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Sultan Nikolaev
Sultan Nikolaev

Nn Model Sugar



Sugar exerts its potent reinforcing effects via both gustatory and post-ingestive pathways. It is, however, unknown whether sweetness and nutritional signals engage segregated brain networks to motivate ingestion. We found in mice that separate basal ganglia circuitries mediated the hedonic and nutritional actions of sugar. During sugar intake, suppressing hedonic value inhibited dopamine release in ventral, but not dorsal, striatum, whereas suppressing nutritional value inhibited dopamine release in dorsal, but not ventral, striatum. Consistently, cell-specific ablation of dopamine-excitable cells in dorsal, but not ventral, striatum inhibited sugar's ability to drive the ingestion of unpalatable solutions. Conversely, optogenetic stimulation of dopamine-excitable cells in dorsal, but not ventral, striatum substituted for sugar in its ability to drive the ingestion of unpalatable solutions. Our data indicate that sugar recruits a distributed dopamine-excitable striatal circuitry that acts to prioritize energy-seeking over taste quality.




Nn Model Sugar


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The Hs1(pro-1) locus confers resistance to the beet cyst nematode (Heterodera schachtii Schmidt), a major pest in the cultivation of sugar beet (Beta vulgaris L.). The Hs1(pro-1) gene was cloned with the use of genome-specific satellite markers and chromosomal break-point analysis. Expression of the corresponding complementary DNA in a susceptible sugar beet conferred resistance to infection with the beet cyst nematode. The native Hs1(pro-1) gene, expressed in roots, encodes a 282-amino acid protein with imperfect leucine-rich repeats and a putative membrane-spanning segment, features similar to those of disease resistance genes previously cloned from higher plants.


A. Schematic representation of the behavioural preparation where mice licked bitter-containing sippers such that detected licks triggered intra-gastric infusions of either glucose or sucralose. B. Hungry mice (N=8) licked the bitter solution significantly more when self-infusing glucose compared to when self-infusing sucralose (t[7]=2.62, * p=0.035), resulting in significantly larger intra-gastric glucose volumes (not shown, t[7]=3.17, p=0.016). C. Reverse microdialysis was used to perfuse DS or VS with dopamine during ingestion of sucralose or a bitter solution. D. Dopamine perfusion in DS (N=6) and VS (N=5) resulted in increases in sucralose intake when compared to aCSF perfusions (Left panel; Perfusion main effect F[1,9]=16.76, p=0.003) The effect was similar in both VS and DS (Two-way RM-ANOVA, striatal region brain perfusion F[1,9]=3.43, p=0.097; dopamine vs. aCSF in DS, t[5]=5.07, Bonferroni * p=0.008; in VS effect was weaker: t[4]=1.33, p=0.51). This is consistent with sweetness-driven dopamine efflux in VS but not DS. Dopamine perfusion in DS and VS resulted in robust increases in bitter intake when compared to aCSF perfusions (Right panel; Perfusion main effect F[1,9]=27.55, p=0.001). Effect was similarly robust in both VS and DS (Two-way RM-ANOVA, striatal region brain perfusion F[1,9]=0.43, p=0.53; dopamine vs. aCSF in DS, t[5]=3.6, Bonferroni *p=0.03; VS: t[4]=3.7, ** p=0.04). E. Cell-specific ablation of D1r-neurones in DS or VS. Top panel: Brief access test for different sucralose concentrations. [Two-way RM-ANOVA, sweetness group F[6,57]=8.23, p=0.000002; group effect F[2,19]=1.2, p=0.32;; sweetness effect F[3,57]=95.8, p= 3x10-22]. Cell-specific ablation of D1r-neurones in VS, but not DS, produced a lower intake of 2 mM sucralose [One-way ANOVA group effect F[2,21]=5.95, p=0.01. Ventral lesion vs. Control, Bonferroni *p=0.04; and vs. DS lesion, Bonferroni * p=0.014], whereas at 6mM sucralose VS Casp intake was higher [One-way ANOVA group effect F[2,21]=5.94, p=0.01; ventral lesion vs. WT-Casp Bonferroni #p=0.012 and Ventral lesion vs. DS-Casp Bonferroni p=0.055]. Bottom panel: Masking bitterness. The concentration of the bitter compound denatonium was fixed at 6mM and different concentrations of sucralose were used. [Two-way RM-ANOVA, sweetener concentration group F[6,57]=5.29, p=0.00021; group effect F[2,19]=1.95, p=0.17; sweetener concentration effect F[3,57]=67.32,, p=9.9x10-19]. Cell-specific ablation of D1r-neurones in VS, but not DS, produced a lower intake of the mixture 6mM denatonium and 6mM sucralose [One-way ANOVA group effect F[2,21]=7.55, p=0.004. Ventral lesion vs. Control, Bonferroni **p=0.012; and vs.DS lesion, Bonferroni ** p=0.007]. F. Effects of cell-specific ablation of D1r-neurones in DS or VS on sugar-driven consumption of unpalatable solutions. Top panel: Licks produced during the ingestion of a bitter mixture that triggers intra-gastric infusions of different D-glucose concentrations. [Two-way RM-ANOVA, glucose concentration group F[6,57]=2.68, p=0.023; group effect F[2,19]=2.75, p=0.089; glucose concentration effect F[3,57]=25.8, p=1.3x10-10]. Bottom panel: Intra-gastric infusions observed during these sessions [Two-way RM-ANOVA, glucose concentration group F[6,57]=8.83, p=8.2x10-7; group effect F[2,19]=4.18, p=0.031; glucose concentration effect F[3,57]=45.87, p=3.3x10-15]. Concentrations: 0.5% [One-way ANOVA group effect F[2,21]=7.07, p=0.005; ventral lesion vs. Control, Bonferroni *p=0.007; and vs.DS lesion, Bonferroni * p=0.023];: 10% [One-way ANOVA group effect F[2,21]=7.09, p=0.005; intake in dorsal lesion vs. Control, Bonferroni **p=0.007; and vs.VS lesion, Bonferroni ** p=0.024]; 25% [One-way ANOVA group effect F[2,21]=5.75, p=0.011; dorsal lesion vs. Control, Bonferroni #p=0.034; and vs.VS lesion, Bonferroni #p=0.018]; 50% [One-way ANOVA group effect F[2,21]=2.16, p=0.142]. G. Licks (top) and infusions (bottom) produced during the conditioning sessions (bitter intake paired with intra-gastric infusions of glucose) prior to the second two-bottle test. Cell-specific ablation of D1r-neurones did not alter intake. [Licks: One-way ANOVA Group Effect F[2,21]=2.27, p=0.13; Infusions: One-way ANOVA Group Effect F[2,21]=1.11, p=0.34]. H-K. Neuroanatomical analyses of the sham cell-specific lesions. When Retrobeads were injected into globus pallidus (GP, targeted by D2r-expressing neurons of DS) of DS-CTL mice (area within dotted line in H), strong labelling was observed in DS (I). Similarly, robust labelling was observed in DS (J) when Retrobeads were injected into the contralateral SNr (K), which is exclusively targeted by D1r-expressing neurons of DS (confront vs. Main Figure 2 in which lesioned case is shown). To allow visualization of the relevant anatomical landmarks, images show the Retrobead fluorescence signal overlaid on a bright field image of the same section.


A. Schematic representation of optical fibre position in ventral pallidum (VP) and B. Substantia nigra, pars reticulata (SNr). C. Optogenetic activation of VP strongly suppresses artificial sweetener intake (N=6, Laser ON vs. OFF effect, paired t-test t[5]=13.1, Boferroni *p=0.0018). D. No effects are observed upon activation of SNr (N=5, t[4]=0.58, p=0.59). E. When a novel artificial sweetener (Rebaudioside A) is paired to light, low intake levels are observed also during subsequent Laser OFF sessions (N=6, t[5]=2.75, Bonferroni p=0.1). F. Again no effects are observed upon activation of SNr (N=5, t[4]=0.96, p=0.39). Importantly note that when licks shown in E (i.e. upon optical stimulation of VP) are compared to those shown in F (i.e. upon optical stimulation of SNr), a strong reduction in Rebaudioside A intake is observed during VP compared to SNr stimulation (two-way repeated-measures ANOVA laser source brain region: F[1,9]=7.09, p=0.026; Main brain region effect F[1,9]=55.25, p=0.00004; Comparison during laser ON sessions: two-sample t-test t[9]=5.97, p=0.00021). G. Animals are treated with a glucose intra-gastric preload previous to access to the sucralose solution. Under these conditions optogenetic activation of VP weakly suppresses intake (N=6). t[5]=2.63, Bonferroni *p=0.046, one-tailed). H. However, optogenetic activation of SNr led to suppressed intake when preceded by sugar gut infusions (N=5). t[4]=4.04, Bonferroni *p=0.032). I. When a sucralose gastric preload is used instead, VP activations leads to strong suppression (N=6). t[5]=7.57, Bonferroni *p=0.002). J. As expected, no effects upon SNr activation are observed when sucralose intra-gastric preloads are used (N=6). t[4]=0.009, p=0.99).


Maple syrup is produced from the sap of maple trees, which is collected from late winter through early spring. The collected sap is clear and only slightly sweet; to produce syrup and sugar, the sap must be concentrated through evaporation (boiling) or reverse osmosis.


Maple trees are a major component of northeastern mesic forests and provide multiple ecosystem services; maple syrup is an iconic and highly valued non-timber forest product with a particularly strong cultural presence in New England. Native Americans have a long history of producing maple sugar, a tradition which was adopted by early settlers. In recent years, the demand for maple products has been on the rise (5, 6, 11). The timber value for maple is also high; however, this use is not considered compatible with syrup production due to the damage caused by drilling tap holes into the trunk (6, 11), except for small niche markets for specialty lumber that are not well developed.


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