-
EU 'concerned' by reports Hungary leaked information to Russia
-
EU chief meets Australian PM as trade talks enter 'last mile'
-
Israel pounds south Beirut, says captured Hezbollah members
-
EU chief to meet Australian PM as trade talks enter 'last mile'
-
Champion Mensik, Medvedev dumped out of Miami Open
-
Jury at US social media addiction trial reports 'difficulty' in finding consensus
-
Stokes eager to lead England recovery after 'hardest period of captaincy'
-
Venezuela protesters demand end to 'hunger' level wages
-
Eight people arrested in Brazil for 'brutal' attack on capybara
-
Audi Q9 – how likely is it to become a reality?
-
Oil slides, stocks rebound on Trump's Iran remarks
-
On Iran, Trump executes his most spectacular U-turn yet
-
Trump announces 'very good' Iran talks denied by Tehran
-
Bill Cosby ordered to pay $19m over sex abuse claim
-
Dodgers eye 'threepeat' as new MLB season welcomes robot umpires
-
Dacia Striker: Stylish and sturdy?
-
Skoda Peaq: New all-electric seven-seater
-
Medvedev ousted by Cerundolo at Miami Open
-
Runway collision kills two pilots at New York airport
-
Italian voters reject Meloni's reforms in referendum blow
-
Bosnian truckers blocked EU freight terminals for a day over visa rules
-
Colombia military aircraft crashes with 125 aboard, many feared dead
-
Rip-offs at the petrol pump?
-
Shakira to wrap up world tour with Madrid residency
-
World gave Israel 'licence to torture Palestinians': UN expert
-
Colombia says 80 troops on crashed aircraft, many feared dead
-
France turns to 2027 race to succeed Macron
-
New Mercedes GLC electric
-
Namibia rejects Starlink licence request
-
Ex-model questioned in France over scout with Epstein links
-
UK sending air defence systems to Gulf: PM
-
Trump administration seeks to ease oil fears but industry wary
-
Blow to Italy's Meloni as she suffers referendum defeat
-
US deploys immigration agents to airports amid shutdown chaos
-
US, TotalEnergies reach 'nearly $1 bn' deal to end offshore wind projects
-
Spurs offer condolences to interim boss Tudor after father's death
-
Iran's true casualty figures unknown as internet blackout hampers monitors
-
Trump's ever-shifting positions on the war with Iran
-
Countries act to limit fuel price rise, cut consumption
-
'Stop, truck one, stop!': transcript of NY plane collision
-
Swiatek splits with coach Fissette after early Miami exit
-
WHO chief urges countries to complete pandemic agreement
-
Trump sees 'regime change' in surprise Iran talks
-
Trump calls off Iran strikes and announces 'very good' talks
-
Russia, Vietnam advance plans for first nuclear power plant
-
New Trump envoy visits Honduras for organized crime-fighting partnership
-
No 'silver bullet' for video game age restrictions: PEGI chief
-
England coach McCullum survives review into Ashes drubbing
-
Mixed results for Lyme disease vaccine hit Valneva shares
-
Far-right French president no certainty despite rise of extremes
'Love hormone'? Not so fast, new study suggests
The "love hormone" oxytocin has long been thought key to behaviours including pairing up with a partner and nurturing offspring, but a new study in prairie voles is raising doubts.
The research found that voles bred to lack functioning receptors for oxytocin were still able to form strong pairs, produce young and nurse -- all behaviours previously believed to depend on the hormone.
Prairie voles are one of the few mammals that mate for life, and are often used to study social behaviours like pair-forming in animals.
In past studies, voles given drugs that stopped oxytocin being processed no longer formed pairs, and mothers failed to produce milk for their young.
Psychiatrist Devanand Manoli and neurobiologist Nirao Shah produced genetically altered prairie voles without working oxytocin receptors, and then observed how the mutant male and female voles behaved.
To their shock, the mutant voles appeared to have no difficulty pairing up with non-genetically altered partners, and mutant females could still deliver and nurse young, unlike those in the drug-driven studies.
"We were certainly surprised," said Manoli, an assistant professor at the University of California, San Francisco.
The results suggest that oxytocin is not the main, or only, driver of activities like partnering or nursing, he said.
"What the genetics reveals is that there isn't a 'single point of failure' for behaviours that are so critical to the survival of the species," he told AFP.
- 'Very complex behaviours' -
That didn't mean there were no differences, however.
Some male mutant voles that paired with ordinary female partners didn't show the aggression towards interloping females that would normally be expected.
And while mutant females produced and nursed litters, some had fewer pups per litter than their counterparts, and fewer of their offspring survived to weaning, the paper published Friday in the journal Neuron explains.
Pups born to mutant mothers also tended to weigh less, suggesting that they were not able to nurse as effectively.
The study only involved pairing of mutant voles with "wild-type" partners, and the researchers said pairings with two mutant partners could produce different results.
Still, as a whole, the findings suggest a different picture of oxytocin's role in several important behaviours.
That could be because animals bred without the receptors developed "other compensatory pathways" that helped them pair up and nurse, said Shah, a professor at Stanford University.
But the researchers suggest it likely means oxytocin is only part of a set of genetic factors that control social behaviour.
"What I think our studies reveal is that there are multiple pathways that regulate these very complex behaviours," said Manoli.
Oxytocin has sometimes been suggested as a way to treat attachment disorders and other neuropsychiatric issues, but there is little settled science on how effective it is.
Now the researchers hope to investigate what other hormones and receptors may be involved in behaviours like pairing and nursing.
"These other pathways might serve as new therapeutic targets," Manoli said.
Z.AbuSaud--SF-PST