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In Vivo Two-Photon Imaging Reveals a Role of Arc in Enhancing Orientation Specificity in Visual Cortex.: Cell, Vol. 126, No. 2. (28 July 2006), pp. 389-402.Cortic al representation s of visual information are modified by an animal's visual experience. To investigate the mechanisms in mice, we replaced the coding part of the neural activity-regul ated immediate early gene Arc with a GFP gene and repeatedly monitored visual experience-ind uced GFP expression in adult primary visual cortex by in vivo two-photon microscopy. In Arc-positive GFP heterozygous mice, the pattern of GFP-positive cells exhibited orientation specificity. Daily presentations of the same stimulus led to the reactivation of a progressively smaller population with greater reactivation reliability. This adaptation process was not affected by the lack of Arc in GFP homozygous mice. However, the number of GFP-positive cells with low orientation specificity was greater, and the average spike tuning curve was broader in the adult homozygous compared to heterozygous or wild-type mice. These results suggest a physiological function of Arc in enhancing the overall orientation specificity of visual cortical neurons during the post-eye-openi ng life of an animal.

Source: Cell, Vol. 126, No. 2. (28 July 2006), pp. 389-402.
Release of mantle helium from forearc region of the Southwest Japan arc: Chemical Geology, Vol. In Press, Corrected ProofShikoku, Japan, is an island located on the forearc region of the western sector of the Southwest (SW) Japan arc that was formed by subduction of the Philippine Sea plate beneath the Eurasian plate. Noble gas isotope analyses were carried out for 30 bubbling gas samples and spring water samples collected in Shikoku. In addition, chemical and carbon isotope analyses were conducted for six gas samples. Observed 3He/4He ratios were 0.17 R/RA to 3.56 R/RA, showing that several samples contain mantle helium components, although some samples contain helium of crustal origin. Geographical distributions of 3He/4He ratios show that high 3He/4He ratios originate mainly from two areas: one along the Median Tectonic Line (MTL), a major active fault in Japan; the other coinciding with a region in which non-volcanic long-period tremors occur, about 30 km deep [Obara, K., 2002. Nonvolcanic deep tremor associated with subduction in southwest Japan. Science 296, 1679-1681]. This fact indicates that fluids liberated from the slab in the forearc region cause deep tremors and fracturing within the crust, thereby easing the transfer of fluids to the surface that are mixed with mantle helium to the surface. An active fault system can also provide an efficient path for mantle helium transfer.

Source: Chemical Geology, Vol. In Press, Corrected Proof
Biosecurity: Towards an anthropology of the contemporary: Anthropology Today (October 2004), pp. 3-7.

Source: Anthropology Today (October 2004), pp. 3-7.
Arc/Arg3.1 is essential for the consolidation of synaptic plasticity and memories.: Neuron, Vol. 52, No. 3. (9 November 2006), pp. 437-444.Arc/Ar g3.1 is robustly induced by plasticity-pro ducing stimulation and specifically targeted to stimulated synaptic areas. To investigate the role of Arc/Arg3.1 in synaptic plasticity and learning and memory, we generated Arc/Arg3.1 knockout mice. These animals fail to form long-lasting memories for implicit and explicit learning tasks, despite intact short-term memory. Moreover, they exhibit a biphasic alteration of hippocampal long-term potentiation in the dentate gyrus and area CA1 with an enhanced early and absent late phase. In addition, long-term depression is significantly impaired. Together, these results demonstrate a critical role for Arc/Arg3.1 in the consolidation of enduring synaptic plasticity and memory storage.

Source: Neuron, Vol. 52, No. 3. (9 November 2006), pp. 437-444.
BDNF function in adult synaptic plasticity: the synaptic consolidation hypothesis.: Prog Neurobiol, Vol. 76, No. 2. (June 2005), pp. 99-125.Interes t in BDNF as an activity-depen dent modulator of neuronal structure and function in the adult brain has intensified in recent years. Localization of BDNF-TrkB to glutamate synapses makes this system attractive as a dynamic, activity-depen dent regulator of excitatory transmission and plasticity. Despite individual breakthroughs, an integrated understanding of BDNF function in synaptic plasticity is lacking. Here, we attempt to distill current knowledge of the molecular mechanisms and function of BDNF in LTP. BDNF activates distinct mechanisms to regulate the induction, early maintenance, and late maintenance phases of LTP. Evidence from genetic and pharmacologica l approaches is reviewed and tabulated. The specific contribution of BDNF depends on the stimulus pattern used to induce LTP, which impacts the duration and perhaps the subcellular site of BDNF release. Particular attention is given to the role of BDNF as a trigger for protein synthesis-depe ndent late phase LTP--a process referred to as synaptic consolidation. Recent experiments suggest that BDNF activates synaptic consolidation through transcription and rapid dendritic trafficking of mRNA encoded by the immediate early gene, Arc. A model is proposed in which BDNF signaling at glutamate synapses drives the translation of newly transported (Arc) and locally stored (i.e., alphaCaMKII) mRNA in dendrites. In this model BDNF tags synapses for mRNA capture, while Arc translation defines a critical window for synaptic consolidation. The biochemical mechanisms by which BDNF regulates local translation are also discussed. Elucidation of these mechanisms should shed light on a range of adaptive brain responses including memory and mood resilience.

Source: Prog Neurobiol, Vol. 76, No. 2. (June 2005), pp. 99-125.
Arc, a growth factor and activity-regul ated gene, encodes a novel cytoskeleton-a ssociated protein that is enriched in neuronal dendrites.: Neuron, Vol. 14, No. 2. (February 1995), pp. 433-445.Neuron al activity is an essential stimulus for induction of plasticity and normal development of the CNS. We have used differential cloning techniques to identify a novel immediate-earl y gene (IEG) cDNA that is rapidly induced in neurons by activity in models of adult and developmental plasticity. Both the mRNA and the encoded protein are enriched in neuronal dendrites. Analysis of the deduced amino acid sequence indicates a region of homology with alpha-spectrin , and the full-length protein, prepared by in vitro transcription/ translation, coprecipitates with F-actin. Confocal microscopy of the native protein in hippocampal neurons demonstrates that the IEG-encoded protein is enriched in the subplasmalemma l cortex of the cell body and dendrites and thus colocalizes with the actin cytoskeletal matrix. Accordingly, we have termed the gene and encoded protein Arc (activity-regu lated cytoskeleton-a ssociated protein). Our observations suggest that Arc may play a role in activity-depen dent plasticity of dendrites.

Source: Neuron, Vol. 14, No. 2. (February 1995), pp. 433-445.
Brain-derived neurotrophic factor induces long-term potentiation in intact adult hippocampus: requirement for ERK activation coupled to CREB and upregulation of Arc synthesis.: J Neurosci, Vol. 22, No. 5. (1 March 2002), pp. 1532-1540.Brai n-derived neurotrophic factor (BDNF) is implicated in long-term synaptic plasticity in the adult hippocampus, but the cellular mechanisms are little understood. Here we used intrahippocamp al microinfusion of BDNF to trigger long-term potentiation (BDNF-LTP) at medial perforant path--granule cell synapses in vivo. BDNF infusion led to rapid phosphorylatio n of the mitogen-activa ted protein (MAP) kinases ERK (extracellular signal-regulat ed protein kinase) and p38 but not JNK (c-Jun N-terminal protein kinase). These effects were restricted to the infused dentate gyrus; no changes were observed in microdissected CA3 and CA1 regions. Local infusion of MEK (MAP kinase kinase) inhibitors (PD98059 and U0126) during BDNF delivery abolished BDNF-LTP and the associated ERK activation. Application of MEK inhibitor during established BDNF-LTP had no effect. Activation of MEK-ERK is therefore required for the induction, but not the maintenance, of BDNF-LTP. BDNF-LTP was further coupled to ERK-dependent phosphorylatio n of the transcription factor cAMP response element-bindin g protein. Finally, we investigated the expression of two immediate early genes, activity-regul ated cytoskeleton-a ssociated protein (Arc) and Zif268, both of which are required for generation of late, mRNA synthesis-depe ndent LTP. BDNF infusion resulted in selective upregulation of mRNA and protein for Arc. In situ hybridization showed that Arc transcripts are rapidly and extensively delivered to granule cell dendrites. U0126 blocked Arc upregulation in parallel with BDNF-LTP. The results support a model in which BDNF triggers long-lasting synaptic strengthening through MEK-ERK and selective induction of the dendritic mRNA species Arc.

Source: J Neurosci, Vol. 22, No. 5. (1 March 2002), pp. 1532-1540.
Sustained Arc/Arg3.1 Synthesis Controls Long-Term Potentiation Consolidation through Regulation of Local Actin Polymerization in the Dentate Gyrus In Vivo: J. Neurosci., Vol. 27, No. 39. (26 September 2007), pp. 10445-10455.Ne w gene expression is necessary for long-term potentiation (LTP) consolidation, yet roles for specific activity-induc ed mRNAs have not been defined. Here we probed the dynamic function of activity-induc ed Arc (activity-regu lated cytoskeletal-a ssociated protein)/Arg3. 1 (activity-regu lated gene 3.1 protein homolog) mRNA using brief, local infusions of antisense (AS) oligodeoxynucl eotides at multiple time points during dentate gyrus LTP in vivo. Surprisingly, early Arc synthesis is necessary for early expression of LTP, whereas sustained synthesis is required to generate stably modified synapses. AS application 2 h after LTP induction results in a rapid and permanent reversal of LTP. This reversal is associated with rapid knockdown of upregulated Arc, dephosphorylat ion of actin depolymerizati on factor/cofilin , and loss of nascent filamentous actin (F-actin) at synaptic sites. Infusion of the F-actin stabilizing drug jasplakinolide during LTP maintenance blocks the ability of AS to reverse LTP. These results couple activity-induc ed expression of Arc to expansion of the actin cytoskeleton underlying enduring LTP. Furthermore, Arc synthesis is required for both the induction and consolidation of LTP elicited by local BDNF infusion, thus identifying Arc as a key molecular effector of BDNF in synaptic plasticity. 10.1523/JNEURO SCI.2883-07.20 07

Source: J. Neurosci., Vol. 27, No. 39. (26 September 2007), pp. 10445-10455.
Arc/Arg3.1: linking gene expression to synaptic plasticity and memory.: Neuron, Vol. 52, No. 3. (9 November 2006), pp. 403-407.Arc/Ar g3.1 is an effector immediate-earl y gene implicated in the consolidation of memories. Although cloned a decade ago, the physiological role of Arc/Arg3.1 in the brain has remained elusive. Four papers in this issue of Neuron address this function. These studies show that Arc/Arg3.1 regulates endophilin 3 and dynamin 2, two components of the endocytosis machinery. Genetic ablation of Arc/Arg3.1 in mice or overexpression in culture suggest that Arc/Arg3.1 regulates AMPA receptor trafficking and synaptic plasticity. Finally, Arc/Arg3.1 knockout mice show memory retention deficits. These recent developments provide new insights into the function of this popular activity-depen dent neuronal marker.

Source: Neuron, Vol. 52, No. 3. (9 November 2006), pp. 403-407.
Identification of genes co-upregulated with Arc during BDNF-induced long-term potentiation in adult rat dentate gyrus in vivo: European Journal of Neuroscience, Vol. 23, No. 6. (March 2006), pp. 1501-1511.

Source: European Journal of Neuroscience, Vol. 23, No. 6. (March 2006), pp. 1501-1511.

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