Sex stereotypes influence adults' perception of babies' cries

Background: Despite widespread evidence that gender stereotypes influence human parental behavior, their potential effects on adults’ perception of babies’ cries have been overlooked. In particular, whether adult listeners overgeneralize the sex dimorphism that characterizes the voice of adult speakers (men are lower-pitched than women) to their perception of babies’ cries has not been investigated. Methods: We used playback experiments combining natural and re-synthesised cries of 3 month-old babies to investigate whether the interindividual variation in the fundamental frequency (pitch) of cries affected adult listeners’ identification of the baby’s sex, their perception the baby’s femininity and masculinity, and whether these biases interacted with their perception of the level of discomfort expressed by the cry. Results: We show that low-pitched cries are more likely to be attributed to boys and high-pitched cries to girls, despite the absence of sex differences in pitch. Moreover, low-pitched boys are perceived as more masculine and high-pitched girls are perceived as more feminine. Finally, adult men rate relatively low-pitched cries as expressing more discomfort when presented as belonging to boys than to girls. Conclusion: Such biases in caregivers’ responses to babies’ cries may have implications on children’s immediate welfare and on the development of their gender identity

Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids

Opiates, one of the oldest known drugs, are the benchmark for treating pain. Regular opioid exposure also induces euphoria making these compounds addictive and often misused, as shown by the current epidemic of opioid abuse and overdose mortalities. In addition to the effect of opioids on their cognate receptors and signaling cascades, these compounds also induce multiple adaptations at cellular and behavioral levels. As omega-3 polyunsaturated fatty acids (n-3 PUFAs) play a ubiquitous role in behavioral and cellular processes, we proposed that supplemental n-3 PUFAs, enriched in docosahexanoic acid (DHA), could offset these adaptations following chronic opioid exposure. We used an 8 week regimen of n-3 PUFA supplementation followed by 8 days of morphine in the presence of this diet. We first assessed the effect of morphine in different behavioral measures and found that morphine increased anxiety and reduced wheel-running behavior. These effects were reduced by dietary n-3 PUFAs without affecting morphine-induced analgesia or hyperlocomotion, known effects of this opiate acting at mu opioid receptors. At the cellular level we found that morphine reduced striatal DHA content and that this was reversed by supplemental n-3 PUFAs. Chronic morphine also increased glutamatergic plasticity and the proportion of Grin2B-NMDARs in striatal projection neurons. This effect was similarly reversed by supplemental n-3 PUFAs. Gene analysis showed that supplemental PUFAs offset the effect of morphine on genes found in neurons of the dopamine receptor 2 (D2)-enriched indirect pathway but not of genes found in dopamine receptor 1(D1)-enriched direct-pathway neurons. Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n-3 PUFA supplementation reversed the effect of chronic morphine on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices. Together these changes outline specific behavioral and cellular effects of morphine that can be reduced or reversed by dietary n-3 PUFAs

Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids

<div><p>Opiates, one of the oldest known drugs, are the benchmark for treating pain. Regular opioid exposure also induces euphoria making these compounds addictive and often misused, as shown by the current epidemic of opioid abuse and overdose mortalities. In addition to the effect of opioids on their cognate receptors and signaling cascades, these compounds also induce multiple adaptations at cellular and behavioral levels. As omega-3 polyunsaturated fatty acids (n-3 PUFAs) play a ubiquitous role in behavioral and cellular processes, we proposed that supplemental n-3 PUFAs, enriched in docosahexanoic acid (DHA), could offset these adaptations following chronic opioid exposure. We used an 8 week regimen of n-3 PUFA supplementation followed by 8 days of morphine in the presence of this diet. We first assessed the effect of morphine in different behavioral measures and found that morphine increased anxiety and reduced wheel-running behavior. These effects were reduced by dietary n-3 PUFAs without affecting morphine-induced analgesia or hyperlocomotion, known effects of this opiate acting at mu opioid receptors. At the cellular level we found that morphine reduced striatal DHA content and that this was reversed by supplemental n-3 PUFAs. Chronic morphine also increased glutamatergic plasticity and the proportion of Grin2B-NMDARs in striatal projection neurons. This effect was similarly reversed by supplemental n-3 PUFAs. Gene analysis showed that supplemental PUFAs offset the effect of morphine on genes found in neurons of the dopamine receptor 2 (D2)-enriched indirect pathway but not of genes found in dopamine receptor 1(D1)-enriched direct-pathway neurons. Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n-3 PUFA supplementation reversed the effect of chronic morphine on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices. Together these changes outline specific behavioral and cellular effects of morphine that can be reduced or reversed by dietary n-3 PUFAs.</p></div

Specific behavioral and cellular adaptations induced by chronic morphine are reduced by dietary omega-3 polyunsaturated fatty acids.

Opiates, one of the oldest known drugs, are the benchmark for treating pain. Regular opioid exposure also induces euphoria making these compounds addictive and often misused, as shown by the current epidemic of opioid abuse and overdose mortalities. In addition to the effect of opioids on their cognate receptors and signaling cascades, these compounds also induce multiple adaptations at cellular and behavioral levels. As omega-3 polyunsaturated fatty acids (n-3 PUFAs) play a ubiquitous role in behavioral and cellular processes, we proposed that supplemental n-3 PUFAs, enriched in docosahexanoic acid (DHA), could offset these adaptations following chronic opioid exposure. We used an 8 week regimen of n-3 PUFA supplementation followed by 8 days of morphine in the presence of this diet. We first assessed the effect of morphine in different behavioral measures and found that morphine increased anxiety and reduced wheel-running behavior. These effects were reduced by dietary n-3 PUFAs without affecting morphine-induced analgesia or hyperlocomotion, known effects of this opiate acting at mu opioid receptors. At the cellular level we found that morphine reduced striatal DHA content and that this was reversed by supplemental n-3 PUFAs. Chronic morphine also increased glutamatergic plasticity and the proportion of Grin2B-NMDARs in striatal projection neurons. This effect was similarly reversed by supplemental n-3 PUFAs. Gene analysis showed that supplemental PUFAs offset the effect of morphine on genes found in neurons of the dopamine receptor 2 (D2)-enriched indirect pathway but not of genes found in dopamine receptor 1(D1)-enriched direct-pathway neurons. Analysis of the D2 striatal connectome by a retrogradely transported pseudorabies virus showed that n-3 PUFA supplementation reversed the effect of chronic morphine on the innervation of D2 neurons by the dorsomedial prefontal and piriform cortices. Together these changes outline specific behavioral and cellular effects of morphine that can be reduced or reversed by dietary n-3 PUFAs

DHA supplementation attenuates the anxiety induced by morphine without altering analgesia or locomotion, established effects of this opiate.

<p><b>A. Wheel running</b> activity was measured over 16h; 3h of light, 12h of dark, 1h of light. The distance run (cm) every hour is shown in the 3 left panels and the total distance run in the column graphs on the right. DHA supplementation did not alter wheel running in male mice receiving saline (Ai) which by day 8 had increased their activity compared with day 1. *, # p<0.05 vs pre-saline injection activity, shown in the solid (control diet) or dashed (DHA group) lines, of the same treatment. B. Total distance run, depicted in the column graphs, shows that morphine reduced wheel running in both DHA and control groups when compared with pre-treatment levels; **, *** p<0.05 and 0.005 respectively vs basal activity in the control group. ##, ### p<0.05 and 0.005 respectively vs basal activity in the DHA group. However, the hourly time bin data show that DHA attenuated this reduction at specific time-points, 5 and 15 h post-morphine injection on day 1, and 5 hours on day 8, *p<0.05, ***p<0.001 vs control morphine at the same timepoint. <b>B. Elevated Plus Maze (EPM).</b> The time spent and frequency of entry into the second, outer half of the EPM was assessed 5h following the last injection of the 8^th day of the morphine or saline injection protocol. Mice on the control diet receiving morphine spent less time and entered less into this region than control mice receiving saline. Supplemental DHA partially reversed this profile. *, ***p<0.05 and 0.001 respectively vs the control saline group, #p<0.05 vs control saline and control morphine. <b>C. Morphine-induced analgesia.</b> The effect of DHA on morphine-induced thermal analgesia was assessed by the tail immersion test at 49.5°C. There was no effect of diet on basal tail-flick latency. Morphine (10mg/kg s.c.) delayed this response in both control and DHA groups (*** p<0.001 vs baseline measures). <b>D. Morphine induced locomotion.</b> i. This effect if morphine was assessed immediately following the first of the daily morphine injections on days 1, 4 and 8 of the TDA morphine injection protocol. The total distance traveled showed no effect of DHA on either the initial locomotor response, or subsequent, sensitized responses, which increased above saline-treated mice on the matching diet, *p<0.05, ***p<0.001 vs saline of the matching control or DHA diet.</p

The expression of genes enriched in D2-, but not D1-, enriched striatal neurons are altered by both supplemental DHA and morphine.

<p><b>A. D1</b> DHA supplementation did not alter the morphine-induced increase in D1 transcript levels. a, c, d; p<0.001, b; p< 0.05. <b>B. Dyn</b> Neither morphine nor DHA altered the expression of Dyn, a gene enriched in D1-neurons. <b>C. Drd2</b> Morphine reduced D2 expression while DHA supplementation increased D2 expression following saline or morphine, a; p<0.0, b; p<0.05, c; p<0.001.<b>D. Enk</b> Morphine increased the expression of Enk, a D2-enriched gene. This was reduced following DHA in either morphine or saline treated mice. a; p<0.01, b; p<0.05.</p

Region-specific effects of dietary DHA and morphine on brain DHA content.

<p><b>A. Frontal cortex.</b> DHA supplementation increased DHA content following saline or morphine treatment with no further effect of morphine. a and b; p<0.05. <b>B. Striatum</b>. Chronic morphine decreased DHA tissue content and DHA supplementation increased DHA content following saline or morphine. a; p<0.01, b; p<0.05. c; p<0.0001.</p