Glucose amplifies the inhibitory effects of food odor and of gel fill.

<p>Animals were treated with glucose 1 hr before testing feeding<b>. </b><i>A</i>) There was no significant difference between the effects of glucose or of ASW on entry into the steady-state. <i>B</i>) Glucose amplified the inhibitory effects of food odor. During the first 2 hours of the meal, animals treated with glucose ate significantly less than did controls (<i>p</i> = 0.05, <i>t</i>(27) = 2.02). There was no significant difference in the subsequent two hours (<i>p</i> = 0.60, <i>t</i>(27) = 0.54). <i>C</i>) Glucose treatment also amplified the inhibitory effect of gut fill at the start of the meal. During the first half hour, glucose-treated animals ate significantly less (<i>p</i> = 0.007, <i>t</i>(44) = 2.79 than did controls, with no significant difference (<i>p</i> = 0.99, <i>t</i>(44) = 0.008); all tests are two-tailed <i>t</i>-tests) in the subsequent period. The dashed line shows steady-state feeding. Standard errors are shown.</p

L-arginine does not amplify the inhibitory effect of gut fill.

<p>In this experiment, 3 groups of animals were examined. One (<i>N</i> = 8) was injected with ASW 10 min before a 4 hr feeding. A second (<i>N</i> = 12) was treated with 2.5 ml of gel injected into the crop before the 4 hr feeding. A third (<i>N</i> = 14) was treated with gel, plus an injection that raised the hemolymph concentration of L-arginine to 250 µM. Standard errors are shown. A) Percent time spent feeding in half-hour intervals over the 4 hr test. Data on animals treated with ASW are not shown. B) The total time spent feeding over the 4 hr test in the three groups. There was a significant difference between the three groups (<i>p</i>(2,31) = 0.036; <i>F</i> = 3.69; one-way analysis of variance). A post-hoc test (Student-Newman-Kuels) showed that at α = 0.05, animals treated with ASW ate significantly more than did animals in the other two groups, with no significant difference between animals treated with gel alone, or with gel and L-arginine.</p

L-arginine augments inhibition caused by the odor of food.

<p>In all experiments, animals were food-deprived for 3 days, and were then allowed <i>ad-libitum</i> access to food for 4 hours. Animals were exposed to food odor for the two hours before the animals were permitted to eat food. In addition, animals were injected either with ASW (<i>N</i> = 37), or with solutions that raised the hemolymph L-arginine by 250 µM (<i>N</i> = 18) or 25 µM (<i>N</i> = 22). Data on the effects of food odor after ASW treatment replicate the data in Figs. 1A and 2. Standard errors are shown. A) The mean percent time spent eating during each half hour of the 4 hours. B) The total time spent feeding during the 4 hours. There were significant differences in the total time spent feeding between the three groups (<i>p</i><0.001, <i>F</i>(2,74) = 13.2; one-way analysis of variance). A post-hoc test (Student-Newman-Kuels) showed that at α = 0.05, animals treated with 250 µM L-arginine ate significantly less than did animals in the other two groups, with no significant difference between animals treated with ASW or with 25 µM L-arginine. Nonetheless, the data in A suggest that 25 µM L-arginine might have had an inhibitory effect during the second hour of the meal. We therefore tested the effect of 25 µM L-arginine against the effect of ASW for each of the four hours of the meal. This comparison used only animals treated with ASW that were run on the days that the effect of 25 µM L-arginine was examined. Pre-treatment with 25 µM L-arginine indeed augmented the effect of pre-exposure to odor during the second period of four hours of the experiment (<i>p</i> = 0.04, <i>t</i>(40) = 2.09), without affecting feeding during the first (<i>p</i> = 0.95, <i>t</i>(40) = 0.51, third (<i>p</i> = 0.85, <i>t</i>(40) = 0.15) or fourth (<i>p</i> = 0.08, <i>t</i>(40) = 1.77) hours.</p

Habituation of excitatory effects of food odor reveals the inhibitory effect.

<p>Animals were pre-exposed to food odor for 24 (<i>N</i> = 13), 2 (<i>N</i> = 27) or 1 (<i>N</i> = 18) hours prior to being given access to food. The percent feeding was then measured over the next 4 hours. During the first hour, there was no significant difference in feeding between animals fed after a 24 hr exposure to seaweed odor and animals fed after a 2 hr pre-exposure to the odor (<i>p</i> = 0.54, <i>t</i>(38) = 0.61; two-tailed <i>t</i>-test)). By contrast, there was a significant difference in feeding between animals pre-exposed to food odor for 1 hour and the combined data from 2 and 24 hour pre-exposures to seaweed odor (<i>p</i> = 0.01, <i>t</i>(56 = 2.60; two-tailed <i>t</i>-test).</p

The NO scavenger PTIO induces fictive feeding when applied to the isolated buccal ganglia.

<p>Fictive feeding was monitored via extracellular recordings from the radula nerve (RN) and from buccal nerve 2 (BN2). Activity in RN is a correlate of radula closing, whereas activity in BN2 is a correlate of retraction. Activity representative of radula retraction was counted as a single burst of fictive feeding. <b>A</b>) In ASW, no fictive feeding was seen, although a single unit in BN2 fired. <b>B</b>) Application of PTIO (at the start of the trace) elicited repeated bursts of fictive feeding. Recordings similar to those shown were observed in 7 separate isolated buccal ganglia preparations. <b>C</b>) Expansion of the boxed area in part B shows overlap between firing in BN2 and RN, indicating that PTIO induced ingestion-like activity. <b>D</b>) Means and standard errors of the number of fictive feeding bursts recorded in 10 min in ASW and after the application of PTIO. PTIO caused a significant increase in fictive feeding (<i>p</i> = 0.02 <i>t</i>(6) = 2.78; two-tailed paired <i>t</i>-test).</p

Block of NO opens an inward current.

<p><b>A</b>) Effect of PTIO and of L-NAME on currents recorded during the last few hundred milliseconds of a voltage clamp experiment performed in TTX. Only currents recorded in response to voltage steps to −90, −60 and −10 mV are shown. Note that both PTIO and L-NAME induce inward currents at −90 and −60 mV, with the currents at −90 mV larger than those at −60 mV. Also note the reversal of the currents at −10 mV. <b>B</b>) Mean and standard errors (hidden by the points) of current amplitudes recorded during the last 500 msec of voltage pulses with and without PTIO or L-NAME (N = 5 for each group). <b>C</b>) The difference in current between values recorded with and without PTIO or L-NAME at the various voltage steps. The data were combined from experiments using the two blockers. Means and standard errors are shown.</p

Effects of NO blockers and donors on other neurons.

<p><b>A</b>) L-NAME had no effect on neuron B8 in 6 of 6 preparations. L-NAME also had no effect on B4 in 5 of 5 preparations (not shown). <b>B</b>) Treatment of an isolated MCC neuron in culture with L-NAME had no effect in 7 of 7 preparations. <b>C</b>) In an isolated, cultured C-PR neuron application of L-NAME caused a depolarization in 5 of 5 preparations. Mean amplitude of depolarization: 13.3±1.07 (SE) mV; Mean latency to spiking: 7.11±1.8 (SE) min. The dashed line marks the −60 mV resting potential.</p

Block of NO depolarizes C-PR in situ.

<p><b>A</b>) Application of the NO scavenger PTIO in an isolated cerebral ganglion preparation depolarized C-PR and caused an increase in EPSPs. <b>B</b>) In the presence of TTX, PTIO still depolarizes C-PR (N = 5 cells in 3 preparation), indicating that part of the effect is direct.</p

The social aetiology of essentialist beliefs

This commentary highlights the importance of attending to the sociocultural contexts that foster essentialist ideas. It contends that Cimpian & Salomon's (C&S's) model undervalues the extent to which the development of essentialist beliefs is contingent on social experience. The result is a restriction of the model's applicability to real-world instances of essentialism-fuelled prejudice and discrimination

SnapShot-Seq-derived timescales for ten human tissues and technical controls.

<p>(<b>A</b>) Lifetimes obtained from total RNA-Seq performed on ten human tissues, using the SOLiD Whole Transcriptome Sequencing method <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0089673#pone.0089673-Tumor1" target="_blank">[23]</a> with RiboMinus rRNA-depletion. <i>T</i>₅, <i>T</i>₃, and <i>T</i>_γ are as defined as in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0089673#pone-0089673-g001" target="_blank">Fig. 1</a>. (<b>B</b>) A comparison of lifetimes across different sequencing methodologies. We performed sequencing on SOLiD (S) or Illumina (I); hybridization-based rRNA depletion with RiboMinus (M) or RiboZero (Z); and compared RNA samples isolated and prepared into libraries on several different days. We performed Illumina total RNA-Seq using the dUTP method <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0089673#pone.0089673-Levin1" target="_blank">[19]</a>. Error bars indicate 95% confidence from Monte Carlo simulations from individual biological samples.</p