Overestimation of Moral Outrage in Twitter Users on Political Topics

Post by Lani Cupo

The takeaway

When people read posts on social media, they are likely to overestimate how much moral outrage the author of the post felt. Further, they are likely to attribute the same level of outrage to a larger group, misperceiving the extent of collective moral outrage.

What's the science?

For a democracy to function, citizens must be able to assess collective moral attitudes, accurately identifying common ground among citizens and understanding what topics are most important to the members of opposing political parties. The use of social media platforms for political conversations can warp and skew social perceptions about the values and opinions of others. It is still unclear how social media, in its current form, might distort perceived outrage among politically-partisan users. This week in Nature, Brady and colleagues examine perceptions of Twitter posts (tweets) to understand how accurately readers can assess moral outrage in the original tweet’s author.

How did they do it?

The authors first conducted a field study using Twitter as a naturalistic study environment. They employed a machine learning algorithm to identify users who often posted high or low levels of outrage while discussing topics in American politics. Then, within 15 minutes of them posting a tweet, the authors invited them to take a survey about how happy or outraged they were while writing the tweet. Then, the authors recruited a separate group of politically-partisan Twitter users to read the tweets and judge how happy or outraged they thought the tweet author was when they wrote the message. In a follow-up study, the authors examined whether overestimating outrage in an individual amplifies the perception of collective moral outrage (i.e. overestimating the outrage of an entire group). To do so, they created two mock Twitter feeds with the tweets from the first experiment that both contained the same amount of outraged tweets based on how the tweet-author rated them, but one feed contained more tweets that were overestimated for outrage (high-overperception feed) and one contained tweets that were not overestimated (low-overperception feed). After exposing different groups of participants to these feeds, they assessed whether they perceived collective outrage to be greater. In a final follow-up study, a new set of participants was shown one of the mock Twitter feeds (either high- or low-overperception) and then asked to assess ten political tweets that contained opinions with either outraged or neutral language. The participants were asked to judge how appropriate the tweet would be in the network they observed, how much they thought the social network they observed liked the opposite political group, and how extreme the network was.

What did they find?

First, the authors found that readers overestimated how outraged the author of the tweet was. Importantly, their ratings correlated with those of the tweet-author (if the tweet-author was slightly outraged, the reader perceived them as outraged), but the reader overestimated the amount of outrage nevertheless. The readers who spent more time on social media to learn about politics were more likely to overestimate outrage, regardless of how politically extreme they were themselves or how strongly they aligned with a political group. Second, in the follow-up experiment, the authors found participants in the high-overperception feed were more likely to judge the collective outrage of their social network as high than those in the low-overperception feed, suggesting that overestimation of social outrage increases the perception of collective outrage. Finally, the authors found the high-overperception network was assessed to be more politically extreme and to dislike their political opponents more. It was also deemed socially acceptable to post tweets with more outrage, showing that overperception of collective outrage altered the perception of social norms in a group.

What's the impact?

This study provides evidence that moral outrage on political topics is overestimated on social media platforms, and this overperception can alter societal expectations in the network. These results provide a foundation to understand how social media may distort social knowledge, especially on controversial political opinions. In time, they may form the basis for countering political antipathy that is amplified on social media platforms.

Access the original scientific publication here

Prefrontal Neurons Regulate the Relationship Between Fear Memory and Pain Perception

Post by Leanna Kalinowski

The takeaway

A small subset of neurons in the prefrontal cortex regulates the association between long-term fear memory and pain perception. Fear memories in these neurons can then be blocked to alleviate chronic hypersensitivity to pain.

What's the science?

Pain and fear are two independent processes that are interrelated in some contexts. For example, when we are faced with a dangerous situation, our fear suppresses our perception of pain; this is a survival mechanism that is well understood. However, long-term fear memories caused by previous exposure to pain can also increase our future sensitivity to pain. This week in Nature Neuroscience, Stegemann and colleagues studied the association between long-term fear memory and pain perception by tagging and manipulating engrams, which are physical traces of memory in the brain.

How did they do it?

In the first experiment, the researchers aimed to identify the engram in the prefrontal cortex that is responsible for recalling previously encoded fear memories. To do this, they first injected a virus into the brain of mice that tags activated cells with mCherry (a fluorescent marker that can be viewed under a microscope). Then, mice received one of three pain stimuli: (1) foot shock, where they received occasional foot shocks over a five-minute period, (2) capsaicin injection, which is a substance that causes acute pain, or (3) fear conditioning, where they are first taught to associate a chamber and tone with a foot shock (training phase), and then are placed into the same chamber four weeks later where they are played the same tone but do not receive foot shocks (recall phase). Importantly, the researchers mixed doxycycline into the mice’s drinking water during the training phase of fear conditioning, as doxycycline temporarily deactivates the virus that tags activated cells with mCherry. This allowed them to only tag the cells being activated during the recall phase.

In the second experiment, the researchers aimed to assess the effects of optogenetically manipulating this engram on fear- and pain-related behaviors. To do this, two groups of mice received a prefrontal cortex injection of either (1) a virus that expresses archeorhodopsin (ArchT), which is a protein that turns off cell activity when exposed to a surgically-implanted fluorescent light, or (2) a virus that expresses channelrhodopsin-yellow fluorescent protein (ChR2-YFP), which is a protein that turns on cell activity when exposed to a fluorescent light. Both sets of mice then underwent the fear conditioning procedure with two rounds of fear recall: once without fluorescent light exposure, and once with fluorescent light exposure. In a different session, the researchers also measured pain behaviors after injecting both groups of mice with capsaicin and delivering the fluorescent light exposure.

In the third experiment, the researchers aimed to assess how the interaction between fear and pain differs in mice experiencing chronic pain. They first measured baseline pain behaviors in mice by measuring how quickly they withdrew their paw from a heat source or from mechanical stimulation. Next, the mice underwent fear conditioning and once again underwent pain behavior testing. Then, mice received one of the following chronic pain manipulations: spared nerve injury or paw inflammation. Finally, the mice underwent a third and final round of pain behavior testing.

In the final experiment, the researchers aimed to assess whether pain hypersensitivity in chronic pain mice can be reversed by silencing the fear memory engram with optogenetics. First, they again injected mice with a virus that expresses ArchT. The mice then underwent fear conditioning with two rounds of fear recall: one without fluorescent light exposure (i.e., cells are kept on), and one with ArchT activation (i.e., cells are turned off). Then, mice received one of the two chronic pain manipulations -- spared nerve injury or paw inflammation -- with pain behaviors being measured both at the peak of pain hypersensitivity and following several weeks of chronic pain hypersensitivity.

What did they find?

First, the researchers were able to identify an engram in the prefrontal cortex that was activated during both long-term fear memory and short-term pain. Results from this experiment informed their experimental manipulations for the remainder of the paper. Then, the researchers first found that optogenetic ArchT activation (i.e., turning off the cells) of the engram reduced both fear memory in the fear recall test, and pain-related behaviors (e.g., flicking, licking, or lifting the injected paw) following the capsaicin injection. They also found that optogenetic ChR2-YFP activation (i.e., turning on the cells) of the engram induced fear memory recall behaviors (e.g., freezing behaviors) even in the absence of auditory and contextual cues. This suggests that acute pain perception contains traces of a long-term fear memory from a previous pain experience. 

Next, the researchers found that while pain behaviors (i.e., rapid paw withdrawal) were not affected by prior fear conditioning in mice without chronic pain, mice with both types of chronic pain had greater pain sensitivity as evidenced by shorter paw withdrawal times. Chronic pain mice exposed to fear conditioning had a further increase in connectivity intensity to the mediodorsal thalamus, which is important for regulating emotion and the negative affect of pain.

Finally, the researchers found that, in mice whose long-term fear memory engrams were silenced, pain behaviors were reduced at both time points in both models of chronic pain. This shows that chronic hypersensitivity to pain can be reversed after suppressing the recall of long-term fear memory.

What’s the impact?

Taken together, results from this study show that a small subset of prefrontal cortex neurons is responsible for mediating interactions between long-term fear memories and pain perception, and they can be manipulated to alleviate pain hypersensitivity following chronic pain. These findings open the door to potential therapeutic strategies for chronic pain patients who experience fear-induced pain hypersensitivity. 

Access the original scientific publication here.

The Impact of Corticosteroid Treatments on Hippocampal Function

Post by Baldomero B. Ramirez Cantu

The takeaway

This study provides evidence that corticosteroid treatments can disrupt the circadian regulation of the hippocampus, leading to impairments in hippocampal function and plasticity.

What's the science?

Circadian rhythms are natural 24-hour cycles that regulate various physiological, biological, and behavioral processes in organisms. Corticosteroid treatments are commonly used to manage inflammatory and immunologic disorders, but they can produce side effects such as mental health issues and memory deficits. Despite their widespread use, the underlying mechanisms behind these side effects remain poorly understood. This week in PNAS, Birnie, Claydon and colleagues identify a molecular basis for the memory deficits in patients treated with corticosteroids and provide insights into the influence of corticosteroid treatment on hippocampal function.

How did they do it?

The authors used a rat model to mimic corticosteroid treatment by administration of the commonly prescribed corticosteroid methylprednisolone (MPL). The rats were housed in a 12-hour light-dark and were administered MPL orally. The authors screened for behavioral, genetic, and neurophysiological changes in the MPL group relative to a control group. They monitored changes in locomotion and body temperature between the two groups in order to screen for any potential impacts of the treatment on these behaviors. They also performed a novel object location task to assess changes in short, intermediate, and long-term memory. RNA sequencing was used to measure changes in gene expression in the two groups. Protein levels were assayed using Western blotting. Intracellular ex-vivo recordings were used to explore changes in synaptic plasticity as a result of corticosteroid treatment.

What did they find?

The authors observed that corticosterone treatment caused disruptions in synaptic physiology and gene expression in the hippocampus. Specifically, the authors found that corticosterone treatment impaired long-term potentiation (a measure of synaptic plasticity that is associated with long-term memory), altered the expression of genes involved in circadian regulation and synaptic plasticity, and disrupted the amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) in the hippocampus. The authors also showed that corticosterone treatment inhibited NMDAR-dependent plasticity, which is a key mechanism underlying learning and memory in the hippocampus.

In addition, their behavioral task found that rats treated with corticosterone exhibited impaired intermediate and long-term memory, but not short-term memory. The authors further investigated the molecular basis for these effects by analyzing gene expression in the hippocampus. They found that corticosterone treatment dysregulated genes that are known to be crucial for memory processing in the hippocampus and circadian regulation, including CAMKII and CLOCK. Crucially, the authors found that the time of day was a potent modulator of hippocampal activity and that this temporal regulation is disrupted by corticosteroid treatment.

What's the impact?

This study sheds light on the underlying mechanisms of the cognitive side effects of long-term corticosteroid treatments, which are very commonly used to treat many inflammatory and immunologic disorders. Furthermore, these findings could lead to the development of new therapeutic approaches for patients who experience cognitive side effects of corticosteroid treatments. 

Access the original scientific publication here.