2 mg/mL ascorbic acid in 0.9% sterile saline, slightly modified from that used by Parish et al. (2001). A total volume of 1.5 μL was injected using the stereotaxic coordinates A/P = −3.0, M/L = −1.2, Autophagy inhibitor D/V = −4.5, with a flat skull position (coordinates in mm, with anterior–posterior and lateral measured from bregma, and ventral from dura). Injections were made at a rate of 0.5 μL/min with a further 2 min allowed for the toxin to diffuse before slow withdrawal of

the capillary, followed by cleaning and suturing of the wound. Rotational asymmetry was assessed using an automated rotometer system (AccuScan Instruments, Columbus, OH, USA) based on the design of Ungerstedt & Arbuthnott (1970). Full body turns were counted and data was expressed as net turns per minute, with rotation toward the side of the lesion given a www.selleckchem.com/p38-MAPK.html positive value. Amphetamine-induced rotational scores were used as an estimate of the extent of DA depletion and were collected over a 40-min test session following 5 mg/kg of d-amphetamine sulphate, i.p. (dissolved in 0.9% sterile saline). Animals were allowed to habituate for 5 min after injection before the

recording of rotations began. Apomorphine-induced rotation reflects the hypersensitivity of the lesioned striatum and this was assessed by testing over a 40-min test session after challenge with 0.1 mg/kg of apomorphine, s.c. (dissolved in a solution of 0.2 mg/mL ascorbic acid in 0.9% sterile saline). Animals were primed on two separate days prior to performing the rotation test for the first time (i.e. priming on Monday and Wednesday, followed with rotation test on Friday).

This avoided a ‘wind-up’ effect that could obscure the rotational responses observed. Animals were allowed to habituate for 5 min after injection before the recording of rotations began. Lateralized sensorimotor integration was measured using a task that was first established in rats by Dowd et al. (2005a) and is based on the classic tests of sensorimotor integration as introduced by Marshall et al. Metformin price (1974). In the current study the corridor test was adapted to mice using a long narrow plastic corridor (60 cm long, 4 cm wide and 15 cm high) with 10 pairs of adjacent pots, each with a diameter of 1 cm (Push cap; LIP Ltd., Galway, Ireland), containing 4-5 sugar pellets (20 mg; TestDiet) that were placed at 5-cm intervals along the length of the corridor (Fig. 1). A clear Perspex lid was placed on top of the apparatus to allow the mice to be observed during testing. Mice were food-restricted and maintained at 85% free-feeding bodyweight throughout habituation and testing. At the first time point, mice were habituated to the corridor by scattering sugar pellets along the floor and allowing them to freely explore for 10 min on two consecutive days prior to testing.

The authors state that they have no conflicts of interest to declare. “
“In 2010, malaria caused approximately 216 million infections in people and 655,000 deaths. In the United States, imported malaria cases occur every year, primarily in returning travelers and immigrants from endemic countries. In 2010, five Plasmodium falciparum malaria cases occurred among crew members of one US commercial airline company (Airline A). This investigation aimed to assess the malaria prevention knowledge, attitudes, and practices (KAP) of Airline A crew members

to provide information for potential interventions. The web link to a self-administered on-line survey was distributed by internal selleck screening library company communications to Airline A pilots and flight attendants (FA) eligible for international

travel. The survey collected demographic information as well as occupation, work history, and malaria prevention education. Of approximately Apoptosis inhibitor 7,000 nonrandomly selected crew members, 220 FA and 217 pilots completed the survey (6%). Respondents correctly identified antimalarial medication (91% FA, 95% pilots) and insect repellents (96% FA, 96% pilots) as effective preventive measures. While in malaria-intense destinations, few FA and less than half of pilots always took antimalarial medication (4% FA, 40% pilots) yet many often spent greater than 30 minutes outdoors after sundown (71% FA, 66% pilots). Less than half in both groups always used insect repellents (46% FA, 47% pilots). Many respondents were unaware of how to get antimalarial medications (52% FA, 30% pilots) and were concerned about their side effects (61% FA, 31% pilots). Overall, FA and pilots demonstrated good knowledge of malaria prevention, but many performed risky activities while practicing only some recommended malaria preventive measures.

Malaria prevention education should focus on advance notification if traveling to a malaria-endemic area, how to easily obtain antimalarial medications, and the importance of practicing all recommended preventive measures. Malaria is BCKDHA a major public health problem worldwide, with approximately 216 million infected people and 655,000 deaths in 2010, mostly affecting developing countries.[1] In the United States, despite recommendations from health agencies, such as the Centers for Disease Control and Prevention (CDC), a steady number of imported malaria cases occur each year, typically from returning travelers and immigrants from malaria-endemic areas. Many US commercial airlines travel regularly to malaria-endemic countries. Data on malaria cases among US airline crew members are scarce; however, previous studies in other countries suggest a low occupational risk for airline crew members traveling to malaria-endemic areas.[2, 3] Long layovers in areas endemic with Plasmodium spp. can increase the risk of malarial infection.

In most cases, IgM titers stay elevated from 3 to 12 months then return to very low levels but can stay elevated for years. IgG antibodies may persist at high titers for many years. Testing

of serial specimens obtained 3 to 4 weeks apart provides the best discriminatory power if the results in the initial specimen are equivocal. When biopsy is performed for lymphadenopathy, histologic changes can be diagnostic. Demonstration of tachyzoites in tissue sections establishes the diagnosis of acute infection. Acute toxoplasmosis in an immunocompetent individual is usually a self-limited disease with resultant chronic, latent infection but no other long-term sequelae. Medical therapy is therefore only indicated when visceral disease is clinically evident or symptoms are severe or persistent or in the setting of pregnancy. The BMN 673 solubility dmso Centers for Disease Control and Prevention recommends Pyrimethamine 25–100 mg daily plus Sulfadiazine 1–1.5

g four times daily for 3–4 weeks. If a patient is allergic to sulfa drugs then clindamycin 600 mg four times daily can be substituted for sulfadiazine. Leucovorin 10–25 mg daily should be prescribed with pyrimethamine to protect the bone marrow. Co-trimoxazole has also been studied in cerebral and ocular disease and found to have efficacy comparable with Pyrimethamine–Sulfadiazine.16,17 Single drug therapy with spiramycin is preferred in pregnancy prior to determination of fetal infection beta-catenin inhibitor in the second trimester, dosed at 1 g three

times daily, without food, and is continued until birth of the neonate or until fetal infection is documented.1,18,19 T gondii primary infection can occur while traveling abroad, often when traveling to countries with T gondii antibody prevalence, as highlighted in this series. We also report periaortic lymphadenopathy related to toxoplasmosis which has not been previously reported. The diagnosis of toxoplasmosis must be considered in returned travelers who present with non-specific symptoms, especially fever, lymphadenopathy, and fatigue. We would like to express our heartfelt thanks to the late Dr J. Dick MacLean, Montreal General Hospital, McGill University Bupivacaine Centre for Tropical Diseases, Montreal, Québec, Canada, for his contributions to this manuscript. The authors state they have no conflicts of interest to declare. “
“The aim of the study was to retrospectively analyze diving fatalities occurring in Primorje-Gorski Kotar County (northern Croatian littoral), Croatia between 1980 and 2010 in order to identify differences between fatally injured tourist and resident divers, as well as temporal changes in the frequency of diver deaths. Medico-legal and police reports of 47 consecutive fatal diving cases were reviewed to determine the frequency of death among divers in relation to year and month of death, age, sex, nationality, organization of diving, diving type, and health condition.

Suppression of the effects of the lack of RpoS by overexpression of SOD or catalase indicated that the damage caused by ROS reduces survival and increases the mutation frequency in a starving P. putida RpoS-deficient strain. Interestingly, although the absence of RpoS in starved P.

putida affected the spectrum of mutations, the spectrum was different from that identified in P. putida lacking the GO repair system (Saumaa et al., 2007). Thus, it is possible that the accumulation of oxidative DNA damage other than GO could elevate the frequency of mutation in these bacteria. There is also another, not exclusive explanation for these differences. It is known that oxidative damage of proteins and membrane components, but not that of VEGFR inhibitor DNA, is a major reason for mortality of cells (Nyström, 2004). Oxidative damage to components of protein synthesis Protein Tyrosine Kinase inhibitor increases mistranslation, and

vice versa, mistranslated proteins are more susceptible to oxidative damage (Dukan et al., 2000). Mistranslation is increased 10–100-fold in E. coli due to amino acid starvation (Sørensen, 2001). Importantly, mistranslation of DNA repair and replication proteins has been demonstrated to create a transient mutator phenotype (Humayun, 1998; Balashov & Humayun, 2002, 2003; Al Mamun et al., 2006). For example, hypermutagenesis in E. coli mutA cells mistranslating aspartate as glycine due to a mutation in the glycine tRNA anticodon was mediated by modifications of DNA polymerase Pol III due to elevated mistranslation (Al Mamun et al., 2006). Additionally, oxidative modification of replication proteins and inactivation of the components of repair pathways have been reported in eukaryotic systems (Graziewicz et al., 2002; Men et al., 2007; Montaner et al., 2007; Bae et al., 2008; Jarrett et al., 2008). Hence, because the elevated mutation frequency Isotretinoin observed by Tarassova et al. (2009) in starving RpoS-deficient

P. putida was associated with an increased death of bacteria and the spectrum of mutations did not resemble that induced by oxidative damage of DNA, the higher mutation frequency in the surviving populations observed in this study might primarily be caused by a decline in DNA replication and repair fidelity due to the oxidative damage of enzymes and/or the errors occurring during the translation of proteins. So far, the role of oxidative damage to proteins in DNA integrity has been underestimated in stationary-phase mutagenesis. It certainly needs more comprehensive investigations. Bacteria have multiple DNA polymerases, each of those with a specific role. DNA polymerase Pol III is a replicative polymerase, and its inactivation is lethal to bacteria. Pol I is involved in Okazaki fragments’ processing and DNA repair synthesis (Okazaki et al., 1971; Cooper & Hanawalt, 1972). Additionally, E.

Overall, evidence suggests that BldG serves as a master switch for both stress-response and developmental gene expression based on its association with multiple anti-sigma factors in S. griseus. Streptomyces and related bacteria

harbor a large number of RNA polymerase sigma factors. For example, Streptomyces coelicolor A3(2), the model microorganism for genetic manipulation, harbors four major and 60 minor sigma factors (including 50 factors involved in extracytoplasmic function and nine in stress-response) (Bentley et al., 2002; Hahn et al., 2003). Streptomyces CYC202 griseus, the streptomycin producer used in this study, retains four major and 48 minor sigma factors (Ohnishi et al., 2008). The presence of these varied sigma factors suggests divergences in the gene expression in this microorganism, and these divergences enable the microorganism to adapt to various environmental and physiological conditions. We studied the role of stress-response sigma factors in S. griseus (streptomycin

mTOR inhibitor producer) with regard to the link between the stress response and morphological and physiological differentiation. In our previous study (Takano et al., 2003), we had characterized an rshA-sigH operon encoding a stress-response sigma factor σH and its antagonist (anti-σH factor) RshA. In that study, the insertion of rshA into a high-copy-number plasmid (pIJ702-rshA) caused marked repression of aerial mycelium formation (Fig. 1a, left) and streptomycin production in S. griseus IFO13350 (the wild-type strain). Therefore, we assumed that this marked phenotypic change was caused by the sequestration of σH and alternative sigma factors by the excess RshA. However, a triple knockout mutant for σH and two σH paralogs (σF and σN) showed the wild-type phenotype (Takano et al., 2007). This finding indicated that

these sigma factors are not directly involved in the control of morphological development and secondary metabolism and suggested that RshA binds to another protein regulating Tenoxicam the expression of developmental genes. In this study, we identified BldG, an anti-sigma factor antagonist, to be such a protein associating RshA. BldG has been characterized for its essential role in the developmental control in S. coelicolor A3(2) (Bignell et al., 2000, 2003). The evidence suggests that the cross-talk between BldG and RshA controls the activity of σH and related stress-response sigma factors in S. griseus. Strains, plasmids, and growth conditions used in this study were as described previously (Takano et al., 2007), except that TA cloning of PCR-generated DNA fragments was done with the help of pMD19 (Takara Shuzo). An integration plasmid pKU463, a derivative of pKU493aad (Komatsu et al., 2010) carrying kanamycin resistance, was obtained from H. Ikeda at Kitasato University. The construction of pIJ702-rshA has been described previously (Takano et al., 2003).

, 2005). European sea bass (Dicentrarchus labrax) in Greece have been affected by a pathogen similar to P. salmonis (Athanassopoulou et al., 2004); also in Hawaii, tilapia populations (Oreochromis mossambicus and Sarotherodon melanotheron), both free-living as well as farmed fish, have suffered a Piscirickettsiosis-type disease (Mauel et al., 2003), suggesting the expansion of this agent to other fish of commercial importance (Marshall et al., 2007). Although the disease affects several fish species of commercial importance, to date the biology, genetics Bleomycin and epidemiology

of P. salmonis have been poorly studied, and so details of relevant aspects of the life cycle of the pathogen are still unknown. The P. salmonis TA locus, named Ps-Tox-Antox, includes its respective regulatory sequences. By in silico comparative genomics of the ps-Tox-Antox locus, we determined that it is homologous to the VapBC TA system of Rickettsia felis and other chromosomal TA operons (Ogata et al., 2005). When the P. salmonis TA genes Selleckchem Quizartinib were cloned and expressed in E. coli for functional analysis, we observed that the characteristics of these genes and their products were similar to other TA systems. Piscirickettsia salmonis strain LF-89 (ATCC VR 1361)

was grown on Blood Cysteine Glucose (BCG) agar plates at 23 °C (modified from Mauel et al., 2008). A single colony was used to inoculate 25 mL of MC5 broth, and was incubated at 23 °C with agitation of 100 r.p.m. Two-day-old bacterial cultures were processed using the AxyPrepTM Multisource Genomic DNA Miniprep Kit (AxyGen Bioscience) according to the manufacturer’s

instructions. Purified P. salmonis DNA was used to construct a genomic DNA library in the plasmid pBluescript SK (+) (Fermentas) and has been described previously (Marshall et al., 2011). The DNA sequenced data were analysed with the softberry server software (http://linux1.softberry.com/berry.phtml) using the algorithms, FgenesB (to find possible ORFs in the sequences), and Bprom (to search for putative bacterial promoters). The products of the ORFs predicted by FgenesB were used in blastp analysis, with the search Vitamin B12 limited to bacterial sequences (http://blast.ncbi.nlm.nih.gov) to determine their possible identities. The putative ORFs were aligned with similar sequences using clustalw (Larkin et al., 2007). The alignments were processed by jalview software (Clamp et al., 2004). Additionally, the primary structure analysis of the new proteins was made by the protparam tool available on the Expasy Proteomic Server (http://www.expasy.org). Thus, the amino acid composition, the hypothetical molecular weight, and the isoelectric point (pI) were all calculated. PCR primers for P. salmonis ps-Tox, ps-Antox, and ps-Tox-Antox genes were designed the Oligo Calc tool (http://www.basic.northwestern.edu/bio-tools/oligocalc.html).

We recommend HSV prophylaxis in people living with HIV with a history of HSV infection who are starting chemotherapy to reduce the incidence and severity of reactivations (level of evidence 1D). We recommend annual influenza vaccination (level of evidence 1B). We recommend vaccination against pneumococcus and hepatitis

Selleckchem Ipilimumab B virus (level of evidence 1D). We recommend that patients with antibodies against hepatitis B core antigen (HBcAb) should be treated with prophylactic antivirals in line with BHIVA hepatitis guidelines (level of evidence 1B). 1 Powles T, Imami N, Nelson M et al. Effects of combination chemotherapy and highly active antiretroviral therapy on immune parameters in HIV-1 associated lymphoma. AIDS 2002; 16: 531–536. 2 Esdaile B, Davis M, Portsmouth S et al. The immunological effects of concomitant highly active antiretroviral therapy and liposomal anthracycline treatment of HIV-1-associated Kaposi’s sarcoma. AIDS 2002; 16: 2344–2347. 3 Alfa-Wali M, Allen-Mersh T, Antoniou A et al. Chemoradiotherapy for anal cancer in HIV patients causes prolonged CD4 cell count suppression. Ann Oncol 2012; 23: 141–147. 4 Moore DA, Gazzard BG, Nelson MR. Central venous line infections in AIDS. J Infect 1997; 34: 35–40. 5 Dega H, Eliaszewicz M, Gisselbrecht M et al. Infections associated with totally implantable venous access

devices (TIVAD) in human immunodeficiency virus-infected patients. J Acquir Immune Defic Syndr Hum Retrovirol 1996; 13: 146–154. 6 Tacconelli E, Tumbarello M, de Gaetano Donati

Pictilisib ic50 K et al. Morbidity associated with central venous catheter-use in a cohort of 212 hospitalized subjects with HIV infection. J Hosp Infect 2000; 44: 186–192. 7 Meynard JL, Guiguet M, Arsac S et al. Frequency and risk factors of infectious complications in neutropenic patients infected with HIV. AIDS 1997; 11: 995–998. 8 Levine AM, Karim R, Mack W et al. Neutropenia in human immunodeficiency Pyruvate dehydrogenase lipoamide kinase isozyme 1 virus infection: data from the women’s interagency HIV study. Arch Intern Med 2006; 166: 405–410. 9 Israel DS, Plaisance KI. Neutropenia in patients infected with human immunodeficiency virus. Clin Pharm 1991; 10: 268–279. 10 Moyle G, Sawyer W, Law M et al. Changes in hematologic parameters and efficacy of thymidine analogue-based, highly active antiretroviral therapy: a meta-analysis of six prospective, randomized, comparative studies. Clin Ther 2004; 26: 92–97. 11 Medina I, Mills J, Leoung G et al. Oral therapy for Pneumocystis carinii pneumonia in the acquired immunodeficiency syndrome. A controlled trial of trimethoprim-sulfamethoxazole versus trimethoprim-dapsone. N Engl J Med 1990; 323: 776–782. 12 Lalezari J, Lindley J, Walmsley S et al. A safety study of oral valganciclovir maintenance treatment of cytomegalovirus retinitis. J Acquir Immune Defic Syndr 2002; 30: 392–400. 13 Williams I, Churchill D, Anderson J et al.

The increasing prevalence of cardiovascular risk factors, such as hypertension and diabetes, and CVD itself in HIV-infected individuals impacts on the morbidity and mortality associated with chronic kidney disease and acute renal failure [25,26]. Family history, Black African ethnicity, viral hepatitis and concomitant administration

of nephrotoxic drugs are also known to increase the risk of developing chronic kidney disease [5]. HIV-related kidney disease is a relatively common cause of renal insufficiency and development of end-stage renal disease (ESRD) requiring dialysis [27]. HIV-associated nephropathy (HIVAN) is considered the most common HIV-related renal disease but, as it is almost exclusively confined to patients of KU-57788 in vitro African descent, there is a suggestion of an additional, genetic influence [27]. Although combination ART has been shown learn more to decrease the incidence of HIVAN and HIV-related ESRD [28,29], the kidney remains susceptible to the toxic effects of ART [27]. As in the general population,

increasing age, female gender, family history, vitamin D deficiency, alcohol intake, smoking and steroid exposure are all risk factors for osteopenia and osteoporosis. However, bone disease occurs at a higher frequency in the HIV-infected population [30]. A meta-analytic review of cross-sectional studies to determine the pooled odds ratios (ORs) of reduced bone mineral density (BMD) and osteoporosis in HIV-positive vs. HIV-negative individuals conducted by Brown & Quagash (2006) found the prevalence of osteoporosis in HIV-infected individuals to be more than three times greater than that in noninfected controls [30]. Individuals receiving ART and PIs had a higher prevalence of reduced BMD and osteoporosis compared with their

respective controls [30]. The increased risk of osteopenia and osteoporosis means that HIV-infected individuals are at greater risk of experiencing fracture. In a population-based study by Triant et al. (2008) [31], the overall fracture prevalence was 2.87 vs. Ureohydrolase 1.77 patients with fractures per 100 persons in HIV-infected vs. noninfected patients, respectively (P<0.0001). The main consequence of the increased survival rate produced by effective ART is that HIV-infected individuals are now exposed to the potential long-term effects of treatment, and are at increased risk of developing age-related rather than HIV-related diseases, such as CVD, liver and kidney disease and osteoporosis. Multiple comorbidities associated with HIV infection affect the treatment choices, quality of life and mortality of people with HIV infection.

Interestingly, those who had disclosed their status to close friends were more likely to report difficulty taking ART than those who had not disclosed their status to close friends. Of the attitudes evaluated (outlined in Fig. 1), not believing in the benefits of ART, concern about the effectiveness of ART in the future, reporting that tablets were an unwanted reminder of HIV infection, negative body image/changes, a negative impact of HIV/AIDS on sex and relationships and a BMN 673 supplier high degree of confidence that unprotected sex was not a risky behaviour were associated with increased likelihood of reporting difficulty taking ART at

a level of α=0.05. A positive health attitude and/or the adoption of positive strategies to manage one’s health was associated with a reduced likelihood of reporting difficulty taking ART. Deeming safe sex to be nonessential because of treatment effects also met the criterion for inclusion in multivariable analysis. The level http://www.selleckchem.com/products/lgk-974.html of support from a range of sources (HIV-positive

friends, close friends, parents, family in general, a counsellor and the respondent’s doctor) was the only socioeconomic factor associated with reported difficulty taking ART at a level of α=0.05. Education level, urbanicity and additional support variables (support from partner/spouse and PLWH groups) also met the criterion for entry into multivariable analyses (see Fig. 1 for the full list of socioeconomic factors investigated). Of the treatment-related variables assessed (see Fig. 1), dosing frequency, the type of regimen taken, the

length of time on ART, and experiencing physical adverse events in the last 12 months or health service discrimination in the last 2 years were associated with reported difficulty taking ART at a level of α=0.05. No additional variables met the criterion for inclusion in the multivariable analyses. Of the disease-related factors assessed (outlined in Fig. 1), diagnosis of an ADI was associated with reported difficulty taking ART at a level of α=0.05. The respondent’s most recent CD4 cell count also met the criterion for inclusion in multivariable analyses. Variables that had shown a significant association in bivariate analyses at the level of α=0.2 were included in multivariable Phosphoprotein phosphatase analysis. Initially, we set up logistic regression models of clusters of variables that were expected to exhibit a high degree of collinearity (step 1 models). At step 1, we created four models: (i) a substance use model, (ii) an other personal factors and attitudes model, (iii) a socioeconomic factor model, and (iv) a treatment-related and disease-related factor model. Variables that remained significantly associated with reported difficulty taking ART at step 1 at the level of α=0.1 were included in the step 2 logistic regression model. The following variables maintained an independent association with reported difficulty taking ART at the level of α=0.

Parallel increases in pri- and pre-miRNA levels at 10 min post-HFS attest to the rapid transcription and processing

of primary transcripts. Changes in mature miRNA expression were detected at 2 h only, indicating a slower processing of hairpin precursors to mature miRNA. Changes in mature miRNA expression were also much smaller (less than twofold). This difference suggests limited precursor processing to mature miRNA. However, the relative differences may also reflect high levels of basal (pre-existing) mature miRNA expression compared with the primary transcripts. In situ hybridization analysis showed no expression of primary miR-132/212 in non-stimulated tissue, whereas mature miR-132 was clearly expressed. Functionally, mGluR activation in the dentate gyrus has been implicated in depotentiation, metaplasticity and NVP-BKM120 research buy long-term depression, rather than LTP (Wu et al., 2004; Kulla & Manahan-Vaughan, 2007; Naie et al., 2007). In agreement with these studies we find that AIDA has no effect on LTP maintenance, but blocks the ability for depotentiation. Thus, LTP is associated with rapid mGluR-dependent transcription miR-132 and miR-212. This miRNA transcription is not required for LTP maintenance under standard

conditions, but could serve to modulate LTP stability through regulation of depotentiation or other mGluR-dependent mechanisms. Taken together, the present results indicate that Alpelisib nmr HFS of the perforant pathway activates two parallel processes: (i) NMDAR-dependent regulation of mature miRNA metabolism; and (ii) mGluR-dependent activation of miR-132 and -212 transcription. The NMDAR-dependent decrease in mature miRNA levels could reflect inhibition of precursor processing or degradation of mature miRNA. As pre-miRNA levels were not detectably altered by NMDAR blockade, the most likely explanation is net degradation (decay) of mature miRNA. At present, little is known about decay mechanisms for miRNAs once they are bound to their mRNA targets. A better understanding of the relationship between cytoplasmic processing (P) bodies (putative sites of mRNA storage and degradation) Racecadotril and translational repression by miRNAs

is likely to be important. While target-bound miRNAs are generally stable, subpopulations of miRNAs may undergo rapid degradation in the context of activity-dependent relief from miRNA inhibition (translational derepression; Parker & Sheth, 2007; Cougot et al., 2008; Franks & Lykke-Andersen, 2008; Tang et al., 2008; Zeitelhofer et al., 2008). This scenario fits with the role of NMDARs in post-transcriptional activation of protein synthesis during LTP. Furthermore, studies in hippocampal neuronal cultures show that NMDAR signaling dynamically alters the localization and composition of dendritically localized P-bodies, as reflected by rapid exchange of the decapping enzyme Dcp1a and the depletion of Argonaute 2, a key protein of the miRNA-RISC (Cougot et al., 2008).