Association between high voltage overhead transmission lines and mental health: a cross-sectional study

We examined the association between residential proximity to 60 Hz high voltage (22-500 kV) overhead transmission lines (HVOTLs) and mental health (MH). The subjects were 223 mothers with a mean age of 37 years. The distance from the subject's residence to the closest HVOTL was measured on a map. MH status was assessed by the SF-36 Health Survey, which was scored on a 0-100 point scale, and an individual with a score of 52 points or less was defined as having poor MH. Logistic regression models were used to examine the association between the distance from the subjects' residence to the closest HVOTL and MH status. The prevalence of poor MH was 15%. Among the 223 subjects, 10 lived within 100 m of a HVOTL. The adjusted odds ratios (OR) for poor MH among those who lived 101-300 m or within 100 m from HVOTL were 1.29 (95% confidence interval (CI): 0.35-10.13) and 1.87 (95% CI: 0.35-10.13), respectively, against the reference category (300+ m). MH status was not significantly associated with the distance between the subject's residence and the closest HVOTL.     

Modulation of neuropeptide FF (NPFF) receptors influences the expression of amphetamine-induced conditioned place preference and amphetamine withdrawal anxiety-like behavior in rats

Many data indicate that endogenous opioid system is involved in amphetamine-induced behavior. Neuropeptide FF (NPFF) possesses opioid-modulating properties. The aim of the present study was to determine whether pharmacological modulation of NPFF receptors modify the expression of amphetamine-induced conditioned place preference (CPP) and amphetamine withdrawal anxiety-like behavior, both processes relevant to drug addiction/abuse. Intracerebroventricular (i.c.v.) injection of NPFF (5, 10, and 20 nmol) inhibited the expression of amphetamine CPP at the doses of 10 and 20 nmol. RF9, the NPFF receptors antagonist, reversed inhibitory effect of NPFF (20 nmol, i.c.v.) at the doses of 10 and 20 nmol and did not show any effect in amphetamine- and saline conditioned rats. Anxiety-like effect of amphetamine withdrawal was measured 24h after the last (14 days) amphetamine (2.5mg/kg, i.p.) treatment in the elevated plus-maze test. Amphetamine withdrawal decreased the percent of time spent by rats in the open arms and the percent of open arms entries. RF9 (5, 10, and 20 nmol, i.c.v.) significantly reversed these anxiety-like effects of amphetamine withdrawal and elevated the percent of time spent by rats in open arms at doses of 5 and 10 nmol, and the percent of open arms entries in all doses used. NPFF (20 nmol) pretreatment inhibited the effect of RF9 (10 nmol). Our results indicated that stimulation or inhibition of NPFF receptors decrease the expression of amphetamine CPP and amphetamine withdrawal anxiety, respectively. These findings may have implications for a better understanding of the processes involved in amphetamine dependence.     

Amygdala protein kinase C epsilon regulates corticotropin-releasing factor and anxiety-like behavior

Corticotropin-releasing factor (CRF), its receptors, and signaling pathways that regulate CRF expression and responses are areas of intense investigation for new drugs to treat affective disorders. Here, we report that protein kinase C epsilon (PKCɛ) null mutant mice, which show reduced anxiety-like behavior, have reduced levels of CRF messenger RNA and peptide in the amygdala. In primary amygdala neurons, a selective PKCɛ activator, ψɛRACK, increased levels of pro-CRF, whereas reducing PKCɛ levels through RNA interference blocked phorbol ester-stimulated increases in CRF. Local knockdown of amygdala PKCɛ by RNA interference reduced anxiety-like behavior in wild-type mice. Furthermore, local infusion of CRF into the amygdala of PKCɛ^−/− mice increased their anxiety-like behavior. These results are consistent with a novel mechanism of PKCɛ control over anxiety-like behavior through regulation of CRF in the amygdala.     

Genetic influences on behavioral inhibition and anxiety in juvenile rhesus macaques

In humans and other animals, behavioral responses to threatening stimuli are an important component of temperament. Among children, extreme behavioral inhibition elicited by novel situations or strangers predicts the subsequent development of anxiety disorders and depression. Genetic differences among children are known to affect risk of developing behavioral inhibition and anxiety, but a more detailed understanding of genetic influences on susceptibility is needed. Nonhuman primates provide valuable models for studying the mechanisms underlying human behavior. Individual differences in threat-induced behavioral inhibition (freezing behavior) in young rhesus monkeys are stable over time and reflect individual levels of anxiety. This study used the well-established human intruder paradigm to elicit threat-induced freezing behavior and other behavioral responses in 285 young pedigreed rhesus monkeys. We examined the overall influence of quantitative genetic variation and tested the specific effect of the serotonin transporter promoter repeat polymorphism. Quantitative genetic analyses indicated that the residual heritability of freezing duration (behavioral inhibition) is h ² = 0.384 ( P  = 0.012) and of 'orienting to the intruder' (vigilance) is h ² = 0.908 ( P  = 0.00001). Duration of locomotion and hostility and frequency of cooing were not significantly heritable. The serotonin transporter polymorphism showed no significant effect on either freezing or orienting to the intruder. Our results suggest that this species could be used for detailed studies of genetic mechanisms influencing extreme behavioral inhibition, including the identification of specific genes that are involved in predisposing individuals to such behavior.     

Attachment Anxiety and Avoidance Influence Pet Choice and Pet-directed Behaviors

Attachment theory is a useful lens through which to examine both perceptions and selection of companion animals. Study 1 compared perceptions of dogs and cats, and found that dogs were perceived as having more positive relationship qualities and secure attachment-related characteristics, whereas cats were perceived as having more negative relationship qualities and avoidant attachment-related characteristics. In addition, people perceived relationships with dogs to involve less avoidance and less anxiety relative to relationships with people. In study 2, which built on the findings of study 1, attachment avoidance was negatively associated with wanting to own a pet, whereas attachment anxiety was positive associated with wanting to own a pet. These attachment dimensions were not associated with wanting to own a dog, but lower avoidance and higher anxiety were associated with wanting to own a cat. Study 3 was a longitudinal study of SPCA-type shelter visitors (510 participants, with 169 reporting a recent pet adoption). Lower attachment anxiety predicted recently adopting a dog rather than a cat, though neither anxiety nor avoidance predicted adopting a cat. Individuals who wanted a pet in order to facilitate human relationships were more likely to adopt a dog than a cat. Those high in attachment avoidance reported turning to their pet as a replacement for human companionship, and those high in attachment anxiety reported feeling more concern about their pets requiring more attention. Attachment anxiety and avoidance may influence the decision whether or not to adopt a pet, as well as the motivation underlying the adoption choice. Attachment also may influence the type of pet chosen (i.e., dog versus cat). In addition, attachment may influence the nature of the human–animal relationship, such as the time spent together, and the security felt regarding the relationship.     

Stress Impacts the Regulation Neuropeptides in the Rat Hippocampus and Prefrontal Cortex

Adverse life experiences increase the lifetime risk to several stress‐related psychopathologies, such as anxiety or depressive‐like symptoms following stress in adulthood. However, the neurochemical modulations triggered by stress have not been fully characterized. Neuropeptides play an important role as signaling molecules that contribute to physiological regulation and have been linked to neurological and psychiatric diseases. However, little is known about the influence of stress on neuropeptide regulation in the brain. Here, we have performed an exploratory study of how neuropeptide expression at adulthood is modulated by experiencing a period of multiple stressful experiences. We have targeted hippocampus and prefrontal cortex (PFC) brain areas, which have previously been shown to be modulated by stressors, employing a targeted liquid chromatography‐mass spectrometry (LC‐MS) based approach that permits broad peptide coverage with high sensitivity. We found that in the hippocampus, Met‐enkephalin, Met‐enkephalin‐Arg‐Phe, and Met‐enkephalin‐Arg‐Gly‐Leu were upregulated, while Leu‐enkephalin and Little SAAS were downregulated after stress. In the PFC area, Met‐enkephalin‐Arg‐Phe, Met‐enkephalin‐Arg‐Gly‐Leu, peptide PHI‐27, somatostatin‐28 (AA1‐12), and Little SAAS were all downregulated. This systematic evaluation of neuropeptide alterations in the hippocampus and PFC suggests that stressors impact neuropeptides and that neuropeptide regulation is brain‐area specific. These findings suggest several potential peptide candidates, which warrant further investigations in terms of correlation with depression‐associated behaviors.     

A quantitative trait locus on chromosome 1 modulates intermale aggression in mice

Aggression between male conspecifics is a complex social behavior that is likely modulated by multiple gene variants. In this study, the BXD recombinant inbred mouse strains (RIS) were used to map quantitative trait loci (QTLs) underlying behaviors associated with intermale aggression. Four hundred and fifty‐seven males from 55 strains (including the parentals) were observed at an age of 13 ± 1 week in a resident‐intruder test following 10 days of isolation. Attack latency was measured directly within a 10‐minute time period and the test was repeated 24 hours later. The variables we analyzed were the proportion of attacking males in a given strain as well as the attack latency (on days 1 and 2, and both days combined). On day 1, 29% of males attacked, and this increased to 37% on day 2. Large strain differences were obtained for all measures of aggression, indicating substantial heritability (intraclass correlations 0.10‐0.18). We identified a significant QTL on chromosome (Chr) 1 and suggestive QTLs on mouse Chrs 1 and 12 for both attack and latency variables. The significant Chr 1 locus maps to a gene‐sparse region between 82 and 88.5 Mb with the C57BL/6J allele increasing aggression and explaining about 18% of the variance. The most likely candidate gene modulating this trait is Htr2b which encodes the serotonin 2B receptor and has been implicated in aggressive and impulsive behavior in mice, humans and other species.     

Perinatal nutrition interacts with genetic background to alter behavior in a parent‐of‐origin‐dependent manner in adult Collaborative Cross mice

Previous studies in animal models and humans have shown that exposure to nutritional deficiencies in the perinatal period increases the risk of psychiatric disease. Less well understood is how such effects are modulated by the combination of genetic background and parent‐of‐origin (PO). To explore this, we exposed female mice from 20 Collaborative Cross (CC) strains to protein deficient, vitamin D deficient, methyl donor enriched or standard diet during the perinatal period. These CC females were then crossed to a male from a different CC strain to produce reciprocal F1 hybrid females comprising 10 distinct genetic backgrounds. The adult F1 females were then tested in the open field, light/dark, stress‐induced hyperthermia, forced swim and restraint stress assays. Our experimental design allowed us to estimate effects of genetic background, perinatal diet, PO and their interactions on behavior. Genetic background significantly affected all assessed phenotypes. Perinatal diet exposure interacted with genetic background to affect body weight, basal body temperature, anxiety‐like behavior and stress response. In 8 of 9 genetic backgrounds, PO effects were observed on multiple phenotypes. Additionally, we identified a small number of diet‐by‐PO effects on body weight, stress response, anxiety‐ and depressive‐like behavior. Our data show that rodent behaviors that model psychiatric disorders are affected by genetic background, PO and perinatal diet, as well as interactions among these factors.