Harnessing social media to challenge scientific misinformation.

Ben Rein is a postdoctoral scholar at Stanford University and a science communicator on social media. In January, 2022, he and his colleagues wrote an open letter to Spotify to combat scientific misinformation. Here, Rein tells his story, sharing thoughts and lessons learned from publishing the open letter.

The virtual disengagement hypothesis: A neurophysiological framework for reduced empathy on social media.

Social media is a hotbed of interpersonal conflict and aggression. Platforms such as Twitter and Instagram are used by more than 62% of the global population, facilitating billions of user interactions every day. However, many of these exchanges involve hostile, insensitive, and antisocial behaviors. This raises the question: is empathy blunted on social media? Substantial evidence demonstrates that humans tend to behave more rudely in virtual settings, but considering the scarcity of physiological data collected under these circumstances, it remains unclear how the neural systems guiding social cognition and empathy may function differently in online interactions. We propose the "Virtual Disengagement Hypothesis," a conceptual framework to explain the prevalence of hostility online. It posits that interactions occurring on social media omit social cues that facilitate the assessment of a social partner's affective state, such as facial expressions and vocal tone, and thus fail to sufficiently recruit brain circuitry involved in empathy, such as the anterior cingulate cortex, insula, and prefrontal cortex. Additionally, interactions on social media occur asynchronously and in a "replayed" context, which may further limit recruitment of empathy systems. As a result of this diminished sensitivity to others' states, users may be predisposed to inconsiderate or outright antisocial behaviors. Given the massive and growing base of users on these platforms, we urge researchers to expand efforts that focus on neuroimaging in virtual settings with a particular emphasis on developing social media-relevant behavioral designs.

MDMA enhances empathy-like behaviors in mice via 5-HT release in the nucleus accumbens.

MDMA (3,4-methylenedioxymethamphetamine) is a psychoactive drug with powerful prosocial effects. While MDMA is sometimes termed an "empathogen," empirical studies have struggled to clearly demonstrate these effects or pinpoint underlying mechanisms. Here, we paired the social transfer of pain and analgesia-behavioral tests modeling empathy in mice-with region-specific neuropharmacology, optogenetics, and transgenic manipulations to explore MDMA's action as an empathogen. We report that MDMA, given intraperitoneally or infused directly into the nucleus accumbens (NAc), robustly enhances the social transfer of pain and analgesia. Optogenetic stimulation of 5-HT release in the NAc recapitulates the effects of MDMA, implicating 5-HT signaling as a core mechanism. Last, we demonstrate that systemic MDMA or optogenetic stimulation of NAc 5-HT inputs restores deficits in empathy-like behaviors in the Shank3-deficient mouse model of autism. These findings demonstrate enhancement of empathy-related behaviors by MDMA and implicate 5-HT signaling in the NAc as a core mechanism mediating MDMA's empathogenic effects.

Making Science Education More Accessible: A Case Study of TikTok's Utility as a Science Communication Tool.

Social media has revolutionized science communication, allowing for rapid dissemination of science-related content to the public. In recent years, video platforms like TikTok and Instagram have implemented recommendation algorithms that track users' interests andsuggest personalized videos. As a result, these apps have become powerful tools for public messaging, facilitating access to audiences that are naturally curious about science. In 2020 I began uploading educational science videos to TikTok which have collectively accumulated more than 48 million views and 8 million "likes." Here I present an analysis of video metrics collected from the TikTok app for a random sampling of 150 videos, searching for factors that predict the number of views a video receives and the level of viewer engagement. Videos with higher view counts were liked and shared at higher rates and sustained viewer attention for longer. Properties like hashtags, sounds, and effects did not significantly influence video views. Interestingly, videos summarizing research papers received the highest levels of engagement, potentially reflecting high demand from lay audiences who are traditionally unable to access scientific literature. Finally, I present survey data demonstrating that 84% of users report feeling more trustful of science & scientists after following this account. Although the generalizability of these findings is limited, the results offer insights into the factors that drive video performance on TikTok and how users engage with scientific content on social media. These findings may help science communicators more effectively reach wider audiences and promote science literacy in new and innovative ways.

Autism risk gene KMT5B deficiency in prefrontal cortex induces synaptic dysfunction and social deficits via alterations of DNA repair and gene transcription.

Large-scale genetic screening has identified KMT5B (SUV420H1), which encodes a histone H4 K20 di- and tri-methyltransferase highly expressed in prefrontal cortex (PFC), as a top-ranking high-risk gene for autism. However, the biological function of KMT5B in the brain is poorly characterized, and how KMT5B deficiency is linked to autism remains largely unknown. Here we knocked down Kmt5b in PFC and examined behavioral and electrophysiological changes, as well as underlying molecular mechanisms. Mice with Kmt5b deficiency in PFC display social deficits, a core symptom of autism, without the alteration of other behaviors. Kmt5b deficiency also produces deficits in PFC glutamatergic synaptic transmission, which is accompanied by the reduced synaptic expression of glutamate receptor subunits and associated proteins. Kmt5b deficiency-induced reduction of H4K20me2 impairs 53BP1-mediated DNA repair, leading to the elevation of p53 expression and its target gene Ddit4 (Redd1), which is implicated in synaptic impairment. RNA-sequencing data indicate that Kmt5b deficiency results in the upregulation of genes enriched in cellular stress response and ubiquitin-dependent protein degradation. Collectively, this study has revealed the functional role of Kmt5b in the PFC, and suggests that Kmt5b deficiency could cause autistic phenotypes by inducing synaptic dysfunction and transcriptional aberration.