Alessandro Piccin

New Dispatch in @currentbiology.bsky.social w/ @RobinPiquet & @dryacinetensaouti.bsky.social highlighting elegant work from the @iordanova.bsky.social lab that formally disentangles whether dopamine signals reward prediction errors or value.

authors.elsevier.com/a/1ldGk3QW8S...

As Chair of the Bordeaux Neurocampus Parity and Inclusion Committee, I’m pleased to share we’ve received generous CNRS funding to expand our inclusion efforts. Thanks to @neurobordeaux.bsky.social and CNRS for the support, which enables us to keep building a more inclusive research environment.

Reference Point-Dependent Reinforcement Learning in Humans and Rats Previous studies indicate that rewards and punishments in reinforcement learning are encoded in a relative manner. Reference point-dependence, a valuation bias shared by eminent adaptation level and p...

🚨 New study alert! 🚨
Ever wondered if rats and humans learn in the same way? 🐭🧑‍🔬
We tested this — and the answer is yes, at least when it comes to how we value rewards in context.
(with @shaunaparkes.bsky.social Lachlan Ferguson, Magdalena Soukupova)

🧵Thread 👇

1/

www.biorxiv.org/content/10.1...

Just UK and NA though... 😢

Merci Dr Y 🙏

Grazie Francesco :)

Thanks Vincent!! It's a full noradrenaline-dopamine project, so a lot of fun questions 😉

It's official! I've been awarded an #MSCA Postdoctoral Fellowship to work w/ @miriammelis.bsky.social in Cagliari 🏖️🇮🇹

#SPICE-FONTS will investigate the role of my fav neurotransmitter #noradrenaline in neurodevelopmental deficits caused by prenatal #cannabis exposure 🤰🌿

Grateful @ec.europa.eu 🙏🇪🇺

Grazie Mario!

Despite the translational failure of CRF1 receptor antagonists (see pmc.ncbi.nlm.nih.gov/articles/PMC...), these results show how some of these compounds might find new life in treating opioid-induced social deficits, which are known for worsening the clinical outcome of opioid use disorders.

At last, we show that, in male mice, antalarmin abolishes morphine-induced firing in neurons co-expressing OXY and AVP, but not in neurons expressing only AVP, thereby suggesting a sex-dependent mechanism of action involving CRF1 receptors and oxytocinergic neurons of the PVN.

Then, we replicate these results using the CRF1 genetic mouse model, and show that CRF1 receptor-deficiency prevents morphine-induced sociability deficits and firing of PVN neurons in a gene expression-dependent manner.

In parallel, we show that antalarmin also eliminates morphine-induced firing of PVN neurons in a sex-dependent manner.

First of all, we show that per os administration of the CRF1 receptor antagonist antalarmin completely abolishes sociability deficits induced by morphine, although exclusively in male mice.

Briefly, we investigated whether #CRF1 receptors play a role in the social deficits induced by #morphine and whether they affect the activity of #oxytocin (OXY) and #vasopressin (AVP) -expressing neurons of the paraventricular nucleus of the hypothalamus (#PVN).

Disruption of the CRF1 receptor eliminates morphine-induced sociability deficits and firing of oxytocinergic neurons in male mice Both genetic and pharmacological studies reveal an essential role for the CRF1 receptor in social behavior deficits induced by a single morphine administration in male, but not in female, mice.

Let's just say that when these experiments took place I had no idea where Wuhan was or how to change a diaper. So, you can just imagine how relieved I am to see this work out! A smooth and positive experience with the new
@elife.bsky.social model, which I recommend.