A mixed methods analysis of maternal response to children's consumption of a palatable food: differences by child weight status.

BACKGROUND: Little is known about how mothers respond to their child eating palatable foods. OBJECTIVES: The objectives of the study are to examine maternal behaviours when children are presented with a large portion of energy-dense palatable food in an experimental setting and to examine differences by child weight status. METHODS: Mother-child dyads (N = 37) (mean child age 70.8 months) participated in a videotaped eating protocol with cupcakes. Anthropometrics were measured. Videos were analysed using discourse analysis and were reliably coded for the presence or absence of the most salient theme. Analysis of variance examined theme presence by child and mother weight status. RESULTS: Mothers disavowed responsibility for their child's eating. Mothers were observed to roll their eyes at the child, throw their hands up in exasperation and distance themselves both physically and emotionally when the child ate the cupcakes voraciously or with high enjoyment. Mothers of children with obesity (vs recommended weight) engaged in more counts of disavowal (p = 0.01). CONCLUSIONS: Mothers of children with obesity distanced themselves from their child, seeming to disavow responsibility for the child's eating of 'junk food'. Mothers may respond to their child's seemingly gluttonous eating by disavowing responsibility due to the stigma of being a parent of a child with obesity.

STRONG MILITARY FAMILIES INTERVENTION ENHANCES PARENTING REFLECTIVITY AND REPRESENTATIONS IN FAMILIES WITH YOUNG CHILDREN.

Military families face many challenges due to deployment and parental separation, and this can be especially difficult for families with young children. The Strong Military Families (SMF) intervention is for military families with young children, and consists of two versions: the Multifamily Group, and a Home-based psychoeducational written materials program. The Multifamily Group was designed to enhance positive parenting through both educational components and in vivo feedback and support during separations and reunions between parents and children (n = 78 parents). In the present study, we examine parenting reflectivity and mental representations in mothers versus fathers in military families, service members versus civilian spouses/parenting partners, and before versus after participation in the SMF Multifamily Group and Home-based interventions. Parenting reflectivity and mental representations were coded from the Working Model of the Child Interview (WMCI; C.H. Zeanah & D. Benoit, 1995). Results suggest that neither parenting reflectivity nor WMCI typology differs between mothers and fathers in military families, or between service members and civilian parenting partners. Furthermore, there was substantial stability in parenting reflectivity and WMCI typology from baseline to posttest, but participation in the Multifamily Group, relative to Home-based, was associated with improvements in both parenting reflectivity and WMCI ratings from baseline to postintervention.

Low-income mothers' feeding goals predict observed home mealtime and child feeding practices.

BACKGROUND: Mothers' goals are important for health behavior change, and engagement in child obesity interventions. It is unknown if maternal feeding goals are associated with observed home mealtime or feeding practices. The objective of this study was to examine the association of four common feeding goals (restrict junk food, promote fruit or vegetable intake, promote autonomy in eating and prevent obesity) with mothers' observed home mealtime and feeding practices. METHODS: Low-income mothers (N = 265) of children (mean child age 70.8 months) participated in a semi-structured interview about child feeding. A coding scheme was developed and reliably applied to identify mothers' feeding goals from transcripts. Mothers' observed home mealtime and feeding practices were reliably coded from home mealtimes and a laboratory eating protocol. Mothers completed a questionnaire and reported demographics. Participant weights and heights were obtained. Regression models were used to test the association of each feeding goal with observed maternal practices, controlling for covariates. RESULTS: The goal of restricting junk food was associated with the child always eating at a table (OR 2.87, 95% CI (1.39-5.96) p = 0.005), but not with the mother restricting junk food. The goal of promoting fruit or vegetable intake was associated with observationally promoting vegetables (OR 1.41, 95% CI (1.09-1.84), p = 0.01). The goals of promoting autonomy and preventing obesity were not associated with any observed maternal home mealtime or feeding practices. CONCLUSIONS: While mothers' goals to restrict junk food and promote fruit or vegetable intake were associated with observed home mealtime and feeding practices, promoting autonomy and preventing obesity were not. Increased understanding of why low-income mothers may not translate certain feeding goals into practices may inform childhood obesity interventions.

Birth order and sibship composition as predictors of overweight or obesity among low-income 4- to 8-year-old children.

OBJECTIVE: This study aimed to examine the association of birth order and number and sex of siblings with overweight or obesity among 4- to 8-year-olds. METHODS: This is a cross-sectional study involving 273 low-income mother-child dyads. Questionnaires and anthropometry were completed. Multiple logistic regression was used to examine the association of birth order, having younger siblings, having older siblings, having at least one brother and having at least one sister with odds of overweight or obesity. Analyses were repeated to additionally include non-biological siblings. Models were adjusted for potential confounders and intermediate variables. RESULTS: Prevalence of child overweight or obesity was 42.5%. Adjusting for covariates, only children and youngest siblings had higher odds of overweight or obesity compared with oldest siblings (odds ratio [OR]: 4.18, 95% confidence interval [CI]: 1.67, 10.46 and OR: 3.21, 95% CI: 1.41, 7.33, respectively). Having one or more younger siblings and having at least one brother were associated with lower odds (OR: 0.38, 95% CI: 0.21, 0.69 and OR: 0.47, 95% CI: 0.28, 0.81, respectively). Including non-biological siblings did not meaningfully change the associations. CONCLUSION: Birth order and sibship composition are associated with overweight or obesity among 4- to 8-year-olds. Future studies identifying the underlying behavioural mechanism can help inform family-based intervention programmes.

Low-income pre-schoolers with higher temperamental surgency enjoy and respond more to food, mediating the path to higher body mass index.

BACKGROUND: Temperament is associated with obesity risk. However, the mechanisms linking temperament and eating behaviour to childhood adiposity are unclear. OBJECTIVES: To examine whether three temperament dimensions (surgency, effortful control and negative lability) are uniquely associated with an increased BMI z score (BMIz) concurrently and an excessive rate of change in BMIz longitudinally through four eating behaviours (food responsiveness, enjoyment of food, emotional overeating and satiety responsiveness) among low-income pre-schoolers, independent of home environment quality. METHODS: 379 pre-schoolers were recruited from Head Start in the Midwest region of the United States. Primary caregivers reported child temperament, eating behaviours and the level of chaos at home. Child BMIz was derived from weight and height measurements at ages 4, 5 and 6 years on average. RESULTS: Path analyses revealed that higher levels of surgency predicted more food responsiveness and enjoyment of food, which was in turn associated with higher concurrent BMIz, independent of effortful control, negative lability and home chaos. CONCLUSION: Low-income surgent pre-schoolers were more likely to have elevated BMIz as they were more inclined to eat in response to external cues and have a high appetitive drive. Obesity prevention programmes might target low-income children with surgent temperaments, and the identified eating behaviours.

Perceptions of low-income mothers about the causes and ways to prevent overweight in children.

BACKGROUND: Childhood overweight and obesity remain major health conditions, affecting nearly one-third of children in the USA. Multiple factors have been identified that contribute to children becoming overweight; however, little is known regarding what low-income mothers perceive to be the causes of and the ways to prevent children from becoming overweight. METHODS: Low-income mothers (n = 286) with children aged 4-8 years participated in semi-structured interviews, during which they were asked for their opinions about the causes of and ways to prevent children from becoming overweight. After themes were identified, interviews were coded for the presence or absence of each theme. RESULTS: The majority of mothers were non-Hispanic White (69.2%) and overweight or obese (77.3%). Additionally, many of the children (41.9%) were overweight or obese. Six causes of children becoming overweight were identified by mothers: types or quantities of food eaten (90.9%); parenting behaviours (44.9%); lack of activity (42.3%); genetics, slow metabolism or medical issues (24.5%); stress or emotion (5.2%); and limited access to resources (3.5%). Five ways to prevent children from becoming overweight identified by mothers included the following: healthy eating (84.9%), more activity (54.8%), limiting screen time (19.9%), limiting sugar-sweetened beverages (12.2%) and drinking more water (6.6%). The majority of mothers (77.1%) reported that they carried out their suggestions to prevent their children from becoming overweight. CONCLUSION: Within this cohort with a high prevalence of maternal and child overweight, most mothers identified many of the evidence-based strategies for childhood obesity prevention. Future intervention development may benefit from focusing on content areas that were less commonly identified by mothers as well as helping mothers translate knowledge to implementation.

Reduced SNAP-25 increases PSD-95 mobility and impairs spine morphogenesis.

Impairment of synaptic function can lead to neuropsychiatric disorders collectively referred to as synaptopathies. The SNARE protein SNAP-25 is implicated in several brain pathologies and, indeed, brain areas of psychiatric patients often display reduced SNAP-25 expression. It has been recently found that acute downregulation of SNAP-25 in brain slices impairs long-term potentiation; however, the processes through which this occurs are still poorly defined. We show that in vivo acute downregulation of SNAP-25 in CA1 hippocampal region affects spine number. Consistently, hippocampal neurons from SNAP-25 heterozygous mice show reduced densities of dendritic spines and defective PSD-95 dynamics. Finally, we show that, in brain, SNAP-25 is part of a molecular complex including PSD-95 and p140Cap, with p140Cap being capable to bind to both SNAP-25 and PSD-95. These data demonstrate an unexpected role of SNAP-25 in controlling PSD-95 clustering and open the possibility that genetic reductions of the protein levels - as occurring in schizophrenia - may contribute to the pathology through an effect on postsynaptic function and plasticity.

A molecular switch for translational control in taste memory consolidation.

In a variety of species memory consolidation following different learning paradigms has been shown to be dependent on protein synthesis. However, it is not known whether modulation of protein synthesis is a critical component of the consolidation process, nor is the identity of any protein(s) subject to translational regulation, known. We report here that phosphorylation of eukaryotic elongation factor-2 (eEF2), an indicator for translational elongation attenuation, is correlated with input that produces taste memory consolidation in the relevant cortex of rat. The temporal pattern of eEF2 phosphorylation is similar to extra-cellular regulated kinase 2 (ERK2) activation and S6K1 phosphorylation, which are known to stimulate translation initiation. In addition, increased eEF2 phosphorylation and increased alphaCaMKII expression is detected in a synaptoneurosomal fraction made from taste cortex following memory consolidation. These results suggest that increased initiation rate together with decreased elongation rate, during memory consolidation, shift the rate-limiting step of protein synthesis, to produce a local switch-like effect in the expression of neuronal proteins.

Interpersonal psychotherapy adapted for the group setting in the treatment of postpartum depression.

Interpersonal psychotherapy (IPT) has demonstrated efficacy in the individual treatment of antepartum and postpartum depression. The current investigation extends prior work by examining the efficacy of a group IPT approach for the treatment of postpartum depression. Depression scores of 17 women diagnosed with postpartum depressive disorder (DSM-IV criteria) decreased significantly from pre- to post-treatment. Follow-up assessments at 6 months revealed continuation of the treatment effect. Results indicate that IPT adapted for a group model has positive implications for the treatment of postpartum depression, demonstrating both short-term and longer-term effects in the reduction of depressive symptomatology. Study limitations include the small sample size, absence of control group, possible bias in therapist's assessments, and lack of monitoring adherence, which may have jeopardized the accuracy of the results.

Are commonly used self-report inventories suitable for screening postpartum depression and anxiety disorders?

OBJECTIVE: The utility of several self-report symptom inventories were examined for detecting postpartum depression (MDD) and anxiety disorders (AD). METHOD: Fifty women (3 or 6 months postpartum), at heightened risk for MDD, completed several depression and anxiety symptom checklists. Psychiatric diagnoses were obtained via SCID interview. RESULTS: Rates of MDD (n=9) and AD (n=9) were equivalent in this sample, with minimal diagnostic overlap. While all the self-report depression inventories screened accurately for MDD, none discriminated AD sensitively and reliably. CONCLUSION: The frequent occurrence of AD emphasizes the need to identify appropriate screening instruments for postpartum anxiety disorders.

ERKI/II regulation by the muscarinic acetylcholine receptors in neurons.

Muscarinic acetylcholine receptors (mAChRs) are known to be involved in learning and memory, but the molecular basis of their involvement is not well understood. The availability of new and specific biochemical tools has revealed a crucial role for the mitogen-activated protein kinase (MAPK) family in learning and memory. Here, we examine the link between mAChRs and MAPK in neurons. Using the MAPK kinase (MEK)-specific inhibitor PD98059, we first demonstrate a necessary role for active ERKI/II in long-term potentiation in vivo. Using phospho-specific antibodies that recognize the activated form of ERKI/II, we find that the level of ERKI/II activation in brain is regulated by mAChRs. Carbachol, a muscarinic agonist, induces prolonged activation of ERKI/II, without effect on the related kinase SAPK/JNK (stress-activated protein kinase/c-Jun N-terminal protein kinase) in primary cortical cultures. ERKI/II activation is Src-dependent and partially phosphoinositide-3 kinase- and Ca(2+)-dependent but is PKC-independent. M1-M4 mAChR subtypes expressed in COS-7 cells can all induce ERKI/II activation using a signal transduction pathway similar to that operating in neurons. The nature of the signal transduction suggests that ERKI/II can serve as a convergence site for mAChR activation and other neurotransmitter receptors.

Frequency-dependent inhibition in the dentate gyrus is attenuated by the NMDA receptor blocker MK-801 at doses that do not yet affect long-term potentiation.

The dual impairment of both long-term potentiation (LTP) in the dentate gyrus and spatial memory by N-methyl-D-aspartate (NMDA) blockers such as 2-aminophosphonovaleric acid (APV) or dizocilpine (MK-801) is considered supportive evidence for the hypothesis that LTP-like mechanisms are involved in spatial memory. However, several studies suggest that, at doses that affect aspects of behavior, LTP is not yet blocked. One possible explanation may be that the blockade of NMDA receptors affect processes other than LTP, which are required for learning. In the present study, we assessed in vivo the effects of the NMDA receptor antagonist MK-801 on LTP and on frequency-dependent inhibition, which has previously been shown to reflect activity of GABAergic interneurons in the rat dentate gyrus. We report here that NMDA receptors are instrumental in frequency-dependent inhibition. Furthermore, frequency-dependent inhibition was found to be more sensitive than LTP to the NMDA antagonist MK-801. Our findings indicate that, in addition to the blockade of LTP, the application of NMDA antagonists affects local circuit activity in the dentate gyrus. The results direct attention to the potential role of interneuronal activity in general and of frequency-dependent inhibition in particular in dentate gyrus related behaviors.

Molecular mechanisms of long-term potentiation in the insular cortex in vivo.

We have investigated molecular mechanisms of synaptic plasticity in the pathway between two forebrain structures important for taste learning, the basolateral amygdala (BLA) and the insular cortex. We report here that in vivo long-term potentiation (LTP) induced by BLA stimulation requires functional NMDA receptors and is modulated by muscarinic acetylcholine receptors. In addition, LTP results in the activation of cortical extracellular regulated kinase 1/2 (ERK1/2) and is blocked by inhibitors of ERK1/2 activation. Previous findings demonstrated the involvement of the same molecular mechanisms in the same cortical area during novel taste learning. The results demonstrate that both synaptic and behavioral plasticity share common molecular mechanisms in the insular cortex.

Specific and differential activation of mitogen-activated protein kinase cascades by unfamiliar taste in the insular cortex of the behaving rat.

Rats were given to drink an unfamiliar taste solution under conditions that result in long-term memory of that taste. The insular cortex, which contains the taste cortex, was then removed and assayed for activation of mitogen-activated protein kinase (MAPK) cascades by using antibodies to the activated forms of various MAPKs. Extracellular responsive kinase 1-2 (ERK1-2) in the cortical homogenate was significantly activated within <30 min of drinking the taste solution, without alteration in the total level of the ERK1-2 proteins. The activity subsided to basal levels within <60 min. In contrast, ERK1-2 was not activated when the taste was made familiar. The effect of the unfamiliar taste was specific to the insular cortex. Jun N-terminal kinase 1-2 (JNK1-2) was activated by drinking the taste but with a delayed time course, whereas the activity of Akt kinase and p38MAPK remained unchanged. Elk-1, a member of the ternary complex factor and an ERK/JNK downstream substrate, was activated with a time course similar to that of ERK1-2. Microinjection of a reversible inhibitor of MAPK/ERK kinase into the insular cortex shortly before exposure to the novel taste in a conditioned taste aversion training paradigm attenuated long-term taste aversion memory without significantly affecting short-term memory or the sensory, motor, and motivational faculties required to express long-term taste aversion memory. It was concluded that ERK and JNK are specifically and differentially activated in the insular cortex after exposure to a novel taste, and that this activation is required for consolidation of long-term taste memory.

Lateral ventricle injection of the protein synthesis inhibitor anisomycin impairs long-term memory in a spatial memory task.

Although protein synthesis inhibition has been shown to affect long-term memory in a wide variety of animal species, cases have been reported in which protein synthesis inhibition failed to affect memory consolidation [S. Wittstock, R. Menzel, Color learning and memory in honey bees are not affected by protein synthesis inhibition, Behav. Neural Biol., 62 (1994) 224-229.]. Most findings argue that the critical time for protein synthesis is during or immediately after training. However, other reports show a second time window, hours after training, where protein synthesis inhibition can cause amnesia [F.M. Freeman, S.P.R. Rose, A.B. Scholey, Two time windows of anisomycin-induced amnesia for passive avoidance training in the day-old chick, Neurobiol. Learn. Mem., 63 (1995) 291-295.][G. Grecksch, H. Matthies, Two sensitive periods for the amnesic effect of anisomycin, Pharmacol. Biochem. Behav., 12 (1980) 663-665.]. In this study, we addressed two questions: (1) Is protein synthesis essential for spatial memory? and (2) At what injection time window(s) will protein synthesis inhibition cause spatial memory amnesia? We report that bilateral intraventricular microinjection of anisomycin (Ani) impairs consolidation of long-term memory, in the hippocampal-dependent Morris water maze spatial memory task. Memory was impaired in a dose-dependent manner without affecting short-term memory. Spatial memory was affected only if Ani was injected 20 min before performing the task and not in any other time window before or after the behavioral test. The inhibition did not affect pre-existing memories or the capability to memorize once the effect of the inhibition diminished.

NMDA receptor and the tyrosine phosphorylation of its 2B subunit in taste learning in the rat insular cortex.

We demonstrate that the NMDA receptor is involved in taste learning in the insular cortex of the behaving rat and describe two facets of this involvement. Blockage of the NMDA receptor in the insular cortex by the reversible antagonist APV during training in a conditioned taste aversion (CTA) paradigm impaired CTA memory, whereas blockage of the NMDA receptor in an adjacent cortex or before a retrieval test had no effect. When rats sampled an unfamiliar taste and hence learned about it, either incidentally or in the context of CTA training, the tyrosine phosphorylation of the NMDA receptor subunit 2B (NR2B) in the insular cortex was specifically increased. The level of tyrosine phosphorylation on NR2B was a function of the novelty of the taste stimulus and the quantity of the taste substance consumed, properties that also determined the efficacy of the taste stimulus as a conditioned stimulus in CTA; however, blockage of the NMDA receptor by APV during training did not prevent tyrosine phosphorylation of NR2B. We suggest that tyrosine phosphorylation of NR2B subserves encoding of saliency in the insular cortex during the first hours after an unfamiliar taste is sampled and that this encoding is independent of another, necessary role of NMDA receptors in triggering experience-dependent modifications in the insular cortex during taste learning. Because a substantial fraction of the NR2B protein in the insular cortex seems to be expressed in interneurons, saliency and the tyrosine phosphorylation of NR2B correlated with it may modulate inhibition in cortex.

Assessment of peer neglect in the preschool years: a short-term longitudinal study.

Examined concurrent and longitudinal relations between different measures of peer neglect in the preschool years. Measures of social competence included peer sociometrics, teacher ratings, and behavioral observations of peer interactions. Participants were sixty 4- to 5-year-old Caucasian boys from low-income family backgrounds. Results indicated that the stability of indicators of peer neglect and social isolation depended on the measure employed. Correlations between different measures suggested heterogeneity in patterns of social adaptation among neglected or isolated preschool children. Results are discussed emphasizing the need to rely on multiple indicators for the assessment of preschool children's social competence.

Long-term potentiation increases tyrosine phosphorylation of the N-methyl-D-aspartate receptor subunit 2B in rat dentate gyrus in vivo.

Long-term potentiation (LTP) is a form of synaptic memory that may subserve developmental and behavioral plasticity. An intensively investigated form of LTP is dependent upon N-methyl-D-aspartate (NMDA) receptors and can be elicited in the dentate gyrus and hippocampal CA1. Induction of this type of LTP is triggered by influx of Ca2+ through activated NMDA receptors, but the downstream mechanisms of induction, and even more so of LTP maintenance, remain controversial. It has been reported that the function of NMDA receptor channel can be regulated by protein tyrosine kinases and protein phosphatases and that inhibition of protein tyrosine kinases impairs induction of LTP. Herein we report that LTP in the dentate gyrus is specifically correlated with tyrosine phosphorylation of the NMDA receptor subunit 2B in an NMDA receptor-dependent manner. The effect is observed with a delay of several minutes after LTP induction and persists in vivo for several hours. The potential relevance of this post-translational modification to mechanisms of LTP and circuit plasticity is discussed.

Carbachol mimics effects of sensory input on tyrosine phosphorylation in cortex.

We have recently shown that in the gustatory cortex of the rat, taste learning enhances protein tyrosine phosphorylation and taste memory is blocked by muscarinic antagonists. A major protein whose tyrosine phosphorylation is stimulated by taste learning in cortex is a 180 kDa synaptic glycoprotein identified as the NMDA receptor subunit 2B (NR2B). Here we report that microinjection of carbachol into the taste cortex modulates protein tyrosine phosphorylation similarly to the effect of unfamiliar taste, and that a 180 kDa protein whose tyrosine phosphorylation is enhanced in vivo by carbachol is NR2B. These data, combined with our previous findings, are in line with the hypothesis that muscarinic input plays a role in encoding new items in memory, and that tyrosine phosphorylation of NR2B is involved in this process.

Modulation of protein tyrosine phosphorylation in rat insular cortex after conditioned taste aversion training.

Protein tyrosine phosphorylation is a major signal transduction pathway involved in cellular metabolism, growth, and differentiation. Recent data indicate that tyrosine phosphorylation also plays a role in neuronal plasticity. We are using conditioned taste aversion, a fast and robust associative learning paradigm subserved among other brain areas by the insular cortex, to investigate molecular correlates of learning and memory in the rat cortex. In conditioned taste aversion, rats learn to associate a novel taste (e.g., saccharin) with delayed poisoning (e.g., by LiCl injection). Here we report that after conditioned taste aversion training, there is a rapid and marked increase in tyrosine phosphorylation of a set of proteins in the insular cortex but not in other brain areas. A major protein so modulated, of 180 kDa, is abundant in a membrane fraction and remains modulated for more than an hour after training. Exposure of the rats to the novel taste alone results in only a small modulation of the aforementioned proteins whereas administration of the malaise-inducing agent per se has no effect. To the best of our knowledge, this is the first demonstration of modulation of protein tyrosine phosphorylation in the brain after a behavioral experience.