Communicating via Video Chat Reduces Inter-Brain Synchrony

Post by Lani Cupo

The takeaway

Synchronous brain activity between mothers and their young adolescent children is impacted when they are communicating via video chat compared to face-to-face. While communicating over video chat, there was reduced inter-brain synchrony.

What's the science?

Technologically-assisted communication (i.e. video chat or videoconferencing) has become especially prominent over the past few years as constraints of the COVID-19 pandemic, remote work, and living far from home necessitate people to connect virtually. Many have reported that connections do not feel the same, or that they experience “Zoom fatigue” after long days on video calls, which may be a result of disruptions to the inter-brain synchrony that underlies human social communication. There is mounting concern that children and adolescents may be especially susceptible to the increased exertion of telecommunication, however, more research is required to investigate the impact of technological communication on developing brains. This week in NeuroImage Schwartz and colleagues used electroencephalograms (EEG) on two brains (mothers and their adolescents) during face-to-face and video chat communications, comparing the synchrony between both conditions.

How did they do it?

140 people (70 mother-child pairs) participated in the study, which took place before the COVID-19 pandemic. The authors filmed all sessions and recorded brain activity from participants with EEG during three conditions: rest, where both participants were in the same room, facing a wall, but not interacting, face-to-face, where participants were in the same room, facing each other, and video chat, where participants were in two separate rooms, communicating through a computer screen. In both interaction conditions, the participants were instructed to discuss a positive topic, either planning a camping trip or planning an amusement park visit. The authors recorded EEG from both the mother and child continuously throughout the experiment. They used a previously defined method of calculating inter-brain connectivity (weighted phase lag index), a technique that aims to reduce correlated noise between participants’ brains that may be caused by shared noise sources, such as sensory stimuli. This is especially important for this study because even in a controlled environment, sensory stimuli in the face-to-face condition may be more similar than in the video-chat condition because participants are in the same room with the same noise sources. The authors also investigated behavioral metrics during both interaction conditions using the well-validated Coding Interactive Behavior manual (CIB). Finally, gaze direction was estimated from the video recordings, coded as either to person, to object, aversion, or unfocused.

What did they find?

Compared to baseline, both face-to-face and video chat communication increased inter-brain connectivity, while rest did not. However, inter-brain connectivity was most enhanced in the face-to-face communication condition, compared to the video chat condition. More specifically, the authors examined 36 possible brain connections between the mother and child’s regions of interest (ROIs). Comparing face-to-face to rest connectivity, they found greater inter-brain connectivity in 9 ROI connections. These ROIs could be categorized into four subgroups, most notably a) both homolog and cross-hemisphere linkage between the mother’s frontal and child’s temporal regions, b) mother’s right frontal region connecting with each of the child's ROIs, and c) the child’s temporal region connecting with mother's frontal and temporal regions. Conducting the same analysis between video chat and rest conditions, the authors report only a single significant connection between the mother’s right frontal and the child’s left temporal regions. This pair of analyses underscore the importance of the mother’s right frontal and child’s left temproal connectivity in mother-child social interactions. Comparing the social communication conditions directly, the authors found a significant difference between groups. Finally, during the face-to-face condition, but not the video chat condition, temporal-temporal synchrony was associated with the mother and child looking at each other, and mother-right-frontal-child-left-temporal connection was associated with the child being empathically engaged.

What's the impact?

This study found that social interaction between mother and child induces synchrony between brain activity in both participants, however, the method of interaction impacts connectivity, with greater synchrony during face-to-face interaction than video chatting or rest. These findings lend insight into the neural processes underlying social communication and highlight a need for future studies to investigate how inter-brain connectivity may change with changing technology.

Access the original scientific publication here

Can Psychedelics Treat Depression?

Post by Anastasia Sares

The takeaway

Recently, there has been rising interest in the possible therapeutic applications of psychedelics. This interest stems from evidence that psychedelic-assisted psychotherapy has been helpful for some people with treatment-resistant depression and other mental health conditions. However, psychedelics can also have negative side effects and require intensive doctor supervision. Thus, scientists are on the hunt for new molecules that might have more therapeutic effects and fewer prohibitive side effects. This week in Nature Neuroscience, Kwan and colleagues reviewed old and new research on the biological mechanisms of psychedelics, providing a resource for future pharmaceutical research.

Getting psychedelics into the brain

To exert their effects on the brain, psychedelic molecules must first get there. This is not an easy task, as the brain and its surrounding fluid are separated from the rest of the body by the blood-brain barrier. The cells of the blood-brain barrier are bound together by tight junctions that prevent molecules from squeezing between them, as they would in the rest of the body. Instead, molecules wanting to get to the brain must cross into these barrier cells and then back out on the other side. Thus, small molecules that are somewhat soluble in both water and fatty cell membranes are best suited to get into the brain, and psychedelics fit these criteria.

Pretending to be serotonin

Once in the brain, psychedelics bind to serotonin receptors, mimicking the action of serotonin itself. There are two important sites on the serotonin receptor that the psychedelic activates: the binding pocket, which receives the nitrogen end of the psychedelic molecule, and a hydrophobic region (a region that repels water), which lines up with a ring of carbons in the psychedelic molecule. These two regions need to be spanned by a distance of exactly two carbons, or the receptor and the molecule won’t line up. In addition, if the carbon ring is free to spin around relative to the nitrogen, the molecule will be less efficient in binding to the receptor, so rigid structures are more effective. LSD is an example of one of these rigid molecules.

What are the effects on neurons?

What happens in the brain when a psychedelic activates a serotonin receptor? There are many different serotonin receptors in the brain, some of which increase neuronal firing while others may decrease it. Overall, the effect of a psychedelic in each region of the brain could depend on the ratio of these different types of serotonin receptors. For example, a number of studies have found that activity in the visual pathway is decreased, while others have suggested that activity in the frontal lobe may increase.

Psychedelics can also increase the presence of molecules related to brain plasticity (the ability of the brain to rewire itself). They can also alter the number of neuronal spines (small protrusions from the dendrites that help the neurons make connections) on neurons. This is generally seen as positive and it may be the reason why therapy with psychedelics can help people with treatment-resistant depression: the therapy and plasticity may work together to reshape a person’s thought patterns. However, not all plasticity is good—there can also be maladaptive plasticity, so it will be important to research this phenomenon in more detail.

Finally, psychedelics may also stimulate non-serotonin receptors, changing levels of other neurotransmitters like dopamine or glutamate, and even in some cases causing cardiac problems (as has been reported in chronic MDMA users).

What are the effects on brain networks?

By the time we arrive at the level of brain networks, the exact mechanisms of psychedelics are much less clear. There are multiple, sometimes contradictory, models of psychedelic action. Some common elements include increased connectivity of the thalamus (a deep brain structure involved in controlling input from different senses) and fragmentation of association cortices (linking information from one brain region to another).

Moving forward

To arrive at effective psychedelic-based therapies, scientists must work to understand what exactly about these compounds is therapeutic. Are the hallucinogenic effects completely independent from the pathways that increase neural plasticity (and if so, could we make a non-hallucinogenic molecule that still has therapeutic benefits)? Or, are the hallucinogenic and the therapeutic activity one and the same?

Access the original scientific publication here.

The Encoding of Aversive Memories

Post by Megan McCullough

The takeaway

The encoding of aversive memories depends on the amygdala modulating activity in the hippocampus. Theta phases in the amygdala coordinate gamma activity and neuronal firing in the hippocampus which is critical to the formation of memories associated with emotional, aversive events.

What's the science?

Humans tend to have a stronger recall of emotional events compared to neutral events. Previous research has implicated the amygdala and the hippocampus in encoding emotional memories. Data has shown that the amygdala modulates emotional memory storage processes in the hippocampus but the mechanism behind this is unclear. This week in Nature Communications, Webb and colleagues investigate the relationship between the amygdala and the hippocampus in encoding emotional memories by simultaneously recording brain activity in the two regions during memory tasks.

How did they do it?

The authors recorded neural activity in both the amygdala and the hippocampus in participants while they performed an emotional memory task. Participants consisted of individuals with drug-resistant epilepsy, and they were assigned to be in one of two cohorts. The participants in Cohort 1 had recording electrodes measuring oscillatory activity in both brain regions during the emotional memory task. The participants in Cohort 2 had microelectrodes recording single neuron activity in the brain regions during the task. The recording of both brain waves and single neuron activity allowed researchers to analyze how activity in one region affects the other during the formation of emotional memories. The emotional memory task involved the participants viewing both neutral and emotional scenes and then performing a recognition memory task for the shown events.

What did they find?

Across both cohorts, the authors found that recall was enhanced for the emotional stimuli compared to the neutral stimuli. First, the authors looked at the brain activity associated with successful recall in the amygdala and hippocampus separately. The encoding of emotional memories was associated with gamma activity in the amygdala. This high-frequency neural activity was not found for successful recall of neutral scenes. In the hippocampus, the authors found that gamma activity was associated with successful recall for both emotional and neutral events. Next, the authors examined how this activity was coupled during memory formation. It was found that the amygdala influenced hippocampal theta oscillations, leading to gamma activity and neuronal firing in the hippocampus. This relationship was correlated with the encoding of emotional visual stimuli. Theta oscillations were transmitted from the amygdala to the hippocampus during the presentation of emotional scenes.

What's the impact?

This study found that the formation of memories of emotional but not of neutral stimuli is dependent on the relationship between brain activity in the amygdala and hippocampus. Theta activity in the amygdala leads to subsequent gamma activity and neuronal firing in the hippocampus. This research suggests that theta burst stimulation in the amygdala could improve memory.

Access the original scientific publication here