Yield response of rice (Oryza sativa L.) genotypes to different types of drought under rainfed lowlands - Part 3. Plant factors contributing to drought resistance

A series of experiments were conducted in drought-prone northeast Thailand to examine the magnitude of yield responses of diverse genotypes to drought stress environments and to identify traits that may confer drought resistance to rainfed lowland rice. One hundred and twenty eight genotypes were grown under non-stress and four different types of drought stress conditions. Under severe drought conditions, the maintenance of PWP of genotypes played a significant role in determining final grain yield. Because of their smaller plant size (lower total dry matter at anthesis) genotypes that extracted less soil water during the early stages of the drought period, tended to maintain higher PWP and had a higher fertile panicle percentage, filled grain percentage and final grain yield than other genotypes. PWP was correlated with delay in flowering (r = -0.387) indicating that the latter could be used as a measure of water potential under stress. Genotypes with well-developed root systems extracted water too rapidly and experienced severe water stress at flowering. RPR which showed smaller coefficient of variation was more useful than root mass density in identifying genotypes with large root system. Under less severe and prolonged drought conditions, genotypes that could achieve higher plant dry matter at anthesis were desirable. They had less delay in flowering, higher grain yield and higher drought response index, indicating the importance of ability to grow during the prolonged stress period. Other shoot characters (osmotic potential, leaf temperature, leaf rolling, leaf death) had little effect on grain yield under different drought conditions. This was associated with a lack of genetic variation and difficulty in estimating trait values precisely. Under mild stress conditions (yield loss less than 50%), there was no significant relationship between the measured drought characters and grain yield. Under these mild drought conditions, yield is determined more by yield potential and phenotype than by drought resistant mechanisms per se. (C) 2002 Elsevier Science B.V. All rights reserved.

“PhenoWorld”: a new multidimensional strategy for studying behaviour in rodents

Tese de Doutoramento em Ciências da Saúde

Low density lipoprotein signaling and pancreatic beta cells protection

SummaryLow-density lipoproteins (LDLs) have an important physiological role in organism transporting cholesterol and other fatty substances to target tissues. However, elevated LDL levels in the blood are associated with the formation of arterial plaques and consequently atherosclerosis. It is therefore important to characterize the intracellular pathways induced upon LDL stimulation as they might be involved in the pathological properties of these lipoproteins. It has been previously found that LDL stimulation of mouse embryonic fibroblasts activates p38 mitogen activated protein kinases (MAPKs). This leads to cell spreading and increase in the wound healing capabilities of the cells. These two responses might occur within atherosclerotic plaques.The aim of this project is to reveal the missing links between LDL particle and activation of p38 MAPK kinase. As previously shown in our lab activation of p38 MAPK kinase by the LDL particles occur independently of classical LDL receptor (LDLR). In this study we have shown that scavenger receptor type Β class I (SR-BI) is responsible for the signal transduction from the LDLs to the p38 MAPK. We have also shown that Mitogen activated kinase kinases (MKKs) that can directly activate ρ 38 MAPK in these conditions are MKK3 and MKK6 but not MKK4. We have also tested some of the intermediate components of the pathway like Ras and PI3 kinase but found that they do not play a role.The data obtained in this study showed a part of molecular mechanism responsible for p38 MAPK activation and subsequent wound healing and can contribute to our knowledge on function of the fibroblasts in the development of the atherosclerotic plaques.Diabetes Mellitus is a condition caused by disordered metabolism of blood glucose level. It is one of the most commonly spread disease in the western world, with the incidence reaching 8% of population in United States. Two most common types of diabetes are type 1 and 2 that differs slightly in the mechanism of the development. However in the basis of both types lies the cell death of pancreatic beta cells. The aim of this work is to improve beta cells survival in different pathophysiological settings. This could be extrapolated to the conditions in which Diabetes develops in humans. We decided to use RasGAP- derived fragment Ν with its strong antiapoptotic effect in beta cells. In our lab we have demonstrated that in the mild stress conditions RasGAP can be cleaved by caspases at the position 455 producing two fragments, fragment Ν and fragment C. Fragment Ν exerts

Intervention précoce en Guidance Interactive et modification de la réactivité neuroendocrinienne chez l'ancien grand prématuré âgé de 12 mois et sa mère

L'étude a pour objectif de mettre en évidence les effets d'une intervention précoce inspirée des thérapies en Guidance Interactive sur la qualité de l'attachement ainsi que sur la réactivité neuroendocrinienne de stress chez des grands prématurés âgés de 12 mois ainsi que chez leurs mères. La population étudiée comprend 48 grands prématurés (<33 semaines de gestation) et leurs mères. Un programme d'intervention précoce a été proposé aléatoirement à la moitié des dyades incluses dans l'étude. Des mesures de cortisol salivaire ont été effectuées à 12 mois lors d'un épisode de stress modéré (la Situation Étrange) tant chez la mère que chez l'enfant. Les mères ayant bénéficié de l'intervention précoce montrent des taux de cortisol plus élevés que celles n'ayant pas bénéficié de l'intervention. Les auteurs font l'hypothèse que ces mères ont pu développer leur sensibilité envers leur enfant et se montrent, par conséquent, plus concernées lors de l'épisode de stress modéré. The present project aims to assess the effects of an early intervention inspired from Interactive Guidance therapy, on later attachment quality and stress reactivity of prematurely born infants and their mothers. The studied population contends 48 preterm born infants (< 33 weeks og gestational age). Half of the dyads receive an intervention program aiming at promoting the parents' responsivity-sensitivity to infant's cues. Infant's and mother's stress reactivity (salivary cortisol) to mild stressors (Strange Situation) will be assessed at 12 months. Mothers with intervention program show higher cortisol levels than the others. The authors postulate that these mothers enhance their caregiving quality and, subsequently, are more prone to be sensitive to infant's cues and to be concerned during the mild stress episode.

GLUT8 is dispensable for embryonic development but influences hippocampal neurogenesis and heart function.

GLUT8 is a glucose transporter isoform expressed at high levels in testis; at intermediate levels in the brain, including the hippocampus; and at lower levels in the heart and several other tissues. GLUT8 is located in an intracellular compartment and does not appear to translocate to the cell surface, except in blastocysts, where insulin has been reported to induce its surface expression. Here, we generated mice with inactivation of the glut8 gene. We showed that expression of GLUT8 was not required for normal embryonic development and that glut8-/- mice had normal postnatal development, glucose homeostasis, and response to mild stress. Adult glut8-/- mice showed increased proliferation of hippocampal cells but no defect in memory acquisition and retention. Absence of GLUT8 from the heart did not alter heart size and morphology but led to an increase in P-wave duration, which was not associated with abnormal Nav1.5 Na+ channel or connexin expression. Thus, absence of GLUT8 expression in the mouse caused complex but mild physiological alterations.

Mice with chronic GSH deficit display phenotypical anomalies that resemble key aspects of schizophrenia

ABSTRACTSchizophrenia is a major psychiatric disorder occurring with a prevalence of 1% in the worldwide population. It develops progressively with psychosis onset in late adolescence or earlyadulthood. The disorder can take many different facets and has a highly diffuse anddistributed neuropathology including deficits in major neurotransmitter systems,myelination, stress regulation, and metabolism. The delayed onset and the heterogeneouspathology suggest that schizophrenia is a developmental disease that arises from interplayof genetic and environmental factors during sensitive periods. Redox dysregulation due to animbalance between pro-oxidants and antioxidant defence mechanisms is among the riskfactors for schizophrenia. Glutathione (GSH) is the major cellular redox regulator andantioxidant. Levels of GSH are decreased in cerebrospinal fluid, prefrontal cortex and postmortemstriatum of schizophrenia patients. Moreover, polymorphisms of the key GSHsynthesizingenzyme, glutamate-cysteine ligase, modifier (GCLM) subunit, are associatedwith the disease, suggesting that GSH deficit is of genetic origin. Here we used miceknockout (KO) for the GCLM gene, which display chronic GSH deficit (~70 to 80% decrease)to investigate the direct link between redox dysregulation and schizophrenia. Accordingly,we evaluated whether GCLM KO compared to normal wildtype mice display behavioralchanges that relate to schizophrenia symptoms and whether their brains showmorphological, functional or metabolic alterations that resemble those in patients.Moreover, we exposed pubertal GCLM mice to repeated mild stress and measured theirhormonal and behavioral stress reactivity. Our data show that chronic GSH deficit isassociated with altered emotion- and stress-related behaviors, deficient prepulse inhibition,pronounced amphetamine-induced hyperlocomotion but normal spatial learning andworking memory. These changes represent important schizophrenia endophenotypes.Moreover, this particular pattern of change indicates impairment of the ventralhippocampus (VH) and related circuitry as opposed to the dorsal hippocampus (DH), which isimplicated in spatial information processing. This is consistent with a selective deficit ofparvalbumin positive interneurons and gamma oscillation in the VH but not DH. Increasedlevels of circulating stress hormones in KO mice following pubertal stress corroborate VHdysfunction as it is involved in negative feedback control of the stress response. VHstructural and functional deficits are frequently found in the schizophrenic brain. Metabolicevaluation of the developing GCLM KO anterior cortex using in vivo magnetic resonancespectroscopy revealed elevated glutamine (Gln), glutamate (Glu), Gln/Glu and N-acetylaspartate(NAA) during the pre-pubertal period. Similar changes are reported in earlyschizophrenia. Overall, we observe phenotypic anomalies in GSH deficient GCLM KO micethat correspond to major schizophrenia endophenotypes. This supports an important rolefor redox dysregulation in schizophrenia and validates the GCLM KO mouse as model for thedisease. Moreover, our results indicate that puberty may be a sensitive period for redoxsensitivechanges highliting the importance of early intervention. Gln, Gln/Glu, Glu and NAAmay qualify as early metabolic biomarkers to identify young at-risk individuals. Since chronictreatment with NAC normalized most metabolic changes in GCLM KO mice, NAC may be oneadjunct treatment of choice for early intervention in patients.RESUMELa schizophrénie est une maladie psychiatrique majeure avec une prévalence de 1% dans lapopulation. Son développement est progressif, les premières psychoses apparaissant àl'adolescence ou au début de l'âge adulte. La maladie a plusieurs présentations et uneneuropathologie étendue, qui inclut des déficits neurochimiques, métaboliques, de lamyélination et de la régulation du stress. L'émergence tardive et l'hétérogénéité de lapathologie suggèrent que la schizophrénie est une maladie développementale, favorisée pardes facteurs génétiques et environnementaux durant des périodes sensibles. La dérégulationrédox, due à un déséquilibre entre facteurs pro-oxidantes et défenses anti-oxidantes,constitue un facteur de risque. Le glutathion (GSH) est le principal régulateur rédox et antioxidantdes cellules, ses taux sont diminués dans le liquide céphalorachidien, le cortexpréfrontal et le striatum de patients. De plus, des variations du gène codant la sous-unitémodulatrice (GCLM) de la glutamate-cystéine ligase, enzyme de synthèse du GSH, sontassociés la maladie, suggérant que le déficit observé chez les patients est d'originegénétique. Nous avons donc utilisé des souris ayant une délétion du gène GCLM (KO), quiont un déficit chronique en GSH (70-80%), afin d'étudier le lien entre une dérégulation rédoxet la schizophrénie. Nous avons évalué si ces souris présentent des altérationscomportementales analogues aux symptômes de la maladie, et des modificationsstructurelles, fonctionnelles et métaboliques au niveau du cerveau, ressemblant à celles despatients. De plus, nous avons soumis les souris à des stresses modérés durant la puberté,puis mesuré les réponses hormonales et comportementales. Les animaux présentent undéficit pré-attentionnel du traitement des informations moto-sensorielles, un déficit pourcertains apprentissages, une réponse accrue à l'amphétamine, mais leurs mémoires spatialeet de travail sont préservées. Ces atteintes comportementales sont analogues à certainsendophénotypes de la schizophrénie. De plus, ces changements comportementaux sontlargement expliqués par une perturbation morphologique et fonctionnelle de l'hippocampeventral (HV). Ainsi, nous avons observé un déficit sélectif des interneurones immunoréactifsà la parvalbumine et une désynchronisation neuronale dans l'HV. L'hippocampe dorsal,impliqué dans l'orientation spatiale, demeure en revanche intact. L'augmentationd'hormones de stress dans le sang des souris KO suite à un stress prépubertal soutien aussil'hypothèse d'une dysfonction de l'HV, connu pour moduler ce type de réponse. Des déficitsstructurels et fonctionnels dans l'hippocampe antérieur (ventral) ont d'ailleurs été rapportéschez des patients schizophrènes. Par de résonance magnétique, nous avons également suivile profil métabolique du le cortex antérieur au cours du développement postnatal des sourisKO. Ces mesures ont révélé des taux élevés de glutamine (Gln), glutamate (Glu), du ratioGln/Glu, et de N-acétyl-aspartate (NAA) durant la période prépubertale. Des altérationssimilaires sont décrites chez les patients durant la phase précoce. Nous avons donc révélédes anomalies phénotypiques chez les souris GCLM KO qui reflètent certainsendophénotypes de la schizophrénie. Nos résultats appuient donc le rôle d'une dérégulationrédox dans l'émergence de la maladie et le potentiel des souris KO comme modèle. De plus,cette étude met en évidence la puberté comme période particulièrement sensible à unedérégulation rédox, renforçant l'importance d'une intervention thérapeutique précoce. Dansce cadre, Gln, Gln/Glu, Glu and NAA seraient des biomarqueurs clés pour identifier de jeunesindividus à risque. De part son efficacité dans notre modèle, NAC pourrait être unesubstance de choix dans le traitement précoce des patients.

RasGAP Shields Akt from Deactivating Phosphatases in Fibroblast Growth Factor Signaling but Loses This Ability Once Cleaved by Caspase-3.

Fibroblast growth factor receptors (FGFRs) are involved in proliferative and differentiation physiological responses. Deregulation of FGFR-mediated signaling involving the Ras/PI3K/Akt and the Ras/Raf/ERK MAPK pathways is causally involved in the development of several cancers. The caspase-3/p120 RasGAP module is a stress sensor switch. Under mild stress conditions, RasGAP is cleaved by caspase-3 at position 455. The resulting N-terminal fragment, called fragment N, stimulates anti-death signaling. When caspase-3 activity further increases, fragment N is cleaved at position 157. This generates a fragment, called N2, that no longer protects cells. Here, we investigated in Xenopus oocytes the impact of RasGAP and its fragments on FGF1-mediated signaling during G2/M cell cycle transition. RasGAP used its N-terminal Src homology 2 domain to bind FGFR once stimulated by FGF1, and this was necessary for the recruitment of Akt to the FGFR complex. Fragment N, which did not associate with the FGFR complex, favored FGF1-induced ERK stimulation, leading to accelerated G2/M transition. In contrast, fragment N2 bound the FGFR, and this inhibited mTORC2-dependent Akt Ser-473 phosphorylation and ERK2 phosphorylation but not phosphorylation of Akt on Thr-308. This also blocked cell cycle progression. Inhibition of Akt Ser-473 phosphorylation and entry into G2/M was relieved by PHLPP phosphatase inhibition. Hence, full-length RasGAP favors Akt activity by shielding it from deactivating phosphatases. This shielding was abrogated by fragment N2. These results highlight the role played by RasGAP in FGFR signaling and how graded stress intensities, by generating different RasGAP fragments, can positively or negatively impact this signaling.

Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe?

The metabolic syndrome may have its origins in thriftiness, insulin resistance and one of the most ancient of all signalling systems, redox. Thriftiness results from an evolutionarily-driven propensity to minimise energy expenditure. This has to be balanced with the need to resist the oxidative stress from cellular signalling and pathogen resistance, giving rise to something we call 'redox-thriftiness'. This is based on the notion that mitochondria may be able to both amplify membrane-derived redox growth signals as well as negatively regulate them, resulting in an increased ATP/ROS ratio. We suggest that 'redox-thriftiness' leads to insulin resistance, which has the effect of both protecting the individual cell from excessive growth/inflammatory stress, while ensuring energy is channelled to the brain, the immune system, and for storage. We also suggest that fine tuning of redox-thriftiness is achieved by hormetic (mild stress) signals that stimulate mitochondrial biogenesis and resistance to oxidative stress, which improves metabolic flexibility. However, in a non-hormetic environment with excessive calories, the protective nature of this system may lead to escalating insulin resistance and rising oxidative stress due to metabolic inflexibility and mitochondrial overload. Thus, the mitochondrially-associated resistance to oxidative stress (and metabolic flexibility) may determine insulin resistance. Genetically and environmentally determined mitochondrial function may define a 'tipping point' where protective insulin resistance tips over to inflammatory insulin resistance. Many hormetic factors may induce mild mitochondrial stress and biogenesis, including exercise, fasting, temperature extremes, unsaturated fats, polyphenols, alcohol, and even metformin and statins. Without hormesis, a proposed redox-thriftiness tipping point might lead to a feed forward insulin resistance cycle in the presence of excess calories. We therefore suggest that as oxidative stress determines functional longevity, a rather more descriptive term for the metabolic syndrome is the 'lifestyle-induced metabolic inflexibility and accelerated ageing syndrome'. Ultimately, thriftiness is good for us as long as we have hormetic stimuli; unfortunately, mankind is attempting to remove all hormetic (stressful) stimuli from his environment.

Effect of intravaginal electrical stimulation on pelvic floor muscle strength

The aim of this study was to evaluate the effect of intravaginal electrical stimulation (IES) on pelvic floor muscle (PFM) strength in patients with mixed urinary incontinence (MUI). Between January 2001 and February 2002, 40 MUI women (mean age: 48 years) were studied. Urge incontinence was the predominant symptom; 92.5% also presented mild stress urinary incontinence (SUI). Selection criteria were clinical history and urodynamics. Pre-treatment urodynamic study showed no statistical differences between the groups. Ten percent of the women in each group had involuntary detrusor contractions. Patients were randomly distributed, in a double-blind study, into two groups. Group G 1 (n=20), effective IES, and group G2 (n=20), sham IES, with follow-up at 1 month. The following parameters were studied: (1) clinical questionnaire, (2) examiner's evaluation of perineal muscle strength, (3) objective evaluation of perineal muscle by perineometry, (4) vaginal weight test, and (5) urodynamic study. The IES protocol consisted of three 20-min sessions per week over a 7-week period using a Dualpex Uro 996 at 4 Hz. There was no statistically significant difference in the demographic data of both groups. The number of micturitions per 24 h after treatment was reduced significantly in both groups. Urge incontinence, present in all patients before treatment, was reduced to 15% in G1 and 31.5% in G2 post-treatment. The subjective evaluation of PFM strength demonstrated a significant improvement in G1. Objective evaluation of PFM force by perineometer showed a significant improvement in maximum peak contraction post-treatment in both groups. In the vaginal weight test, there was a significant increase in average number of cone retentions post-treatment in both groups. With regard to satisfaction level, after treatment, 80% of the patients in G1 and 65% of the patients in G2 were satisfied. There was no statistically significant difference between the groups. There was a significant improvement in PFM strength from both effective and sham electrostimulation, questioning the effectiveness of electrostimulation as a monotherapy in treating MUI.

Efeito do stressor moderado sobre o desafio social e o crescimento na tilália-do-nilo

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Plasma corticosterone elevation inhibits the activation of nuclear factor kappa B (NFKB) in the Syrian hamster pineal gland

We evaluated how the mild stress-induced increase in endogenous corticosterone affected the pineal gland in Syrian hamsters (Mesocricetus auratus). The animals were maintained under constant light for 1 day, instead of a cycle of 14:10-h, to increase the circulating corticosterone levels during the daytime. The nuclear translocation of nuclear factor kappa B (NFKB), which is the pivotal transcription factor for stress and injury, presented a daily rhythm in normal animals. NFKB nuclear content increased linearly from the onset of light [Zeitgeber Time 0 (ZT0)] until ZT11 and decreased after ZT12 when the plasma corticosterone peak was detected in normal animals. However, the 24-h profiles of the two curves were different, and they did not clearly support an exclusive relationship between corticosterone levels and NFKB content. Therefore, we tested the effect of increased endogenous corticosterone through inducing mild stress by maintaining daytime illumination for one night. This stressful condition, which increased daytime corticosterone levels, resulted in a daytime decrease in NFKB nuclear content, and this was inhibited by mifepristone. Overall, this study shows that NFKB has a daily rhythm in Syrian hamster pineal glands and, by increasing endogenous corticosterone with a stressful condition, NFKB activity is regulated. Therefore, this study suggests that the pineal gland in the Syrian hamster is a sensor of stressful conditions.

Influence of manure scrapers on dairy cows in cubicle housing systems

Manure scrapers are widely used in dairy cow loose-housing systems. In order to evaluate the effects of the scrapers on the cows, we assessed their impact on the animals' cardiac activity, feeding behaviour, and the behavioural reactions of cows confronted with different types of scrapers. In part I of the study, we measured cardiac activity (mean R–R interval and RMSSD, a parameter of heart-rate variability) whilst observing the behaviour of 29 focal cows on three farms during situations with and without active manure scrapers. Lower RMSSD values were observed during scraping events while cows were either lying, standing or walking in the alleyway, standing completely in the lying cubicle, or standing half in the lying cubicle (P=0.03), but only tended to differ while directly confronted with the scraper (P=0.06). This indicates that dairy cows experienced at least some mild stress during manure-scraping events. In part II, the feeding behaviour of 12 cows on each of two farms was recorded by means of a jaw-movement sensor and compared between situations with the manure-scraping event following forage provision either within or outside the main daily feeding period (i.e. within 1 or after 2 h from forage provisioning, respectively). The duration of night-time feeding (P=0.049) and the number of feeding bouts (P=0.036) were higher when a manure-scraping event took place within the main daily feeding period, indicating that the cows' feeding behaviour had been disturbed. In part III, we observed the cows' behaviour on 15 farms during eight manure scraping events per farm, where each of five farms had one of three different scraper types. We assessed the cows' immediate reactions when confronted with the scraper. In addition, we recorded the number of animals present in the alleyways before and after the manure-scraping events. The more cows that were present in the alleyways before the scraping event, the lower the proportion of cows showing direct behavioural reactions both with (P=0.017) and without (P=0.028) scraper contact, and the higher the number of cows that left the alleyways (P<0.001). Scraper type did not influence the proportion of cows showing behavioural reactions. In conclusion, our results show that dairy cows perceive the manure-scraping event negatively in some situations, that feeding behaviour may be disturbed when scrapers are active during the main feeding period, and that cows avoid the scraper during crowded situations.

Epilepsy in mice deficient in the 65-kDa isoform of glutamic acid decarboxylase

γ-Aminobutyric acid (GABA), the major inhibitory neurotransmitter in the mammalian brain, is synthesized by two glutamate decarboxylase isoforms, GAD65 and GAD67. The separate role of the two isoforms is unknown, but differences in saturation with cofactor and subcellular localization suggest that GAD65 may provide reserve pools of GABA for regulation of inhibitory neurotransmission. We have disrupted the gene encoding GAD65 and backcrossed the mutation into the C57BL/6 strain of mice. In contrast to GAD67−/− animals, which are born with developmental abnormalities and die shortly after birth, GAD65−/− mice appear normal at birth. Basal GABA levels and holo-GAD activity are normal, but the pyridoxal 5′ phosphate-inducible apo-enzyme reservoir is significantly decreased. GAD65−/− mice develop spontaneous seizures that result in increased mortality. Seizures can be precipitated by fear or mild stress. Seizure susceptibility is dramatically increased in GAD65−/− mice backcrossed into a second genetic background, the nonobese diabetic (NOD/LtJ) strain of mice enabling electroencephalogram analysis of the seizures. The generally higher basal brain GABA levels in this backcross are significantly decreased by the GAD65−/− mutation, suggesting that the relative contribution of GABA synthesized by GAD65 to total brain GABA levels is genetically determined. Seizure-associated c-fos-like immunoreactivity reveals the involvement of limbic regions of the brain. These data suggest that GABA synthesized by GAD65 is important in the dynamic regulation of neural network excitability, implicate at least one modifier locus in the NOD/LtJ strain, and present GAD65−/− animals as a model of epilepsy involving GABA-ergic pathways.

Increased dopamine turnover in the prefrontal cortex impairs spatial working memory performance in rats and monkeys.

The selective activation of the prefrontal cortical dopamine system by mild stress can be mimicked by anxiogenic beta-carbolines such as FG7142. To investigate the functional relevance of elevated levels of dopamine turnover in the prefrontal cortex, the current study examined the effects of FG7142 on the performance of spatial working memory tasks in the rat and monkey. FG7142 selectively increased prefrontal cortical dopamine turnover in rats and significantly impaired performance on spatial working memory tasks in both rats and monkeys. Spatial discrimination, a task with similar motor and motivational demands (rats), or delayed response performance following zero-second delays (monkeys) was unaffected by FG7142. Further, biochemical analysis in rats revealed a significant positive correlation between dopamine turnover in the prefrontal cortex and cognitive impairment on the delayed alternation task. The cognitive deficits in both rats and monkeys were prevented by pretreatment with the benzodiazepine receptor antagonist, RO15-1788, which blocked the increase in dopamine turnover and by the dopamine receptor antagonists, haloperidol, clozapine, and SCH23390. These findings indicate that excessive dopamine activity in the prefrontal cortex is detrimental to cognitive functions mediated by the prefrontal cortex.

Teaching our children when to eat:how parental feeding practices inform the development of emotional eating-a longitudinal experimental design

Background: Emotional eating in children has been related to the consumption of energy-dense foods and obesity, but the development of emotional eating in young children is poorly understood. Objectives: We evaluated whether emotional eating can be induced in 5-7-y-old children in the laboratory and assessed whether parental use of overly controlling feeding practices at 3-5 y of age predicts a greater subsequent tendency for children to eat under conditions of mild stress at ages 5-7 y. Design: Forty-one parent-child dyads were recruited to participate in this longitudinal study, which involved parents and children being observed consuming a standard lunch, completing questionnaire measures of parental feeding practices, participating in a research procedure to induce child emotion (or a control procedure), and observing children's consumption of snack foods. Results: Children at ages 5-7 y who were exposed to a mild emotional stressor consumed significantly more calories from snack foods in the absence of hunger than did children in a control group. Parents who reported the use of more food as a reward and restriction of food for health reasons with their children at ages 3-5 y were more likely to have children who ate more under conditions of negative emotion at ages 5-7 y. Conclusions: Parents who overly control children's food intake may unintentionally teach children to rely on palatable foods to cope with negative emotions. Additional research is needed to evaluate the implications of these findings for children's food intake and weight outside of the laboratory setting. This trial was registered at clinicaltrials.gov as NCT01122290.