The field began with the initial observation that the activity of

The field began with the initial observation that the activity of dopamine neurons resembles a reward prediction error from formal reinforcement-learning theory [4], and now subsumes an elaborate framework that can potentially account for the functions of many different parts of the brain. It is likely

that this approach will continue to be useful as we embark on the attempt to understand how different RL component processes are ultimately combined together to produce integrated behavior. Nothing declared. Papers of particular interest, published within the period of review, have been highlighted as: • of special interest This work was supported by an NIH Ganetespib cost conte center grant on the neurobiology of social decision making (P50MH094258-01A1), NIH grant DA033077-01 (supported by OppNet, NIH’s Basic Behavioral and Social Science Opportunity Network) and National Science Foundation grant 1207573 to JOD. “
“Current Opinion in Behavioral Sciences 2015, 1:101–106 This find more review comes from a themed issue on Cognitive neuroscience Edited by Cindy Lustig and Howard Eichenbaum 2352-1546/© 2014 Published by Elsevier Ltd. The prefrontal cortex is often described as subserving decision-making and executive control.

Decision-making research focuses on the PFC function in action selection according to perceptual cues and reward values 1 and 2]. Executive control research focuses on the PFC function in learning and switching between behavioral rules or sets that guide action 1, 3, 4, 5, 6, 7, 8, 9 and 10]. These two lines of research have often been carried out independently. Here we review recent findings and outline a theoretical framework unifying these two conceptual approaches of PFC function. There is converging evidence that the computation of expected rewards driving action selection primarily involves the ventromedial PFC (vmPFC) 11, 12 and 13]. The vmPFC, especially its ventral portion (often referred to as the medial orbitofrontal cortex), enables to convert distinct subjective reward scales

into a ‘common currency’ scale for allowing value comparison 14, 15, 16 and 17] that drives selection. Reward values are generally associated with action outcomes rather than actions per se. Consistently, the Protein tyrosine phosphatase vmPFC is involved in predicting action outcomes 18, 19, 20, 21• and 22], suggesting that the vmPFC encodes action-outcome associations for selecting actions according to reward values. By contrast, selecting actions according to perceptual cues involves the lateral premotor cortex 9, 23, 24 and 25]. However, when expected rewards and perceptual cues are not linked to specific actions, decisions are presumably made between more abstract action sets that may subsequently guide the selection of specific actions according to stimuli.

However, a genome-wide association study (GWAS) for GLS resistanc

However, a genome-wide association study (GWAS) for GLS resistance has not yet been reported with Chinese maize germplasm. Accordingly, the objectives in this study were to (1) assess phenotypic variation among 161 Chinese maize inbred lines under artificial inoculation with a propagule Y27632 suspension, (2) identify genetic loci conferring

GLS resistance by performing a genome-wide association study of GLS resistance using 41,101 SNP markers in the population, and (3) identify candidate genes for GLS resistance. The results obtained here will help to drive the breeding process towards improvement of GLS resistance. An association mapping panel with 161 Chinese maize inbred lines was planted in a plant pathology nursery at Shenyang, Liaoning Province, China (41.48° N, 123.25° E), in 2010 and 2011, using complete randomized blocks with two replicates. Each plot was planted in single rows, 0.67 m apart and 4.5 m long, with a total of 20 plants per row. Among these lines, the inbred lines Shen 137 and Dan 340 were used as resistant and susceptible controls, respectively [15]. The association mapping panel was artificially inoculated during the bugle stage (V9–V11 developmental stage) with a

10-mL propagule suspension containing 2.5 × 104 conidia following the method of Dong et al. [10]. During the maize milky maturity stage, the disease reaction on each plant was scored on a R428 molecular weight scale with five levels (G1, G3, G5, G7, and G9) that represent the percentage of the infected foliar area (PIFA) as follows: G1 ≤ 5% PIFA and absence of symptoms; G3 = 6%–10% PIFA with few and sparse lesions; G5 = 11%–30% PIFA with lesions reaching the ear leaf

and a few lesions occurring on the leaves above the ear; G7 = 31%–70% PIFA with lesions reaching the leaves above the ear; G9 ≥ 71% PIFA with premature plant death before physiological maturity (black layer formation in kernels) [4] and [10]. GLS resistance was evaluated by PIFA for all plants in each row and the average score for the row comprised the phenotypic data. All the phenotypic data collected in 2010 and 2011 were summarized as percentages (e.g. PIFA). An arcsine transformation was performed and statistical tests Depsipeptide manufacturer were conducted using Statistical Analysis System (SAS) software [29]. A PROC UNIVARIATE normal plot was used to test whether the data was normally distributed. A standard analysis of variance (ANOVA) was performed using PROC GLM to determine variation in disease response. The general linear model procedure was used to analyze the effects of environments, block, inbred lines, and the interactions between these factors. Estimates of the variance components associated with all model terms were calculated using the PROC MIXED option.

In cases where the margin of a section is transparent and free of

In cases where the margin of a section is transparent and free of black stains when it is held against sunlight or a bright flame, the section is carefully washed with water and poured onto with an acidic and ideally hot solution (Ac. Ocalic. 0.5, Nat. sulfuros. 0.5, Aq. 200). The section is then gently swung in the solution until the margin is perfectly white and stain free.

If necessary, the acid solution can be changed. Should stains still persist, one has either the option to be satisfied with the result or otherwise restart the process with potassium solution after washing the slice in water. A repetition is also advisable selleck inhibitor if the staining was very intense and the layers are thus not distinguishable after the first staining. In such a manner, de-staining can be carried to the extreme. The more de-staining is carried out the brighter the entire slice becomes. This however also applies to the delicate fibres, especially cortical fibres, which can be de-stained to the point where they will fade. If a slice that is too bright and brown it can be stained darker and blue when covered in alkaline solution, an ammonia solution or carbonic lithium. The slice – from now onwards placed on an object slide – is dried in absolute alcohol and the celloidin

is removed with ether alcohol. If the slice was covered with celloidin prior to cutting, it is best to make sure that the side of the slice that was covered with celloidin is Alectinib clinical trial placed facedown on the stage. It is then lightened in carboxylox (ac.

Carbol. 2. Xyl.6.). One drains the carboxylol a little and presses at least eight layers of blotting paper quickly and strongly on the slice. The uppermost page of blotting paper should not become wet, as parts of the slide will stick to it. The slice is then poured over with warm or Xylol-thinned Canada-balm and covered with a thin glass plate. During microscopy, it is best to look without Docetaxel aperture using an Abbé microscope. The cortex, whose white matter connections are to be described here, is delimited anteriorly by a frontal plane [fr], which passes tangential to the posterior end of the splenium (Fig. 1 and 2). The natural boundary for the white matter of the occipital lobe, the confluence of the posterior horn in the cella lateralis of the lateral ventricle – the opening of the posterior horn – lies just behind this plane. On the convexity of the medial surface this plane cuts the most anterior part of the precuneus (Fig. 2). On the lateral convexity (Fig. 1) it cuts the gyrus at the end of the Sylvian fissure [supramarginal gyrus], whose most posterior cortical indentation extents into the depths. On the lateral convexity of this three-sided piece of brain, two sulci can be seen running dorso-ventrally [e,k], and three sulci running posterior-anteriorly [s.o. I-III], which all impact on the shape of the underlying white matter due to their depth.

An MRI scan will be performed with diffusion weighted and perfusi

An MRI scan will be performed with diffusion weighted and perfusion weighted sequence to assess for the presence of a penumbra. Patients without penumbra will not be excluded, as there is evidence that there may be benefit to ischemic cells after reperfusion selleck products [25] and [29], however the mechanism and effect could be quite different, and so these two groups should be considered separately. This will be recorded and patients will be later placed into two groups, penumbra and no penumbra for analysis. As it would be prohibitively time consuming to require reading the MRI for a diffusion perfusion mismatch

prior to randomization, the presence or absence of penumbra should be analyzed later through subgroup analysis. Selumetinib research buy This would also avoid unnecessary HBO2T treatment delays. If no exclusion exists, patient will be randomized to standard of care plus HBO2T or standard of care plus a sham treatment of air at minimal pressure increase to maintain patient blinding. HBO2T will

consist of one session of 100% oxygen at 2.4 ATA for 90 min. The selection of this dose is based on several factors. First, the FDA has approved HBO2T at a dose of 2.4 ATA for 90 min for numerous conditions and it is well tolerated [30]. Second, this dose, and limitation to a single treatment, (a single exposure) at this pressure is also more consistent with animal studies which have shown efficacy of HBO2T in cerebral ischemia [13], [15], [16], [17], [18], [31], [32], [33], [34], [35], [36], [37] and [38]. All patients enrolled will undergo repeat NIHSS, mRS scale, Barthel index [39] and Glasgow outcomes scale [40] at 7 days performed by an examiner blinded to their treatment. These assessments will be repeated at 90 days with a follow-up appointment to clinic, similar to the outcomes in the NINDS (National Institute of Neurologic Diseases) trial which found tPA to be effective [3]. Primary outcome will be the mRS, and NIHSS scores as in the NINDS trial. Secondary outcomes will include the Barthel index score, Glasgow outcome scale score,

length of hospital stay, rates of ICH, mortality crotamiton and discharge location. Sample size would be determined based on a 20% absolute difference in good outcome (score 0–1 on the modified Rankin scale) at three months. In the original tPA trial, approximately 25–28% of the placebo group and 39–47% of the tPA group achieved this outcome [3]. If this 6 h trial shows safety and efficacy, a second tier could be added extending to 12 h for patients with a documented penumbra. To determine whether use of HBO2T in the acute state after traumatic brain injury is effective at improving functional and mortality outcomes. To determine whether use of HBO2T in the acute state after traumatic brain injury is effective at reducing elevated intracranial pressure (ICP).

MaβFS plasmid DNA was isolated using a Tianpure Mini Plasmid Kit

MaβFS plasmid DNA was isolated using a Tianpure Mini Plasmid Kit (Tiangen Biotech, Beijing) and inserts were sequenced using a Bigdye terminator chemistry kit (ABI, Perkin-Elmer) on an ABI 3130 XL DNA sequencer (ABI, Perkin-Elmer). DNA

sequence data were assembled and analyzed using DNAMAN software, and putative amino acid sequences were analyzed in GenBank databases using the NCBI BLAST program. Schematic structures of MaβFS1 Selleckchem Navitoclax and MaβFS2 were drawn in a gene structure display server (GSDS, The theoretical isoelectric points (pI) and molecular weights (MW) of the proteins were computed using the Compute pI/MW Tool ( tools/pi_tool.html). Alignment of the deduced protein sequences was performed using DNAMAN and CLUSTAL_X Afatinib supplier version 1.83. A joint unrooted phylogenetic tree was constructed by MEGA4 using the neighbor-joining method. Total RNA of the root, stem, leaf and flower of Asian peppermint were extracted using the RNAprep Pure Plant Kit (Tiangen Biotech, Beijing), and a 2 μg aliquot of RNA per sample was used to synthesize first-strand cDNA. The expression levels of MaβFS were investigated

using quantitative real time-PCR (qRT-PCR), which was performed with a Quant qRT-PCR Kit (Tiangen Biotech, Beijing) in an ABI PRISM 7000 sequence detection system (Applied Biosystems, Foster City, CA, USA), with reactions subjected to the following program: 95 °C for 1 min, 41 cycles of 95 °C for 10 s, and 56 °C for 30 s. To normalize the PCRs for the amount of added RNA the β-actin gene from peppermint (MaACT, GenBank accession no. AW255057) was selected

as the endogenous control. For each sample, the MaβFS Ct value (meaning the number of cycles required for the fluorescence signal to cross the threshold) of each sample was normalized to the Ct value of β-actin. The relative value of gene expression was analyzed using the 2− ΔΔCt method [42]. The relative expression levels of MaβFS in stems, leaves and flowers were presented relative to average root levels. The primer pairs, MaβFS F2 and MaβFS R2, and MaACT F and Etofibrate MaACT R, are listed in Table 1. Compared with the commercial pBI121 vector, the modified pBI121 plasmid used here replaced the uidA gene (encoding GUS) of the original vector with a fragment possessing multiple cloning sites including Sma I and Spe I, but preserving the npt II gene encoding npt II gene driven by the NOS promoter and NOS terminator. The npt II gene confers resistance to aminoglycoside antibiotics, such as kanamycin. The full ORF sequence of the MaβFS1 gene with Sma I and Spe I was cloned into the Sma I and Spe I sites of the modified pBI121 to form the transformation vector MaβFS1-pBI121. The orientation and integrity of MaβFS1 in the construct were confirmed by sequencing. The plasmids were then transferred into Agrobacterium tumefaciens strain AGL1.

In some experiments 10 μM L-thiocitrulline (nitric oxide synthase

In some experiments 10 μM L-thiocitrulline (nitric oxide synthase inhibitor) or 10 μM SB203580 (MAPK p38 inhibitor) were added for further 7 or 14 days, respectively. Immunohistochemistry using the avidin–biotin technique was performed to detect cholinergic neurons, as described previously (Zassler and Humpel, 2006). All incubations were processed free-floating at 4 °C for 2 days including 0.1% Triton, allowing good penetration of the antibody into the slices from Dabrafenib supplier both sides. Fixed slices

were rinsed 30 min with 0.1% Triton/PBS (T-PBS) at room temperature and pre-treated for 20 min with 20% methanol/1% H2O2/PBS. Then the slices were washed three times for 10 min with PBS, blocked with 20% horse serum/0.2% BSA/T-PBS and then incubated with the primary antibody against JQ1 datasheet goat anti-choline‐acetyltransferase (1:750, Millipore, USA) in 0.2% BSA/T-PBS for 2 days at 4 °C. Slices were washed and incubated with secondary biotinylated anti-goat antibody (1:200, Vector Laboratories), for 1 h at room temperature. After rinsing three times in PBS, slices were incubated in avidin–biotin complex solution (ABC; Elite Standard PK 6100, Vector Laboratories) for 1 h, then washed three times in 50 mM Tris-buffered saline (TBS) and the signal was detected using 0.5 mg/ml 3,3′diaminobenzidine (DAB) in TBS

with 0.003% H2O2 as substrate. Slices were then rinsed in PBS and mounted on glass slides. Slices were extracted in 100 μl ice-cold sodium-phosphate buffer (PBS) with protease-inhibitor cocktail (Sigma, Germany) using an ultrasonic device (Branson sonifier 250) and centrifuged at 16 000 ×g for 10 min at 4 °C. Inflammatory markers and MMP-2 were analyzed in slice extracts using a rat Multiplex ELISA (SearchLight®; Aushon Biosystems), as described previously ( Marksteiner et al., 2011 and Pirchl Methamphetamine et al., 2010). All neuronal counts

were based on individual sections and show total number of neurons per slices. The number of microscopically detectable immunoreactive ChAT+ neurons was counted in the whole slice visualized under a 40× objective by an investigator blinded to the treatment code. Quantitative data are presented as mean ± SEM. Multistatistical analysis was obtained by one way ANOVA, followed by a subsequent Fisher PLSD posthoc test by comparing controls against the respective treatments, where p < 0.05 represents statistical significance. This study was supported by the Austrian Science Funds (P191220-B05 and L429-B05). We thank Ursula Kirzenberger-Winkler for excellent technical help. "
“Musashi (Msi) was first identified in the external sensory organ in the peripheral nervous system (PNS) of Drosophila and is required for asymmetric cell division of the sensory organ precursor (SOP) cell of the Drosophila adult external sensory organ, and it functions by controlling the expression of Tramtrack69 (TTK69) ( Nakamura et al., 1994). Msi contains two RNA recognition motifs (RRMs) as a highly conserved RNA-binding domain.

In jüngerer Zeit wurde Kupfermangel bei 100 % schwer unterernährt

In jüngerer Zeit wurde Kupfermangel bei 100 % schwer unterernährter Kinder während der Verbesserung ihres Ernährungszustands nachgewiesen [74]. Die Schwierigkeiten, bei unterernährten Kindern zur Verbesserung ihres Ernährungszustands den Bedarf an Kupfer und anderen Mineralstoffen durch ein speziell zugeschnittenes Nahrungsmittelangebot zu decken, sind bereits diskutiert worden [75]. Heutzutage ist ein spezieller

Verweis auf die langfristige Einnahme von Zinksupplementen erforderlich, die sekundären Kupfermangel auslösen kann [76]. Kupfermangel infolge übermäßiger Aufnahme von Zink ist in mehreren Fallstudien beschrieben worden [77], [78], [79], [80] and [81]. Darüber hinaus wurde oxidativer Stress infolge von Kupfermangel mit einer beschleunigten Abnahme kognitiver Fähigkeiten bei der Alzheimer-Krankheit in Verbindung gebracht; hier besteht allerdings noch weiterer Klärungsbedarf [82]. Toxische Effekte im Zusammenhang mit Kupfer sind bei Personen, die nicht an der Wilson-Krankheit leiden, selten. Akute Toxizität wurde mehrfach bei Personen beschrieben, die versehentlich oder in Selbstmordabsicht höhere Dosen an Kupfer eingenommen hatten. Je nach der Kupferdosis Ibrutinib price kann das Ausbleiben einer geeigneten und rechtzeitigen Behandlung zum Tode führen [83], [84],

[85], [86], [87] and [88]. Bei niedrigeren Dosen gehen die ersten Reaktionen auf eine akute Exposition gegenüber Kupfer vom Magen aus und führen zu vagaler Stimulation, wodurch als Reflexantwort Übelkeit und Erbrechen ausgelöst werden [89], [90] and [91]. Ist die eingenommene Kupferdosis etwas höher, wird Erbrechen zusätzlich durch direkte Stimulation des Brechzentrums im Hypothalamus ausgelöst. Der Mechanismus, der im Zusammenhang mit höheren Kupferdosen zu Durchfall führt, ist jedoch noch nicht ausreichend aufgeklärt. Bei klinischen Studien an gesunden Männern und Frauen unter Einsatz verschiedener Kupfersalze, Wasserquellen und Kupferdosen

wurde Übelkeit als der erste negative Effekt einer kontrollierten, akuten Exposition gegenüber Kupfer beschrieben [92], [93], [94] and [95]. Daten, die zu den akuten negativen Auswirkungen von Kupfer vorliegen, haben dazu geführt, dass die Weltgesundheitsorganisation STK38 (WHO) eine Kupferkonzentration von 2 mg Cu/l im Trinkwas-ser als sicher für den menschlichen Konsum festgelegt hat. Das wichtigste und bekannteste Beispiel für chronische Kupfertoxizität ist die Wilson-Krankheit, eine autosomal rezessiv vererbte Krankheit, die auf eine Mutation im ATP7B-Gen zurückgeht [96]. Die Wilson-Krankheit ist beim Menschen die Hauptursache für die Akkumulation von Kupfer in der Leber und stellt ein natürliches Modell für die schwerwiegenden toxischen Wirkungen eines Kupferüberschusses dar [10], [11] and [12].

Furthermore, in such ecosystems the effect of anthropogenic nutri

Furthermore, in such ecosystems the effect of anthropogenic nutrient inputs are more evident, and phytoplankton abundance is strongly related to such nutrients, mainly nitrogen compounds. In general, the overall average phytoplankton abundance in the study area was 1.45 × 104 cells l−1, this average being 2–4 times lower than in other Egyptian coastal areas, which can have abnormal algal blooms as a consequence of freshwater discharges and other terrestrial sources of nutrients (El Sherif & Gharib 1994, Abdel-Aziz et al. 2006,

Gharib & Dorgham 2006, Shams El-Din & Abdel Halim 2008). In an earlier study, Dowidar (1988) recorded that the algal bloom in the Egyptian coastal area during the winter was due mainly to the low grazing impact of both zooplankton and phytophagous fish (principally sardines), whereas the spring blooms in the present study HSP inhibitor coincided with a 6.00°C increase in water temperature from 18.00°C to 24.00°C and a decline in phosphorus concentrations (0.07 ± 0.05 μM). On the other hand, the phytoplankton abundance decreased in winter as a consequence of relatively low temperatures, even though nutrient levels, especially phosphate levels, were high during this period. However, the increase in phytoplankton abundance in spring was also typically nutrient-limited in both the eastern Mediterranean high throughput screening ( Dorgham et al. 1987) and the whole of that sea (

Kideys et al. 1989, Delgado 1990, Polat & Piner 2002). Phytoplankton reflects water quality through changes in its community structure, patterns of distribution and the proportion of sensitive species. Throughout the study, the phytoplankton in the waters off the Matrouh beaches was dominated by diatoms. Similar findings were reported from most Egyptian coastal waters by Shams El-Din & Dorgham (2007) in Abu-Qir bay, Gharib & Dorgham (2006) in the Western Harbour, and Shams El-Din & Abdel Halim (2008) in the coastal waters of three tourist villages in western Alexandria. The decline in Bacillariophyta abundance could be due to nutrient limitation resulting from the lack of phosphorus

and silicates in the water (reactive Prostatic acid phosphatase P and Si concentrations were below or near the detection limit). Diatoms were more frequent (common: 84 species, rare: 36 species) than Pyrrophyta (common: 25 species, rare: 27 species). The bloom of Pseudo-nitzschia spp. was probably a response to higher nutrient concentrations. It is known that, in the Western Harbour and at El-Maadia on the Alexandria coast, such blooms have occurred in response to coastal eutrophication ( Abdel-Aziz et al. 2006, Gharib & Dorgham 2006). This hypothesis is supported by the strong positive correlation between Pseudo-nitzschia spp. and the different nutrient salts. Relatively higher phytoplankton abundances were recorded in the Matrouh lagoon (beaches 4–7), the high numbers of diatoms reflecting the general eutrophic nature of this semi-enclosed basin (Labib 1994).


CRPcys-XL binds GpVI, platelets are activated, leadi


CRPcys-XL binds GpVI, platelets are activated, leading to their aggregation [11] and [18]. Subsequently, Selleckchem PCI 32765 a small set of triple-helical peptides containing primary sequence from collagen I was used to identify GFOGER as a motif that binds integrins α1β1 and α2β1 [12]. To cater for the possibility that cross-linking may similarly be required to support cellular activation via clustering of integrins, these and subsequent peptides, such as GFOGERcys (Table 1), generally included terminal Cys residues. We then synthesized two large sets of peptides (Toolkits) encompassing the entire triple-helical domains of the homotrimeric collagens II and III in 56 and 57 peptides, respectively [3] and [14]. We use three examples of Toolkit peptides in this paper (Table 1). With the aid of their helix-inducing host sequence, all these peptides fold to form canonical collagen triple helices of similar stability to native collagen [23]. Toolkit peptides have facilitated the systematic mapping of receptors [3], [14] and [33] and structural binding proteins [3], [15] and [16] onto collagens II and III. see more Applications for triple-helical peptides may be developed in several ways: the Toolkit approach might be applied to collagen I using heterotrimeric peptides [5], [25] and [28]. Collagen-mimetic peptides are used in biomaterials [24] and may also

have diagnostic applications. For example, the identification of a site that bound von Willebrand factor

(VWF) using the Toolkits [16] enabled the development of a defined, collagen-mimetic peptide mixture of VWF-, GpVI- and integrin-binding peptides that can support thrombus formation under shear conditions [22], BCKDHA valuable for diagnostic purposes. Although the heterogeneity of these peptides is increased by random oxidation of their terminal cysteine residues (Fig. 1), the latter provide a valuable means of introducing higher-order structure through chemical crosslinking. Their role has not been investigated in any depth, and forms an important focus of this report. Here, we provide a framework for investigating cross-linked polymeric collagen peptides that complements work on fibril-forming collagen peptides where cysteine aids helix stabilization [13] and [21]. We also investigate the enhancement of adhesive properties conferred by the oxidation of cysteine upon storage, where the main use of peptides is to investigate cell–collagen interaction using solid-phase adhesion methodology. Peptides were synthesized as C-terminal amides on TentaGel R-Ram resin using an Applied Biosystems Pioneer peptide synthesizer as described previously [23]. Fractions containing homogeneous product were identified by analytical HPLC on an ACEphenyl300 (5 μm) column, characterized by MALDI and electrospray mass spectrometry, pooled and freeze-dried. Where applicable, biotin was coupled to the N-terminal group by addition of N-(biotinyloxy)succinimide (5 equiv.

In conclusion it can be said that each of the above hypotheses ma

In conclusion it can be said that each of the above hypotheses may explain part of the variation between species. However, a quantitative prediction for a species based on measurement RG7422 mw of another one cannot be made due to the complexity of physiology and ecology. Only empirical data are appropriate to gain insight in the metabolism of a particular arthropod species. The research was funded by the Austrian Science Fund (FWF): P20802-B16. We greatly appreciate the help with electronics by G.

Stabentheiner and with data evaluation by M. Bodner, M. Brunnhofer, M. Fink, P. Kirchberger, A. Lienhard, L. Mirwald and A. Settari. Many thanks also to two anonymous reviewers for very helpful comments. “
“Olfactory coding follows an orderly sequence of information flow that is comparable across animal species (Ache and Young, 2005 and Hildebrand and Shepherd, 1997). The primary sensory cells express a large repertoire of receptor proteins (the olfactory receptors). Axons of receptor cells converge onto olfactory glomeruli in the antennal lobe (insects) or olfactory bulb (mammals). From there, this orderly information is relayed to higher-order brain areas. Because each glomerulus collects information from one receptor neuron

family, odor information is encoded in the pattern of physiological activity across glomeruli. This combinatorial information constitutes the basis of olfactory processing, and has been investigated using techniques as diverse as single cell recording (Krofczik Ion Channel Ligand Library et al., 2008), patch-clamp (Wilson et al., 2004), multi-unit recordings (Lei et

al., 2004) and optical imaging (Friedrich and Korsching, 1997 and Joerges et al., 1997). The capacity of optical imaging to record from many neurons at the same time while knowing their spatial relationships has made this technique particularly fruitful for unraveling the neural basis of olfactory processing (Galizia and Menzel, 2001). In insects, it is possible to identify comparable glomeruli across animals (Berg et Staurosporine mw al., 2002, Galizia et al., 1999a and Laissue et al., 1999), making this approach even more powerful, and allowing for the generation of a functional atlas of odor-response patterns, as done in the honeybee (Galizia et al., 1999b and Sachse et al., 1999) ( In most species, multiple olfactory systems coexist. In rodents, for example, several parallel olfactory systems code for odors: the main olfactory system, the vomeronasal system, the Grueneberg organ and the septal organ, with different occurrences depending on the species (Breer et al., 2006). Most importantly, while some odors are coded exclusively within one of these organs, others can be coded in parallel in several of these organs. In insects, parallel processing in multiple olfactory tracts has evolved in several lineages (Galizia and Rossler, 2010). In social hymenoptera (e.g.