Focus on the role of seed tannins and pectolytic enzymes in the color development of Pinot noir wine.

Maceration techniques which promote the extraction of color pigments and tannin from grapes are often sought in Pinot noir winemaking to optimise color stability; alternatively, exogenous grape tannins may be included during fermentation. To examine the effect of seed-derived tannins and the use of pectolytic enzymes on color development in wines, conventional must preparations of Vitis vinifera L. cv Pinot noir grapes were compared with wines made using a supplementary addition of either a commercial seed tannin product or previously fermented seeds, while in a complementary experiment, seeds were sequentially removed during fermentation. After 6 months bottle aging, wines supplemented with either a commercial seed tannin solution (0.4 â€‹g/L), or fermented seeds (20% w/w seeds) had from 60% to 95% higher tannin concentration than the untreated wine, and up to 60% more monomeric anthocyanins. Conversely, when a third of the seeds were removed from the fermenting wine, the concentration of both tannin and non-bleachable pigments was 20-30% lower than in untreated wines and the wine hue had more red-purple tones. Exploration of the use of pectolytic enzymes in conjunction with seed removal was also found to have a significant impact on wine color parameters. Further insights on the timing of egress of tannin precursors from seeds was obtained from histochemical examination of the seeds that had been removed during alcoholic fermentation.

Grape skins as supplements for color development in Pinot noir wine.

A particular challenge to making wine from Pinot noir grapes is the delicate flavor, light color and poor ageing potential of the wine. Conventional Pinot noir must preparations were compared with those made using a skin-based supplement to assess the impact on non-bleachable (sulfur resistant) pigments in the wine. When supplemented with either fresh grape pomace of Pinot noir, Pinot gris or Chardonnay grapes; Pinot noir grape marc or a commercial liquid grape skin extract, the additional seeds and pulp from the supplements were shown to compromise the development of stable pigments in the wine. To compare the relative merits of tannin derived from grape skins and seeds, the supplements used in a parallel experiment were the skins alone of the same three grape varieties and at six months bottle age, the stable pigment concentration was found to exceed the amount attributable to the supplement. A third experiment used fermented grape skins as the supplement, with 85% of the supplementary anthocyanin recovered as stable pigment complexes in the wine. Notably, this series of experiments showed that supplements containing grape seeds appeared to compromise non-bleachable pigment formation in the wine while skin only supplements stimulated their development.

Relative Timing Between Kappa Opioid Receptor Activation and Cocaine Determines the Impact on Reward and Dopamine Release.

Negative affective states can increase the rewarding value of drugs of abuse and promote drug taking. Chronic cocaine exposure increases levels of the neuropeptide dynorphin, an endogenous ligand at kappa opioid receptors (KOR) that suppresses dopamine release in the nucleus accumbens (NAc) and elicits negative affective states upon drug withdrawal. However, there is evidence that the effects of KOR activation on affective state are biphasic: immediate aversive effects are followed by delayed increases in reward. The impact of KOR-induced affective states on reward-related effects of cocaine over time is not known. We hypothesize that the initial aversive effects of KOR activation increase, whereas the delayed rewarding effects decrease, the net effects of cocaine on reward and dopamine release. We treated rats with cocaine at various times (15 min to 48 h) after administration of the selective KOR agonist salvinorin A (salvA). Using intracranial self-stimulation and fast scan cyclic voltammetry, we found that cocaine-induced increases in brain stimulation reward and evoked dopamine release in the NAc core were potentiated when cocaine was administered within 1 h of salvA, but attenuated when administered 24 h after salvA. Quantitative real-time PCR was used to show that KOR and prodynorphin mRNA levels were decreased in the NAc, whereas tyrosine hydroxylase and dopamine transporter mRNA levels and tissue dopamine content were increased in the ventral tegmental area 24 h post-salvA. These findings raise the possibility that KOR activation-as occurs upon withdrawal from chronic cocaine-modulates vulnerability to cocaine in a time-dependent manner.

Lateral hypothalamic melanocortin receptor signaling modulates binge-like ethanol drinking in C57BL/6J mice.

Binge ethanol drinking is a highly pervasive and destructive behavior yet the underlying neurobiological mechanisms remain poorly understood. Recent work suggests that overlapping neurobiological mechanisms modulate feeding disorders and excessive ethanol intake, and converging evidence indicates that the melanocortin (MC) system may be a promising candidate. The aims of the present work were to examine how repeated binge-like ethanol drinking, using the 'drinking in the dark' (DID) protocol, impacts key peptides within the MC system and if site-specific manipulation of MC receptor (MCR) signaling modulates binge-like ethanol drinking. Male C57BL/6J mice were exposed to one, three or six cycles of binge-like ethanol, sucrose or water drinking, after which brain tissue was processed via immunohistochemistry (IHC) for analysis of key MC peptides, including alpha-melanocyte stimulating hormone (α-MSH) and agouti-related protein (AgRP). Results indicated that α-MSH expression was selectively decreased, while AgRP expression was selectively increased, within specific hypothalamic subregions following repeated binge-like ethanol drinking. To further explore this relationship, we used site-directed drug delivery techniques to agonize or antagonize MCRs within the lateral hypothalamus (LH). We found that the nonselective MCR agonist melanotan-II (MTII) blunted, while the nonselective MCR antagonist AgRP augmented, binge-like ethanol consumption when delivered into the LH. As these effects were region-specific, the present results suggest that a more thorough understanding of the MC neurocircuitry within the hypothalamus will help provide novel insight into the mechanisms that modulate excessive binge-like ethanol intake and may help uncover new therapeutic targets aimed at treating alcohol abuse disorders.

Effect of grape bunch sunlight exposure and UV radiation on phenolics and volatile composition of Vitis vinifera L. cv. Pinot noir wine.

The effect of canopy leaf removal and ultraviolet (UV) on Pinot noir grape and wine composition was investigated in this study. Limited basal leaf removal in the fruit zone was conducted, compared to shaded bunches. The UV exposure was controlled using polycarbonate screens to block UV radiation, and acrylic screens to pass the UV. The results showed that bunch sunlight and UV exposure significantly increased the Brix and pH in the grape juice, and increased substantially wine colour density, anthocyanins, total pigment, total phenolics and tannin content. Bunch sunlight and UV exposure affected terpene alcohols, C13-norisprenoids and other volatile composition of the wine differently. Sunlight exposure and UV resulted in increase of nerol, geraniol and citronellol but not linalool. Sunlight exposure slightly increased the concentration of ß-ionone, but the increase was not statistically significant for UV treatment. Neither sunlight nor UV treatment showed any impact on the concentration of ß-damascenone.

Pinot Noir wine composition from different vine vigour zones classified by remote imaging technology.

The relationship between grapevine vigour and grape and wine composition was investigated in this study. Own-rooted Pinot Noir grapevines were grown in a commercial vineyard in Tasmania, Australia, with uniform vineyard management practices. Vine vigours were determined by plant cell density (PCD) obtained from aerial photography. As vine vigour decreased, total soluble solid in grapes, total phenolics and anthocyanins in wines increased, while titratable acidity and yield decreased. Wines from the ultra low vine vigour zone had the highest concentrations of esters and alcohols. Higher level of linalool, nerol, geraniol, vitispirane, and ß-ionone were observed in ultra low vigour and low vigour zones, but there was no obvious trend for citronellol and ß-damascenone. Principal component analysis and discriminant analysis of the volatiles illustrated the differences among wines from the four vine vigour zones.

Central neuropeptide Y modulates binge-like ethanol drinking in C57BL/6J mice via Y1 and Y2 receptors.

Frequent binge drinking has been linked to heart disease, high blood pressure, type 2 diabetes, and the development of ethanol dependence. Thus, identifying pharmaceutical targets to treat binge drinking is of paramount importance. Here we employed a mouse model of binge-like ethanol drinking to study the role of neuropeptide Y (NPY). To this end, the present set of studies utilized pharmacological manipulation of NPY signaling, immunoreactivity (IR) mapping of NPY and NPY receptors, and electrophysiological recordings from slice preparations of the amygdala. The results indicated that central infusion of NPY, a NPY Y1 receptor (Y1R) agonist, and a Y2R antagonist significantly blunted binge-like ethanol drinking in C57BL/6J mice (that achieved blood ethanol levels >80 mg/dl in control conditions). Binge-like ethanol drinking reduced NPY and Y1R IR in the central nucleus of the amygdala (CeA), and 24 h of ethanol abstinence after a history of binge-like drinking promoted increases of Y1R and Y2R IR. Electrophysiological recordings of slice preparations from the CeA showed that binge-like ethanol drinking augmented the ability of NPY to inhibit GABAergic transmission. Thus, binge-like ethanol drinking in C57BL/6J mice promoted alterations of NPY signaling in the CeA, and administration of exogenous NPY compounds protected against binge-like drinking. The current data suggest that Y1R agonists and Y2R antagonists may be useful for curbing and/or preventing binge drinking, protecting vulnerable individuals from progressing to the point of ethanol dependence.

Blockade of the corticotropin releasing factor type 1 receptor attenuates elevated ethanol drinking associated with drinking in the dark procedures.

BACKGROUND: Drinking in the dark (DID) procedures have recently been developed to induce high levels of ethanol drinking in C57BL/6J mice, which result in blood ethanol concentrations (BECs) reaching levels that have measurable affects on physiology and/or behavior. The present experiments determined whether the increased ethanol drinking caused by DID procedures can be attenuated by pretreatment with CP-154,526; a corticotropin releasing factor type-1 (CRF1) receptor antagonist. METHODS: In Experiment 1, male C57BL/6J mice received ethanol (20% v/v) in place of water for 4 hours, beginning with 3 hours into the dark cycle. On the fourth day, mice were given an intraperitoneal injection of one of the 4 doses of CP-154,526 (0, 1, 3, 10 mg/kg) 30 minutes before receiving their ethanol bottle. In Experiment 2, C57BL/6J mice had 2 hours of access to the 20% ethanol solution, beginning with 3 hours into the dark cycle on days 1 to 3, and 4 hours of access to the ethanol bottle on day 4 of DID procedures. Mice were given an intraperitoneal injection of one of the 4 doses of CP-154,526 (0, 1, 3, 10 mg/kg) 30 minutes before receiving their ethanol bottle on day 4. Tail blood samples were collected immediately after the 4-hour ethanol access period on the fourth day of each experiment. Additional control experiments assessed the effects of CP-154,526 on 4-hour consumption of a 10% (w/v) sucrose solution and open-field locomotor activity. RESULTS: In Experiment 1, the vehicle-treated group consumed approximately 4.0 g/kg/4 h of ethanol and achieved BECs of approximately 30 mg%. Furthermore, pretreatment with the CRF1 receptor antagonist did not alter ethanol consumption. On the other hand, procedures used in Experiment 2 resulted in vehicle-treated mice consuming approximately 6.0 g/kg/4 h of ethanol with BECs of about 80 mg%. Additionally, the 10 mg/kg dose of CP-154,526 significantly reduced ethanol consumption and BECs to approximately 3.0 g/kg/4 h and 27 mg%, respectively, relative to vehicle-treated mice. Importantly, the 10 mg/kg dose of the CRF1R antagonist did not significantly alter 4-hour sucrose consumption or locomotor activity. CONCLUSIONS: These data indicate that CRF1R signaling modulates high, but not moderate, levels of ethanol drinking associated with DID procedures.

The CRF-1 receptor antagonist, CP-154,526, attenuates stress-induced increases in ethanol consumption by BALB/cJ mice.

BACKGROUND: Corticotropin-releasing factor (CRF) signaling modulates neurobiological responses to stress and ethanol, and may modulate observed increases in ethanol consumption following exposure to stressful events. The current experiment was conducted to further characterize the role of CRF1 receptor (CRF1R) signaling in stress-induced increases in ethanol consumption in BALB/cJ and C57BL/6N mice. METHODS: Male BALB/cJ and C57BL/6N mice were given continuous access to 8% (v/v) ethanol and water for the duration of the experiment. When a baseline of ethanol consumption was established, animals were exposed to 5 minutes of forced swim stress on each of 5 consecutive days. Thirty minutes before each forced swim session, animals were given an intraperitoneal injection of a 10 mg/kg dose of CP-154,526, a selective CRF1R antagonist, or an equal volume of vehicle. The effect of forced swim stress exposure on consumption of a 1% (w/v) sucrose solution was also investigated in an ethanol-naïve group of BALB/cJ mice. RESULTS: Exposure to forced swim stress significantly increased ethanol consumption by the BALB/cJ, but not of the C57BL/6N, mice. Stress-induced increases in ethanol consumption were delayed and became evident approximately 3 weeks after the first stressor. Additionally, forced swim stress did not cause increases of food or water intake and did not promote delayed increases of sucrose consumption. Importantly, BALB/cJ mice pretreated with the CRF1R antagonist showed blunted stress-induced increases in ethanol intake, and the CRF1R antagonist did not influence the ethanol drinking of non-stressed mice. CONCLUSIONS: The present results provide evidence that CRF1R signaling modulates the delayed increase of ethanol consumption stemming from repeated exposure to a stressful event in BALB/cJ mice.