open question why specific neural processes support encoding of a particular item. An answer to this question would help to resolve current debates about which Memory functions are actually supported by the hippocampus, and why activity in the neural networks of the hippocampus is involved in, or even necessary for, some Memory processes but not for others. In this review, we first summarize findings on the electrophysiological activity within the hippocampus during different Memory processes. We try to differentiate whether the hippocampus is merely involved in these processes, or whether the hippocampus appears to be necessary for them. Based on a distinction between a more general "encoding state" and the more specific process of "content-specific Memory Formation", we review data on neural representations within hippocampus and neocortex. We suggest that during Memory Formation, the hippocampus renders neural representations more sparse by providing an inhibitory signal to the neocortex.
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Memory Formation by neuronal synchronization.
Brain research reviews, 2006Co-Authors: Nikolai Axmacher, Guillén Fernández, Christian E Elger, Florian Mormann, Juergen FellAbstract:Cognitive functions not only depend on the localization of neural activity, but also on the precise temporal pattern of activity in neural assemblies. Synchronization of action potential discharges provides a link between large-scale EEG recordings and cellular plasticity mechanisms. Here, we focus on the role of neuronal synchronization in different frequency domains for the subsequent stages of Memory Formation. Recent EEG studies suggest that synchronized neural activity in the gamma frequency range (around 30-100 Hz) plays a functional role for the Formation of declarative long-term memories in humans. On the cellular level, gamma synchronization between hippocampal and parahippocampal regions may induce LTP in the CA3 region of the hippocampus. In order to encode spatial locations or sequences of multiple items and to guarantee a defined temporal order of Memory processing, synchronization in the gamma frequency range has to be accompanied by a stimulus-locked phase reset of ongoing theta oscillations. Simultaneous gamma- and theta-dependent plasticity leads to complex learning rules required for realistic declarative Memory Formation. Subsequently, consolidation of declarative memories may occur via replay of newly acquired patterns in so-called sharp wave-ripple complexes, predominantly during slow-wave sleep. These irregular bursts induce longer lasting forms of synaptic plasticity in output regions of the hippocampus and in the neocortex. In summary, synchronization of neural assemblies in different frequency ranges induces specific forms of cellular plasticity during subsequent stages of Memory Formation.
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Rhinal-hippocampal connectivity determines Memory Formation during sleep.
Brain : a journal of neurology, 2005Co-Authors: Juergen Fell, Guillén Fernández, Carlo Schaller, Christian E Elger, Martin T Lutz, Edgar Kockelmann, Wieland Burr, Christoph HelmstaedterAbstract:Compared with waking state attention, volition and semantic processing play a minor role during sleep. Thus, investigating declarative Memory Formation during sleep may allow us to isolate mnemonic core processes. The most feasible approach to Memory Formation during sleep is the analysis of dream memories. Lesion and imaging studies have demonstrated that encoding of declarative memories, i.e. consciously accessible events and facts, depends on operations within the rhinal cortex and the hippocampus, two substructures of the medial temporal lobe. Successful Memory Formation is accompanied by a transient rhinal-hippocampal interaction. Consequently, the ability to memorize dreams may be related to mediotemporal connectivity. Therefore, we recorded EEG during sleep from rhinal and hippocampal depth electrodes implanted in 12 epilepsy patients (eight women, mean age 41.1 +/- 6.4 years). They were awakened during rapid eye movement sleep (REM) and asked to recall their dream. Via coherence analyses we show that rhinal-hippocampal connectivity values are approximately twice as large for patients with good dream recall versus those patients with poor recall. This suggests that rhinal-hippocampal connectivity is a key factor in determining declarative Memory Formation.
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rhinal hippocampal theta coherence during declarative Memory Formation interaction with gamma synchronization
European Journal of Neuroscience, 2003Co-Authors: Juergen Fell, Peter Klaver, Hakim Elfadil, Carlo Schaller, Christian E Elger, Guillén FernándezAbstract:The hippocampus and the rhinal cortex, two substructures of the medial temporal lobe, together play a crucial role in human declarative Memory Formation. To investigate in detail the mechanism connecting these two structures transiently during Memory Formation we recorded depth EEG in epilepsy patients from within the hippocampus and the rhinal cortex. During this recording, patients performed a single-trial word list-learning paradigm with a free recall Memory test following a distraction task. Rhinal-hippocampal EEG coherence and spectral power at both locations in the time interval up to 2 s after onset of word presentation were analysed in the frequency range 1-19 Hz. Successful as opposed to unsuccessful Memory Formation was associated with a general rhinal-hippocampal coherence enhancement, but without alterations in spectral power. Coherence increases in the theta range were correlated with the previously reported Memory-related changes in rhinal-hippocampal gamma phase synchronization. This correlation may suggest an interaction of the two mechanisms during declarative Memory Formation. While theta coherence might be associated with slowly modulated coupling related to an encoding state, rhinal-hippocampal gamma synchronization may be more closely related to actual Memory processes by enabling fast coupling and decoupling of the two structures.
Sheena A. Josselyn - One of the best experts on this subject based on the ideXlab platform.
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Reprint of: disrupting Jagged1-Notch signaling impairs spatial Memory Formation in adult mice.
Neurobiology of learning and memory, 2013Co-Authors: Derya Sargin, Leigh C.p. Botly, Gemma Higgs, Alexander Marsolais, Paul W. Frankland, Sean E. Egan, Sheena A. JosselynAbstract:It is well-known that Notch signaling plays a critical role in brain development and growing evidence implicates this signaling pathway in adult synaptic plasticity and Memory Formation. The Notch1 receptor is activated by two subclasses of ligands, Delta-like (including Dll1 and Dll4) and Jagged (including Jag1 and Jag2). Ligand-induced Notch1 receptor signaling is modulated by a family of Fringe proteins, including Lunatic fringe (Lfng). Although Dll1, Jag1 and Lfng are critical regulators of Notch signaling, their relative contribution to Memory Formation in the adult brain is unknown. To investigate the roles of these important components of Notch signaling in Memory Formation, we examined spatial and fear Memory Formation in adult mice with reduced expression of Dll1, Jag1, Lfng and Dll1 plus Lfng. We also examined motor activity, anxiety-like behavior and sensorimotor gating using the acoustic startle response in these mice. Of the lines of mutant mice tested, we found that only mice with reduced Jag1 expression (mice heterozygous for a null mutation in Jag1, Jag1 +/ ) showed a selective impairment in spatial Memory Formation. Importantly, all other behavior including open field activity, conditioned fear Memory (both context and discrete cue), acoustic startle response and prepulse inhibition, was normal in this line of mice. These results provide the first in vivo evidence that Jag1–Notch signaling is critical for Memory Formation in the adult brain.
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Disrupting Jagged1-Notch signaling impairs spatial Memory Formation in adult mice.
Neurobiology of learning and memory, 2013Co-Authors: Derya Sargin, Leigh C.p. Botly, Gemma Higgs, Alexander Marsolais, Paul W. Frankland, Sean E. Egan, Sheena A. JosselynAbstract:It is well-known that Notch signaling plays a critical role in brain development and growing evidence implicates this signaling pathway in adult synaptic plasticity and Memory Formation. The Notch1 receptor is activated by two subclasses of ligands, Delta-like (including Dll1 and Dll4) and Jagged (including Jag1 and Jag2). Ligand-induced Notch1 receptor signaling is modulated by a family of Fringe proteins, including Lunatic fringe (Lfng). Although Dll1, Jag1 and Lfng are critical regulators of Notch signaling, their relative contribution to Memory Formation in the adult brain is unknown. To investigate the roles of these important components of Notch signaling in Memory Formation, we examined spatial and fear Memory Formation in adult mice with reduced expression of Dll1, Jag1, Lfng and Dll1 plus Lfng. We also examined motor activity, anxiety-like behavior and sensorimotor gating using the acoustic startle response in these mice. Of the lines of mutant mice tested, we found that only mice with reduced Jag1 expression (mice heterozygous for a null mutation in Jag1, Jag1(+/-)) showed a selective impairment in spatial Memory Formation. Importantly, all other behavior including open field activity, conditioned fear Memory (both context and discrete cue), acoustic startle response and prepulse inhibition, was normal in this line of mice. These results provide the first in vivo evidence that Jag1-Notch signaling is critical for Memory Formation in the adult brain.
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Neuronal Competition and Selection During Memory Formation
Science (New York N.Y.), 2007Co-Authors: Jin-hee Han, Adelaide P. Yiu, Rachael L. Neve, Steven A. Kushner, Christy J. Cole, Anna Matynia, Robert A.m. Brown, John F. Guzowski, Alcino J. Silva, Sheena A. JosselynAbstract::Competition between neurons is necessary for refining neural circuits during development and may be important for selecting the neurons that participate in encoding memories in the adult brain. To examine neuronal competition during Memory Formation, we conducted experiments with mice in which we manipulated the function of CREB (adenosine 3´,5´-monophosphate response element–binding protein) in subsets of neurons. Changes in CREB function influenced the probability that individual lateral amygdala neurons were recruited into a fear Memory trace. Our results suggest a competitive model underlying Memory Formation, in which eligible neurons are selected to participate in am emory trace as af unction of their relative CREB activity at the time of learning.
Ronald L Davis - One of the best experts on this subject based on the ideXlab platform.
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MicroRNA function in Drosophila Memory Formation.
Current opinion in neurobiology, 2016Co-Authors: Germain U. Busto, Tugba Guven-ozkan, Ronald L DavisAbstract:MicroRNAs (miRs) are small non-coding RNAs that regulate protein expression through post-transcriptional mechanisms. They participate in broad aspects of biology from the control of developmental processes to tumorigenesis. Recent studies in Drosophila show that they also regulate activity-dependent and sensory-specific protein expression and support olfactory Memory Formation. Among the hundreds of miRs described, several have been demonstrated to be required for normal learning, Memory, or for the development of neuronal circuits that support Memory Formation. Fly models of human diseases offer promise of identifying miRs whose expression becomes dysregulated and part of the pathological state, providing models for understanding brain disorders and drug discovery.
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identification of genes that promote or inhibit olfactory Memory Formation in drosophila
Genetics, 2015Co-Authors: Erica Walkinshaw, Caitlin Farkas, Daniel Richter, Eric P Nicholas, Krystyna Keleman, Ronald L DavisAbstract:Genetic screens in Drosophila melanogaster and other organisms have been pursued to filter the genome for genetic functions important for Memory Formation. Such screens have employed primarily chemical or transposon-mediated mutagenesis and have identified numerous mutants including classical Memory mutants, dunce and rutabaga. Here, we report the results of a large screen using panneuronal RNAi expression to identify additional genes critical for Memory Formation. We identified >500 genes that compromise Memory when inhibited (low hits), either by disrupting the development and normal function of the adult animal or by participating in the neurophysiological mechanisms underlying Memory Formation. We also identified >40 genes that enhance Memory when inhibited (high hits). The dunce gene was identified as one of the low hits and further experiments were performed to map the effects of the dunce RNAi to the α/β and γ mushroom body neurons. Additional behavioral experiments suggest that dunce knockdown in the mushroom body neurons impairs Memory without significantly affecting acquisition. We also characterized one high hit, sickie, to show that RNAi knockdown of this gene enhances Memory through effects in dopaminergic neurons without apparent effects on acquisition. These studies further our understanding of two genes involved in Memory Formation, provide a valuable list of genes that impair Memory that may be important for understanding the neurophysiology of Memory or neurodevelopmental disorders, and offer a new resource of Memory suppressor genes that will aid in understanding restraint mechanisms employed by the brain to optimize resources.
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olfactory Memory Formation in drosophila from molecular to systems neuroscience
Annual Review of Neuroscience, 2005Co-Authors: Ronald L DavisAbstract:The olfactory nervous system of insects and mammals exhibits many similarities, which suggests that the mechanisms for olfactory learning may be shared. Molecular genetic investigations of Drosophila learning have uncovered numerous genes whose gene products are essential for olfactory Memory Formation. Recent studies of the products of these genes have continued to expand the range of molecular processes known to underlie Memory Formation. Recent research has also broadened the neuroanatomical areas thought to mediate olfactory learning to include the antennal lobes in addition to a previously accepted and central role for the mushroom bodies. The roles for neurons extrinsic to the mushroom body neurons are becoming better defined. Finally, the genes identified to participate in Drosophila olfactory learning have conserved roles in mammalian organisms, highlighting the value of Drosophila for gene discovery.