, 2010) and overgeneralized autobiographical memory is often asso

, 2010) and overgeneralized autobiographical memory is often associated with depression and PTSD (Sumner et al., 2010). Deficits in pattern separation may therefore represent a circuit-based endophenotype for these different disorders. The finding that increasing adult hippocampal neurogenesis is sufficient to improve pattern separation suggests that neurogenesis may be harnessed to treat disorders with pattern separation deficits (Sahay et al., 2011) Interestingly, naturalistic interventions such as voluntary exercise have been shown to improve pattern separation in rodents (Creer et al., 2010). It is possible that increased adult hippocampal neurogenesis mediates some of the beneficial

effects of exercise on pattern separation. Chronic antidepressant treatments, which are known to stimulate adult hippocampal neurogenesis, may also exert some of their behavioral effects through enhancing pattern selleck compound separation; however this is yet to be demonstrated. Unraveling the molecular mechanisms underlying the plasticity of neural stem cells and adult-born neurons and identification of proneurogenic small molecules

(Pieper et al., 2010 and Wurdak et al., 2010) will BGB324 clinical trial catalyze the development of novel strategies to treat pattern separation deficits. Olfaction is at the heart of mammalian life, playing critical and often necessary roles in mother-infant attachment, kin recognition, mate selection and recognition, food selection, predator avoidance, and homing. Each of these basic functions can include prolonged changes in internal state and the external chemical environment and often require remarkably precise separation

of highly tuclazepam overlapping odorant stimulus patterns. Enhanced survival of newly generated olfactory bulb interneurons due to a springtime eruption of novel environmental odors could coincide with the need for enhanced pattern separation and the perceptual acuity necessary for navigating this rich olfactory world. In fact, prolonged enrichment of the odor environment enhances the survival (Rochefort et al., 2002) of adult-generated olfactory bulb interneurons and odor perceptual learning and memory (Mandairon and Linster, 2009). Together, these findings suggest that adult neurogenesis in the OB, as in the DG, may provide a mechanism for adapting to relatively stable changes in the environment, allowing for shifts in olfactory pattern separation and ultimately olfactory acuity. Perturbed experience dependent regulation of olfactory bulb neurogenesis may result in unlimited pattern separation, which could come at the expense of pattern completion and perceptual stability. Given the ephemeral nature of odors, excessive pattern separation could lead to an overrepresentation of feature representation in slightly shifting stimuli, with each successive presentation of even the same stimulus being perceived as unique.

The steeper I-V relation observed in the absence of the GABAergic

The steeper I-V relation observed in the absence of the GABAergic input should reduce the dynamic range of the ERG b-wave light responses in D1R−/− and GABACR−/− mice. Indeed, the rod-driven b-wave stimulus-response curves, both in the dark and at each background light intensity, obtained from both D1R−/− and GABACR−/− mice displayed a systematic ∼2-fold decrease in their dynamic range, defined as the range of intensities covering between 5% and

95% of the maximal response ( Figure 6), which served as a reason for decreased overall operational range, as illustrated click here in Figures 1C, 2B, and 2D. Altogether, our results argue that GABACRs buy Everolimus mediate a tonic, sensitizing chloride current that hyperpolarizes WT rod DBCs and decreases their input resistance, thereby extending the amplitude and operational range of their depolarizing light responses. In

the final set of experiments, we aimed to identify the cellular source of the dopamine-dependent GABAergic input onto rod DBCs. Electrophysiological studies have described the most prevalent GABACR-mediated chloride currents in rod DBC axon terminals (e.g., Eggers and Lukasiewicz, 2006). However, their dendrites also display a distinct GABACR-mediated chloride conductance, documented in ferret (Shields et al., 2000), which is consistent with specific GABACR immunostaining of rod DBC dendrites and its absence in GABACR−/− rod DBCs ( McCall et al., 2002). Figure 7 shows that short GABA puffs evoked GABACR-mediated chloride currents in both the axonal and dendritic terminals of the same WT rod DBCs in the mouse. Complete suppression of GABA-dependent currents could only be achieved by blocking both GABAA and GABAC receptors. Interestingly, the relative Rolziracetam contributions of GABAAR- and GABACR-dependent currents were similar for dendrites and axon terminals ( Figures 7C and 7D). The latter finding is consistent with results obtained for rat ( Euler and Wässle, 1998)

and for mouse ( McCall et al., 2002) rod DBC axon terminals. Therefore, both axons and dendrites could be considered as potential sites of sustained GABAergic inputs. Furthermore, both axons and dendrites of rod DBCs are located postsynaptically to cells displaying strong immunostaining for D1R and GABA (amacrine and horizontal cells, respectively; Figure 1D and Figure S4). The expression pattern of KCC2 on both rod DBC axons and somas immediately adjacent to the relatively short dendrites (Figures 4C and 4D) predicts an efficient chloride extrusion over the whole length of the rod DBC and therefore does not favor either amacrine or horizontal cells as a major source of the GABAergic input.

Our data demonstrate that in the spinal cord, the level of N-cadh

Our data demonstrate that in the spinal cord, the level of N-cadherin expression is not uniform but rather varies markedly between different progenitor groups along the dorsoventral axis in accordance to their expression of Foxp4. How might discrepancies in cadherin expression affect NPC function? Studies of germline stem cells in the Drosophila have shown that the level of E-cadherin plays

an important role in sustaining the stem cell pool and gating their differentiation behavior ( Song et al., 2002 and Voog et al., 2008). When E-cadherin function is blocked, germline stem cells lose contact with their niche and prematurely differentiate ( Song et al., 2002 and Voog et al., 2008). Remarkably, as little as JQ1 2-fold differences in E-cadherin levels can influence whether a germline stem cell remains in contact with the niche or differentiates ( Jin et al., 2008). Moreover, cells that express higher levels of E-cadherin can displace other cells from selleck products the niche, thus favoring the expansion of E-cadherinhigh cells over time ( Jin et al., 2008). By analogy, groups of vertebrate NPCs that express lower or higher levels of N-cadherin might have different adhesive properties, which could similarly influence their self-renewal capacity and

propensity for differentiation. The reduced expression of N-cadherin in the pMN, for example, could explain why MNs are among the first cells to differentiate in the spinal Rebamipide cord and why pMN cells rapidly lose their stem cell characteristics when grown in vitro compared to other progenitor groups ( Mukouyama et al., 2006). The differential expression of cadherins may thus be one way in which

the morphogen signals that pattern the developing nervous system ensure that different populations of NPCs expand and differentiate in a stereotyped manner. In many tissues, the expansion of the stem cell pool is proportional to the size and numbers of cells that make up the niche. If the niche is enlarged or contracted, stem cell numbers are accordingly changed (Voog and Jones, 2010). In the embryonic nervous system, NPCs do not depend upon support cells; rather they form their own niche microenvironment through AJs contacts within the neuroepithelium (Zhang et al., 2010). These observations raise the question of whether there are comparable mechanisms for limiting the “size” of the NPC niche and expansion of progenitors. Our data suggest that the transcriptional regulation of N-cadherin is a means by which the embryonic NPC niche could be regulated. Previous work by Kondoh and colleagues has shown that Sox2 directly activates N-cadherin expression (Matsumata et al., 2005). Our results extend those findings by identifying Foxp4 binding sites in the Cdh2 locus that likely mediate its repressive effects on N-cadherin.

9 mM and ∼6 mM, respectively When applied

9 mM and ∼6 mM, respectively. When applied Galunisertib mouse over the rostral lumbar segments, an aCSF composed of 0.9 mM [Ca2+]o and 6 mM [K+]o triggered an episode of locomotor-like activity in all preparations tested (n = 7; Figure 1H). Blind whole-cell recordings were performed from ventromedial neurons in the L1-L2 region to further investigate the relationship between changes in ionic concentrations and firing properties. Interneurons were identified by their high input resistance (604 ± 75 MΩ, n = 18) and the absence of antidromic response

to ventral root stimulation. A few minutes after NMA and 5-HT were applied, and long before the locomotor-like activity emerged, all interneurons (n = 18) were spiking (Figure 2A). Simultaneous recordings with ion-sensitive microelectrodes and intracellular pipettes enabled linking changes in ionic

concentrations to the cellular activity (Figures S2A and S2B). Half of the recorded neurons switched their firing pattern from spiking to bursting, either at the onset of locomotor-like activity (3/8 neurons; Figure 2B) or during ongoing locomotion (5/8 neurons). Superfusion of riluzole (5 μM) to block INaP progressively reduced the amplitude of membrane oscillations, which then became undetectable ( Figures 2D and 2E). As described previously ( Tazerart et al., 2007; Zhong et al., 2007), the ventral root burst progressively decreased in amplitude with little effect on the cycle frequency until locomotor-like activity disappeared ( Figure S2C). Furthermore, when preincubated for 45 min before the application of NMA/5-HT, riluzole (5 μM) Selleck BVD-523 prevented the emergence of locomotion (n = 3,

Figure S2D). The following set of experiments was performed to assess whether locomotor-related changes in [Ca2+]o and [K+]o may initiate intrinsic bursting properties. Whole-cell recordings were performed in neonatal rat slice preparations from spinal Ribonucleotide reductase interneurons (n = 187) located in the area of the locomotor CPG (ventromedial part of L1-L2). To discriminate the effect of ionic changes from that of neurotransmitters in generating membrane oscillations, we omitted the application of NMA and 5-HT. Reducing [Ca2+]o to 0.9 mM while keeping [K+]o at 3 mM did not affect the firing pattern (Figure 2F, left). Bursting could be induced only when reducing [Ca2+]o further to 0.3 or 0.0 mM (Figure 2G). At a constant [Ca2+]o (1.2 mM), pacemaker activities could not be evoked by increasing [K+]o to near 6 mM (Figure 2F, right) and appeared only at values above 9 mM (Figure 2G). A striking observation was the synergistic effect of reducing [Ca2+]o and increasing [K+]o on the generation of bursts. A concomitant reduction of [Ca2+]o to 0.9 mM and increase of [K+]o to 6 mM induced bursts in 25% of neurons (Figures 2G and 2H). These bursts were attributable to INaP as they were reversibly abolished by low concentrations of TTX (0.

, 2009, Walther et al , 2009 and MacEvoy and Epstein, 2011), but

, 2009, Walther et al., 2009 and MacEvoy and Epstein, 2011), but they are still far smaller than the likely representational capacity of the human visual system. Theoreticians have argued that the simple statistical properties of natural scenes explain selectivity to low-level features in peripheral sensory areas (Olshausen and Field, 1996 and Smith and Lewicki, 2006). Behavioral data suggest that low-level natural scene statistics also influence the perception of scene categories (Oliva and Torralba, 2001 and Torralba and Oliva, 2003). Though several qualitative theories have

been proposed that link the object statistics of natural scenes with human scene perception (Biederman, 1981 and Palmer, 1975), none have provided an objective, quantitative framework to support this link. The current study provides such a framework. Our data-driven, model-based approach shows that scene categories encoded in the human brain can be derived www.selleckchem.com/products/gdc-0068.html from the co-occurrence statistics of objects in natural scenes.

This further suggests that the brain exploits natural scene statistics at multiple levels of abstraction. If this is true, then natural scene statistics might be used as a principled means Selleckchem Nintedanib to develop quantitative models of representation throughout the visual hierarchy. The work reported here could be extended in several ways. For example, although the spatial distribution of objects within a scene appears to influence the representation of the scene (Biederman et al., 1982, Green and Hummel, 2006 and Kim and Biederman, 2011), the modeling framework used here whatever makes no assumptions about the spatial distribution of objects within scenes. More sophisticated models that incorporate spatial statistics or other mediating factors such as attention may provide further

information about the representation of scenes and scene categories in the human brain. The experimental protocol used was approved by the UC Berkeley Committee for the Protection of Human Subjects. All fMRI data were collected at the UC Berkeley Brain Imaging Center using a 3 Tesla Siemens Tim Trio MR scanner (Siemens, Germany). For subjects S1, S3, and S4, a gradient-echo echo planar imaging sequence, combined with a custom fat saturation RF pulse, was used for functional data collection. Twenty-five axial slices covered occipital, occipitoparietal, and occipitotemporal cortex. Each slice had a 234 × 234 mm2 field of view, 2.60 mm slice thickness, and 0.39 mm slice gap (matrix size = 104 × 104; TR = 2,009.9 ms; TE = 35 ms; flip angle = 74°; voxel size = 2.25 × 2.25 × 2.99 mm3). For subject S2 only, a gradient-echo echo planar imaging sequence, combined with a custom water-specific excitation (fat-shunting) RF pulse was used for functional data collection. In this case, 31 axial slices covered the entire brain, and each slice had a 224 × 224 mm2 field of view, 3.50 mm slice thickness, and 0.

, 2009), and irradiation ( Mexis et al , 2009, Narvaiz et al , 19

, 2009), and irradiation ( Mexis et al., 2009, Narvaiz et al., 1992 and Prakash et al., 2010). Compared Selleckchem Sunitinib to hydro, thermal, and chemical methods, ionizing radiation has the advantage of retaining the functional quality of nuts. However, radiation efficacy varies among studies due to different sample conditions during treatment. Although low water activity (aw) is one key to controlling microbial growth, it actually presents a significant impediment to microbial inactivation. According to Laroche et al. (2005), the thermal inactivation rates for Saccharomyces cerevisiae and Lactobacillus plantarum are not monotonically dependent on initial aw (0.10–0.70).

Additionally, the effect of aw on thermal resistance of Salmonella Typhimurium varied with solute type (glycerol, sucrose, glucose, or polyethylene glycol) ( O’Donovan-Vaughan and Upton, 1999). Given that the surrounding humidity can alter the surface aw of nuts during processing and storage, it is important to quantify inactivation rates as a function of this critical variable. Therefore, the objectives of this study were to: (1) quantify the relationship between aw and the D10-value for low-energy X-ray inactivation of Salmonella on almonds and walnuts, (2) quantify post-irradiation survival of Salmonella on nuts during storage, and (3) determine the impact of X-ray irradiation on the sensory quality. Shelled

raw whole almonds (Nonpareil) and walnuts (Juglans regia) from the 2009 crop were purchased in a single lot of each from retail sources located in California. Upon acquisition, 200 g of each nut type were vacuum-packaged and stored at 4 °C until testing. PLX-4720 concentration Kernel and bulk density were measured in a graduated cylinder nearly using the platform scale method (AOAC 971.25) ( AOAC, 2000). For moisture content determination, samples were ground using a IDS55 coffee bean grinder (Mr. Coffee, Cleveland, OH) for ~ 30 s, and ~ 2 g (5 replications) was dried in an oven at 102 °C to constant weight (~ 48 h). An FP-200 Nitrogen Analyzer (Leco Corp., St. Joseph, MI: compliance with AOAC 990.03) was used for protein

analysis, and a Soxhlet fat extractor was used according to AOAC 948.22 ( AOAC, 2000) for total fat content. Salmonella Enteriditis PT30 (SE PT30), originally isolated from raw almonds implicated in the 2000 and 2001 outbreaks, was previously obtained from Dr. Linda Harris (University of California — Davis) and preserved at − 80 °C in Tryptic Soy Broth (TSB) (Difco, Becton Dickinson, Sparks, MD) containing 20% glycerol. To compare serovars, three strains of Salmonella Tennessee (S13952, S13972, and S13999) were obtained from the Food Science and Human Nutrition culture collection at Washington State University (Pullman, WS) and preserved under the same condition as SE PT30. The inoculation procedure of Danyluk et al. (Danyluk et al., 2005) was followed with slight modifications.

, 2007; Ying et al , 2008) Further, an important recent report d

, 2007; Ying et al., 2008). Further, an important recent report demonstrated that FGF10 determines the timing of the transition from neural epithelium to radial progenitor, a key event in neurogenesis (Sahara and O’Leary, 2009). Our study does not assess the role of MEK in mediating the FGF10 effect since recombination Perifosine in our study occurred after the neural epithelium stage. However, our finding that Mek deletion prevents an important step in radial progenitor fate transition in late embryogenesis clearly has parallels with the FGF10 result at an earlier stage in radial progenitor development. Importantly,

FGFs have previously been implicated in glial development ( Naruse et al., 2006; Seuntjens et al., Kinase Inhibitor Library 2009; Song and Ghosh, 2004). We suggest that FGF effects on regulating radial progenitor fate transitions are mediated via MEK/ERK signaling. Our findings provide strong evidence for an important interaction between MEK signaling and the CNTF/LIFRβ-gp130/JAK-STAT cascade, a major cytokine signaling pathway that promotes astrogenesis (Bonni et al., 1997). It has been well established that an increase in the gp130 expression level in radial progenitors at midembryogenesis is vital for initiating astrogenesis (He et al., 2005; Nakashima et al., 1999a). Importantly, we have demonstrated here that MEK was required

for the expression of gp130 by radial progenitors. Consequently, CNTF failed to induce STAT3 phosphorylation and GFAP expression efficiently in Mek1,2\Nes isothipendyl mutant progenitor cultures.

Our data suggest that MEK and CNTF/JAK-STAT pathways work contiguously in regulating astrogenesis. Thus, MEK signaling promotes gliogenic fate transition by radial progenitors, and then CNTF/JAK-STAT signaling induces further differentiation of astrocyte precursors. Progression along the oligodendrocyte lineage was also profoundly affected by Mek deletion. In line with our results, partial inhibition of ERK/MAPK signaling by deletion of Braf or Erk2 has previously been shown to inhibit CNS myelination, though the effect on radial progenitor fate transition to OPC was unclear ( Fyffe-Maricich et al., 2011; Galabova-Kovacs et al., 2008). Here, we have completely eliminated ERK/MAPK signaling by deleting Mek1/2 and show that the generation of OPCs in the developing cortex is almost completely blocked. MEK regulation of neurogenesis was not definitively addressed in this study due to uncertainty about the timing of recombination in relation to the major phases of neurogenesis which occur earlier than gliogenesis. A recent study showed a requirement for ERK2 in regulating the proliferation of neurogenic precursors at E14, although results were complex in that some layer markers showed depletion after Erk2 deletion but other layer markers showed expansion ( Pucilowska et al., 2012). Here, our data suggest prolonged neurogenesis at late embryonic stages in Mek-deleted cortices.

Fernandez et al (2003) identified Eimeria species in samples con

Fernandez et al. (2003) identified Eimeria species in samples containing from two to eight oocysts originated from experimental infections, using the same methodology. Yet, Haug et al. (2007) observed

that there is a variation in the detection of each Eimeria species, depending on the number of oocysts used and the technique adopted for DNA extraction. selleck products In field samples, many factors may interfere in the success and effectiveness of diagnosis by PCR, especially in regards to the presence of contamination. According to Haug et al. (2007) the DNA extraction process in stool samples is influenced by the formation of inhibitors of Taq DNA polymerase that affect the reaction. At least three Eimeria species were simultaneously identified using a multiplex PCR. These data are consistent with literature that reveals the occurrence of mixed infections in animals, thus hindering the accurate diagnosis of the species applying techniques traditionally Romidepsin mw used ( Long and Joyner, 1984, Shirley, 1995 and Williams, 2001). In Japan, Kawahara et al. (2008) identified E. brunette 65.6%, E. maxima and E. necatrix 50%, E. tenella 37.5%,

and E. acervulina at 25% in the properties evaluated, using real time PCR for the detection of ITS-1. In China Sun et al. (2009) identified E. tenella, E. praecox and E. acervulina in more than 70% of the properties. Yet in South Korea, Lee et al. (2010) identified a high prevalence of the seven species emphasizing E. acervulina, E. tenella and E. brunetti. These data reinforce the idea that several factors influence the presence and prevalence of Eimeria species in each region. The morphological evaluation of oocysts also resulted in the diagnosis of a wide variety of species in the farms. Luchese et al. (2007) also identified frequencies ranging from 45.52%, 18%, 14% and 12.32% for E. maxima, E. brunetti, E. tenella and E. acervulina, respectively, through the morphology.

Terra et al. (2001), evaluated 60 carcasses of slaughtered broiler chickens in the city of Monte Alegre do Sul, Brazil, and identified frequencies of 90% for E. maxima, 86.4% for E. tenella, 86% for E. mitis, and 25% for E. acervulina and E. necatrix, through the morphology. However, Santos et al. (2003) failed to identify the occurrence Linifanib (ABT-869) of Eimeria species in farms of São Paulo state using morphology, considering the observed overlap in the measurements of oocysts among species and the occurrence of infections caused by mixed infections, preventing diagnosis. According to this data ( Table 1), morphology could be a sensitive method for the discrimination of Eimeria species in field trials. Nevertheless, morphology is a technique with A sort of limitations to be used as a single tool for diagnosis of Eimeria species. It means that results obtained with this method should be carefully interpreted ( Woods et al., 2000 and López et al., 2007).

caninum and T gondii tissue cysts ( Weiss et al , 1999) For sig

caninum and T. gondii tissue cysts ( Weiss et al., 1999). For signal amplification, the avidin–biotin complex immunoperoxidase step was performed (DakoCytomation, Denmark) and the slides stained with diaminobenzidine tetrahydrochloride (DAB – DakoCytomation). Counter staining was performed with Harris hematoxylin (10%) and slides were later mounted on coverslips to be read under light microscope (Nikon, Japan). Direct detection was also attempted by the detection of Nc5 locus in the IHC positive samples, using DNA extraction, primer

sets and amplification protocols as previously described ( Furuta selleckchem et al., 2007). The need to observe N. caninum in wildlife animals has been pointed out as a possible way to understand some obscure aspects of the parasite’s cycle ( Gondim, 2006). There are indications that the presence of birds in cattle-raising farms could be associated with the increase of seroprevalence and abortions related to N. caninum ( Bartels et al., 1999 and Otranto

et al., 2003). In T. gondii epidemiological chain, birds are considered parasite’s reservoir, since those animals are frequently preyed upon by its definitive hosts, felids ( Elmore Selumetinib concentration et al., 2010). The same pattern of events may be observed in the relationship between dogs and birds, which may lead to speculations towards if birds may also perform the role of N. caninum reservoirs in nature. Epidemiological studies for these protozoa frequently employ antibody detection to estimate population infection rates. Serological positivity to T. gondii in birds is usually low, which is not compatible with direct detection in different tissues ( Dubey, 2002). Serological analysis by IFAT of samples gathered from wild birds maintained in captivity and free-ranging birds for the presence of antibodies to N. caninum were inconclusive, since specific IgG antibodies to N. caninum were not detected. The absence of detectable levels of specific IgG against N. caninum in birds is not a surprise, since it has been already shown that experimentally infected pigeons and different chicken models present

an abrupt antibody seroconversion, from despite a brief detection period ( Furuta et al., 2007 and Mineo et al., 2009). Additionally, the same phenomenon has been described in experimental infections of wild birds with T. gondii ( Mineo et al., 2009 and Vitaliano et al., 2010). The lack of detection of circulating antibodies specific to the parasite in the tested species may be partially attributed to the serological assay employed, which is based on a secondary antibody raised for chickens. Although the assay seems to work properly with some wildlife species, IgG domains of different bird species is variable and might not present the same homology with chicken antibodies, fact that may dampen the serological diagnosis in wild life animals. Unfortunately, it is uncommon to find commercial conjugates specific for wild life animals, which limits applied research focusing those species.

To test whether the neural activity is modulated according to the

To test whether the neural activity is modulated according to the temporally discounted values of individual targets, we also applied the following two models: equation(model 2) S=a0+a1DVL+a2DVR+a3(DVchosen−DVunchosen)+a4C,S=a0+a1DVL+a2DVR+a3(DVchosen−DVunchosen)+a4C, equation(model 3) S=a0+a1DVchosen+a2DVunchosen+a3(DVL−DVR)+a4C.S=a0+a1DVchosen+a2DVunchosen+a3(DVL−DVR)+a4C.

The set of independent variables in each of these three models forms the basis Proteasome inhibitor for the same vector space. Therefore, these three models account for the same amount of variance in the neural activity, and are used to test the statistical significance for different independent variables. To test whether the regression coefficients associated with the temporally discounted values of individual targets are significantly correlated, we repeatedly (n = 10,000) shuffled the spike counts randomly across trials and estimated the p-value from

the frequency of such shuffles in which the correlation coefficient between the regression 3-MA cell line coefficients exceeded the value obtained from the original data (Figure 4). To test whether the activity related to temporally discounted values differs for the intertemporal choice and control tasks, we applied a regression model that includes a series of interaction terms between the dummy variable indicating the task performed by the animal and other variables related to the animal’s choice and Cell press temporally discounted values as follows. equation(model 4) S=a0+a1(DVL+DVR)+a2(DVL−DVR)+a3(DVchosen−DVunchosen)+a4C+a5T+a6T×(DVL+DVR)+a7T×(DVL−DVR)+a8T×(DVchosen−DVunchosen)+a9T×C,S=a0+a1(DVL+DVR)+a2(DVL−DVR)+a3(DVchosen−DVunchosen)+a4C+a5T+a6T×(DVL+DVR)+a7T×(DVL−DVR)+a8T×(DVchosen−DVunchosen)+a9T×C,where

T denotes the task (0 and 1 for the choice and control task, respectively). To test whether the activity was modulated by the magnitude and delay of reward expected from a given target, we also applied the following regression model. equation(model 5) S=a0+a1M+a2DL+a3DR+a4Mchosen+a5Dchosen+a6C,S=a0+a1M+a2DL+a3DR+a4Mchosen+a5Dchosen+a6C,where M denotes the position of the large-reward target (0 and 1 for the trials in which the large reward was assigned to the leftward and rightward targets, respectively), DL (DR) the delay of the reward from the left (right) target, and Mchosen and Dchosen the magnitude and delay of the reward chosen by the animal. The statistical significance of each regression coefficient was determined with a t test (p < 0.05), and the significance for the effect of the reward delays (DL and DR) was adjusted for multiple comparison using the Bonferroni correction.