Spatial exploration induces <i>ARC</i>, a plasticity‐related immediate‐early gene, only in calcium/calmodulin‐dependent protein kinase II‐positive principal excitatory and inhibitory neurons of the rat forebrain

Vazdarjanova, Almira; Ramírez‐Amaya, Víctor; Insel, Nathan; Plummer, Thane K.; Rosi, Susanna; Chowdhury, Shantanu; Mikhael, Dalia M.; Worley, Paul F.; Guzowski, John F.; Barnes, Carol A.

doi:10.1002/cne.21003

Cited by 231 publications

(228 citation statements)

References 70 publications

Supporting

Mentioning

190

Contrasting

Order By: Relevance

“…Whereas very low levels of Arc mRNA are found in rats taken directly from their home cages ("caged control"), Arc expression is robustly, yet transiently, induced by behavioral experience. A recent study showed that Arc is induced exclusively in α calcium-calmodulin kinase II (αCaMKII) expressing principal neurons in the striatum, hippocampus, and neocortex (Vazdarjanova, Ramirez-Amaya, Insel, Plummer, Rosi, Chowdhury, Mikhael, Worley, Guzowski, & Barnes, 2006). The tight association of Arc expression with αCaMKII supports the hypothesis that Arc and αCaMKII act as "plasticity partners", which promote synaptic modifications that accompany learning in principal neurons (Vazdarjanova et al, 2006).…”

Section: Activity-regulated Arc Transcriptionmentioning

confidence: 96%

Networks of neurons, networks of genes: An integrated view of memory consolidation

Miyashita

Kubík

Lewandowski

et al. 2008

Neurobiology of Learning and Memory

Self Cite

142

120

View full text Add to dashboard Cite

Investigations into the mechanisms of memory formation have abided by the central tenet of the consolidation theory-that memory formation occurs in stages which differ in their requirement for protein synthesis. The current most widely accepted hypothesis posits that new memories are encoded as neural activity-induced changes in synaptic efficacy, and stabilization of these changes requires de novo protein synthesis. However, the basic assumptions of this view have been challenged by concerns regarding the specificity of the methods used to support the claim. Studies on immediateearly genes (IEGs), in particular Arc, provide a distinct and independent perspective on the issue of the requirement of new protein synthesis in synaptic plasticity and memory consolidation. The IEG Arc and its protein are dynamically induced in response to neuronal activity, and are directly involved in synaptic plasticity and memory consolidation. Although we provide extensive data on Arc's properties to address the requirement of genomic and proteomic responses in memory formation, Arc is merely one element in a network of genes that interact in a coordinated fashion to serve memory consolidation. From gene expression and other studies, we propose the view that the stabilization of a memory trace is a continuous and ongoing process, which does not have a discrete endpoint and cannot be reduced to a single deterministic "molecular cascade". Rather, memory traces are maintained within metastable networks, which must integrate and update past traces with new ones. Such an updating process may well recruit and use many of the plasticity mechanisms necessary for the initial encoding of memory.

show abstract

Section: Activity-regulated Arc Transcriptionmentioning

confidence: 96%

Networks of neurons, networks of genes: An integrated view of memory consolidation

Miyashita

Kubík

Lewandowski

et al. 2008

Neurobiology of Learning and Memory

Self Cite

142

120

View full text Add to dashboard Cite

show abstract

“…Expression of these genes is regulated by excitatory synaptic transmission and, in the hippocampus, is closely related to place cell activity (Guzowski et al 1999;Guzowski 2002;Vazdarjanova et al 2006). IEGs can also be used to examine reactivation of individual neurons during two separate events.…”

Section: Identification Of Reactivated Neuronsmentioning

confidence: 99%

New methods for understanding systems consolidation

Tayler

Wiltgen

2013

Learn. Mem.

View full text Add to dashboard Cite

According to the standard model of systems consolidation (SMC), neocortical circuits are reactivated during the retrieval of declarative memories. This process initially requires the hippocampus. However, with the passage of time, neocortical circuits become strengthened and can eventually retrieve memory without input from the hippocampus. Although consistent with lesion data, these assumptions have been difficult to confirm experimentally. In the current review, we discuss recent methodological advances in behavioral neuroscience that are making it possible to test the basic assumptions of SMC for the first time. For example, new transgenic mice can be used to monitor the activity of individual neurons across the entire brain while optogenetic approaches provide precise control over the activity of these cells using light stimulation. These tools can be used to examine the reactivation of neocortical neurons during recent and remote memory retrieval and determine if this process requires the hippocampus.

show abstract

“…23,24 Spatial exploration also increases Arc expression, and does so specifically in glutamatergic neurons of hippocampus and neocortex. 58 Thus, the increased expression of Fos and Arc during training may reflect not just neuronal activation, but more specifically synaptic plasticity.…”

Section: Disclosure Statementmentioning

confidence: 99%

Effects of Skilled Training on Sleep Slow Wave Activity and Cortical Gene Expression in the Rat

Hanlon

Faraguna

Vyazovskiy

et al. 2009

Sleep

142

131

View full text Add to dashboard Cite

SO FAR. IN MAMMALS, THE BEST CHARACTERIZED marker of sleep homeostasis is slow wave activity (SWA), the power density in the electroencephalogram (EEG) between 0.5 and 4 Hz during NREM sleep. SWA is high at sleep onset and declines during sleep, suggesting that it may reflect the accumulation of sleep pressure as a function of duration and/or intensity of prior waking. 1,2 Why and how SWA should reflect sleep homeostasis, however, is still unclear.We hypothesized that SWA is high at sleep onset because it reflects the occurrence, during waking, of widespread synaptic potentiation in cortical and subcortical areas. 3,4 This increase would be detrimental in the long term, because stronger synapses need more energy, space, and cellular supplies, and may lead to saturation of the ability to learn. Sleep would thus be crucial to renormalize synaptic strength to an energetically sustainable level. Molecular and electrophysiological markers of synaptic potentiation increase after waking in rat cortex and hippocampus, while markers of synaptic depression do so after sleep. 5,6 Moreover, in rats and humans, procedures presumably leading to synaptic potentiation or depression result in SWA increases and decreases, respectively. 7-12 More specifically, a study in humans using highdensity EEG found that performing a visuomotor learning task produced a local increase in SWA during subsequent sleep. 7 The increase was restricted to the right parietal cortical areas presumably modified by learning. 13 Moreover, it was specific for NREM sleep, reversible within the first 90 minutes of sleep, and correlated with the improvement in performance after sleep. 7 However, there is no direct evidence that the motor adaptation task used in that study activates neurons in parietal cortex, nor that it causes synaptic potentiation specifically in that region.Previous studies have suggested that activity-dependent genes activated during a specific waking experience may be reactivated during sleep, perhaps to potentiate the same synapses previously engaged during waking. 14 Ribeiro and colleagues found that the exposure to a new environment for 3 hours 15 results in the immediate cortical and hippocampal induction, during waking, of plasticity-related gene zif-268, 16 followed by its downregulation during NREM sleep, and then again by its increased expression during REM sleep (relative to NREM sleep). Intriguingly ~ 3 min of NREM sleep were enough to downregulate waking-induced zif-268 expression, and ~ 2 min of REM sleep were sufficient to detect its selective reinduction, even if both NREM and REM rats were awake during the last 30 min before sacrifice. Another study 17 recently found, using fluorescent in situ hybridization, that the number of hippocampal CA1 neurons showing induction of Arc and/or Homer1a was similar during "rest" periods before and after the exploration of a new environment. However, more cells were active during both exploration and post-task rest than during exploration and pre-task rest. Based on these findings, it h...

show abstract

Spatial exploration induces ARC, a plasticity‐related immediate‐early gene, only in calcium/calmodulin‐dependent protein kinase II‐positive principal excitatory and inhibitory neurons of the rat forebrain

Cited by 231 publications

References 70 publications

Networks of neurons, networks of genes: An integrated view of memory consolidation

Networks of neurons, networks of genes: An integrated view of memory consolidation

New methods for understanding systems consolidation

Effects of Skilled Training on Sleep Slow Wave Activity and Cortical Gene Expression in the Rat

Contact Info

Product

Resources

About