The Other-Race Effect (ORE) Across Development

Greg Reynolds and Kelly Roth have conducted ample research on facial processing in infancy as we learned from the talk on “The development of attentional biases for faces in infancy: A developmental systems perspective” (Reynolds & Roth, 2018). As the title suggests, this work reviewed the development of different attentional biases found in facial processing in infancy, from preferences for faces over objects, human faces over other-species faces, mother’s faces over other faces, female faces over male faces, and same-race faces over other-race faces. Of particular importance in today’s society is the development of racial categorization in facial processing. The other-race effect, or ORE, specifically refers to a “disadvantage for processing and recognizing individual exemplars of other-race faces in comparison to own-race faces” (Reynolds & Roth, 2018). The ORE develops early in infancy, albeit weakly: 3-month-olds show evidence of the ORE, yet it is relatively easily extinguished with exposure to other-race faces. However, from 3 to 9 months, the ORE increases and is not so easily diminished (Reynolds & Roth, 2018). Interestingly and pointedly, the ORE develops before the other-species effect (OSE). The OSE details a preference in facial processing for human faces over those of other species; it does not fully develop until 6 to 9 months. The ORE and OSE are examples of perceptual narrowing – a “developmental process that occurs as infants gain extensive experience with stimuli specific to their native environment” (Reynolds & Roth, 2018). This raises the question does perceptual narrowing in infancy allow for sub-divisions in other-race categorization (e.g. Black vs Asian faces), or is it a broader categorization, such as own-race vs. all other races?

Quinn and colleagues set out to answer this question in their article “Narrowing in categorical responding to other-race face classes by infants” (Quinn, Lee, Pascalis, & Tanaka, 2016). Using a familiarization/novelty-preference procedure, they found that the ORE differentially allows for sub-categorization across development. 6-month-old Caucasian infants formed a preference for White faces over Black and Asian faces, yet they maintained distinct categories of Black vs Asian faces. However, 9-month-old Caucasian infants lost the distinction between other-race faces (Quinn et al., 2016). This is consistent with previous findings that the ORE, while present at 3-months, strengthens from 6- to 9-months (Reynolds and Roth, 2018). Clearly the ORE represents an unconscious attentional bias, but it is important to note that the ORE is easily avoided with early dynamic exposure to other-race faces, such as in-person interaction or diverse picture books (Reynolds & Roth, 2018). It is likely that the lack of distinct racial categorization would also fail to manifest if exposure to other-race faces was increased in infancy.

Works Cited: 

Reynolds, G., Roth, K. “The development of attentional biases for faces in infancy: A developmental systems perspective.” Frontiers in Psychology, vol. 9, no. 222, 2018, pp. 1-16., doi:10.3389/fpsyg.2018.00222.

Quinn, P., Lee, K., Pascalis, O., Tanaka, J. “Narrowing in categorical responding to other-race face classes by infants.” Developmental Science, vol. 19, no. 3, 2016, pp. 362-371, doi:10.1111/desc.12301.

Neuromodulation of Aggressiveness in Violent Offenders

In a 2019 study published in the journal Neuroscience, Andrés Molero-Chamizo of the University of Huelva, Spain acted as the lead researcher examining the effects of anodal transcranial direct current stimulation (tDCS) on self-reported aggressiveness in prisoners with violent offenses. tDCS is a non-invasive, painless form of neurostimulation in which electrodes placed on the head deliver a low-intensity electrical current to a specific part of the brain. Anodal tDCS refers to the excitation of neuronal activity, whereas cathodal tDCS inhibits neuronal activity. In this particular study, Molero-Chamizo and his team of researchers applied anodal tDCS stimulation bilaterally to the prefrontal cortex. They chose to activate this area of the brain because reduced activity in the prefrontal cortex has been associated with aggression and violence. The researchers split their 41 male participants into two groups: 15 murderers and 26 non-murderers. The researchers had the participants fill out the Buss-Perry Aggression Questionnaire (BAQ) before and after their tDCS treatments. The questionnaire asks participants how much they agree with statements such as, “Sometimes I fly off the handle for no good reason.” The tDCS was applied for 15 minutes per day for three consecutive days. After the treatment, both inmate groups displayed a reduction in their self-perceived aggression. The BAQ evaluates four dimensions of aggression: anger, hostility, verbal aggression, and physical aggression. Aside from the non-murderer group failing to show a significant reduction in hostility, both groups displayed significant reductions in all dimensions of aggression.

Molero-Chamizo plans to follow up this study with one that includes a few improvements to the procedure in order to address some of the limitations from the first study. The initial study was only single-blinded and the control group consisted of prisoners that received no tDCS. For the following study, Molero Chamizo plans to include the university’s psychology students in the participant pool as well as acquiring saliva samples to measure cortisol levels before and after the tDCS treatment. Cortisol is an indicator of stress and could possibly suggest some aspect of aggressiveness. He also aims to examine the long-term effects of this particular type of tDCS treatment.

Both Andrés Molero-Chamizo and Joe Vukov’s work present two different aspects of neuromodulation.  The article by Molly J. Crockett that the class read in preparation for Joe Vukov’s talk deals with the question of how brain chemistry affects morality. Throughout her essay, she presents evidence indicating that our moral judgements are not fixed, but malleable. Although we typically view our moral judgements as inherently personal, distinctive, and indicative of who we are as people, they are often affected by neuromodulator levels, stress, hunger, and so forth. Joe Vukov’s presentation dealt with very similar questions. Although we see our moral intuitions as intrinsic, inborn elements of ourselves, they are undoubtedly shaped and cultivated by our particular upbringing. It’s easy to imagine that you’d have very different political or religious beliefs depending on what part of the world you were born in or to what type of parents you were brought up with, even though we see our political and religious beliefs as a reflection of our moral character. Following the same path, Molero-Chamizo’s work provides a more concrete example that morality is not fixed. Reducing aggressiveness certainly does not entail moral goodness, but this study does have an underlying goal of finding a possible avenue for reducing instances of violent crime, which is embedded in morality.

This type of work can have major implications. Societies are structured around a shared moral code, but we are now finding evidence that our moral intuitions can be tinkered with. Research such as this brings with it a collection of ethical questions regarding neuromodulators’ effect on moral judgments and whether it should be permissible to dabble with another’s moral inclinations.

Links: 

https://www.sciencedirect.com/science/article/abs/pii/S0306452218307498

https://www.vox.com/future-perfect/2019/3/9/18256821/prisoner-brain-study-spain-aggression-neurointervention-ethics

Sleep enhances memory consolidation

We currently live in a sleep-deprived society, due to stressful jobs, irregular working shifts etc. that can lead to hippocampal function and memory impairments. Scientists Ralitsa Todorova and Michaël Zugaro at the Collège de France focus on the importance of sleep and its great impact on stabilizing our memories while we sleep. The hippocampus during active periods of sleep has the capacity to spontaneously reactivate itself and transmit information to the cortex for memory consolidation. They focused on the silence period during sleep of rats’ brains that emitted delta waves in which a small group of neurons that were involved when the spatial memory task took place and remained active and isolated for long-term memory formation. During the period in which the hippocampus was reactivating memory traces to the cortex it was also determining the group of active neurons of the delta waves that reorganized the cortical circuits for long-term memory and allowed rats to do well at the spatial task.

Scientists know now that sleep is essential for memory consolidation and it involves reactivation of memory traces, however, the neurocognitive mechanisms of that process are still unknown. Eitan Schechtman et al. from the Department of Psychology at Northwestern University has been studying sleep-related reactivation with TMR (targeted memory reactivation) by presenting subjects after a spatial-memory task with auditory cues (for some sets of items) during sleep that enhanced their memory compared to the non-cue items. They concluded that the neural mechanism for the auditory cue items with TMR led to the reactivation of multiple memory items concurrently in parallel and individualistically in humans’ brains to enhance their memory.

In conclusion, these findings emphasize the importance of sleep to positively impact the neuronal connectivity in the brain for memory consolidation Scientists have shown that the tool TMR has the potential to enhance memory consolidation. There are new studies arising with the use of TMR during sleep with the hope to use it as a beneficial method for example for children to improve their school performance.

Works cited:

Schechtman, E., Antony, J. W., Lampe, A., Wilson, B. J., Norman, K. A., & Paller, K. A. (2019). Multiple memories can be simultaneously reactivated during sleep as effectively as a single memory. doi: 10.1101/662015

CNRS. (2019, October 18). A new discovery: How our memories stabilize while we sleep. ScienceDaily. Retrieved November 26, 2019 from www.sciencedaily.com/releases/2019/10/191018125514.htm

Fear, Anxiety & PTSD: Neural Mechanisms Enhanced Through Fear-Leaning

Fear, Anxiety & PTSD: Neural Mechanisms Enhanced Through Fear-Leaning

            According to the National Center for Post-Traumatic Stress Disorder (PTSD), 7-8 out of every 100 people will have PTSD at some point in their lives. On October 22^nd 2019, Dr. Michael Fanselow, a distinguished professor and researcher at the University of California, Los Angeles, presented on his continuing research over the “Neurobehavioral perspectives on the distinction between fear and anxiety” (2015) and “Induction and Expression of Fear Sensitization Caused by Acute Traumatic Stress” (2016), wherein he explores what happens in a single traumatic experience that causes lifelong symptoms characterizing PTSD. Dr. Fanselow reported that 10-20% of individuals exposed to traumatic events would go on to develop symptoms of PTSD. Some important symptoms of PTSD include fear and avoidance of things associated with an event, persistence of this fear for at least 30 after the event has taken place, high rates of symptoms presenting along with other anxiety disorders and/or substance abuse, increased propensity acquire new phobias, resistance to exposure and extinction therapy, increased arousal, and exaggerated response to startling stimuli.

            Fear is generally thought of in an associative way, and the quintessential model of this type of fear learning is Pavlovian conditioning. Classic Pavlovian fear conditioning is characterized by cues presented at the time of trauma provoking fear memories and responses. Dr. Fanselow emphasized that the main focus of current biobehavioral research is to treat PTSD with extinction and exposure therapy. However, as previously stated, a major component of PTSD is that individuals become more resistant to this kind of therapy. Dr. Fanselow’s research takes on a new approach to possible treatments of PTSD by considering how a non-associative model called stress-enhanced fear learning (SEFL). This model is not bound by the cues that are specifically associated with the traumatic event, advancing the hypothesis that many symptoms of PTSD are derived from a form of sensitization rather than the context of the trauma.

By evaluating new neurobiological mechanisms associated with more sensitized, or heightened, behavioral responses, Dr. Fanselow and colleagues suggest that targeting certain neural components of this fear response pathway in order to better treat PTSD. Given the results of his study, Dr. Fanselow suggests blocking a steroid hormone glucocorticoid receptors in the brain’s fear center, or amygdala, would be effective in preventing the negative effects of stress-enhanced fear learning.

            An article published by Neuroscience News entitled “PTSD has strong genetic component like other psychiatric disorders” explores other biological mechanisms explaining persisting PTSD symptoms. This article presents a collaborative study done among scientists from the University of California San Diego School of Medicine, the Psychiatric Genomics Consortium’s PTSD working group, and a non-profit organization called Cohen Veterans Bioscience. Researchers used these global collaborations to recruit thousands of participants suffering from PTSD as well as a control group from a variety of backgrounds and a wide range of neuro-diversity. The long-term goal that researchers hoped to achieve was to "develop tools that might help clinicians predict who is at greatest risk for PTSD and personalize treatment approaches." The study assessed the genomes, in an approach referred to as a genome-wide association study (GWAS), of these participants and found that there were consistent DNA markers associated with being at higher risk for developing PTSD.

            The findings of this study suggest that there may be a way to assess individuals who are at high risk for developing PTSD and provide them with proactive treatments, such as encouraging therapy at an early age so as to lower the risk of developing PTSD if they are faced with a traumatic event.

            Both in the study showing PTSD to be linked to genetics and Dr. Fanselow’s research, we see how important it is to explore the mechanisms of PTSD in different ways in order to provide the best treatment to those who suffer the symptoms. Although there is much work to be done in order to truly understand the neural and biological basis of PTSD, these studies are important gateways into more individualized treatment from an illness that so many people suffer from in their lifetimes.

Dr Fanselow’s Research:

Perusini, J.N., Meyer, E.M., Long, V.A., Rau, V., Nocera N., Avershal, J., Maksymetz, J., Spigelman, I., & Fanselow, M.S. (2016) Induction and Expression of Fear Sensitization Caused by Acure Traumatic Stress. Neuropsychopharmacology, 41, 45-57. PMC4677128

Perusini, J.N., & Fanselow, M.S. (2015) Neurobehavioral perspectives on the distinction between fear and anxiety. Learning and Memory, 22, 417-425. PMC4561408

PTSD Article:

Buschman, H. (2019, October 9) PTSD has strong genetic component like other psychiatric disorders. Neuroscience News, Retrieved from https://neurosciencenews.com/ptsd-genetics-15048/

Depression's Impact on the Individual and Societal Level

          It is all too common to hear loads of numbers being thrown out on the news and in academia discussing the increasing rates of depression. Many people claim to have the answers—just drink more water, make sure to exercise, delete all social media—but these solutions cannot seem to make a dent in the number of those suffering from these disorders. Different medications and forms of therapy are known to provide aide to certain individuals, but this is not a problem with a one-size-fits-all solution. Continuing research in discovering ways to reduce the growing numbers of those diagnosed with depression is crucial alongside understanding the impact this disorder can have on an individual’s life.  

            Professor Vukov highlighted the work of Molly J. Crockett in understanding neurochemical modulation of moral judgment and behavior. Crockett focused on the effects of modulating serotonin specifically in her work. In the first experiment, one group of participants were given citalopram (blocks serotonin reuptake) or atomoxetine (a noradrenaline reuptake inhibitor) or a placebo. The researchers found that in personal moral scenarios, citalopram increased harm aversion. In the next study, the researchers examined how serotonin impacts views of fairness. They blocked serotonin with tryptophan which caused increased rejection of unfair offers in an ultimatum game. Citalopram reduced the rejection of unfair offers. In a third study, the team sound that depleting serotonin increases costly punishment behaviors and made fairness goals less salient. Overall, the pattern of results suggests that serotonin depletion decreased the value of social exchange and increased the value of revenge.  

            These results demonstrating effects of neurochemical manipulations on morality may have potential normative implications. The researchers showed that moral judgments and decisions are sensitive to fluctuations in brain chemistry. However, certain moral judgments appear to be more sensitive to nonnormative factors than others. For example, making judgments about physical harms change more depending on serotonin levels compared to more impersonal or indirect harm situations. The power of this neuromodulation is also affected by individual differences such as variations in empathy. This is explained given how genotypic variability affects how one’s nervous system reacts to changes in neurotransmitter levels. Therefore, moral judgments are not fixed but are contingent on neuromodulator levels. This raises the question of the possible impact of depression on morality.

            Looking at data from two annual college undergraduate surveys from 2007 to 2018 by Duffy and colleagues, researchers found a board worsening of mental health indicators including depression and anxiety. The data suggests that something shifted around 2012 or 2013. Some speculate that this was around the time that smartphones and social media switched from being optional to mandatory among adolescents. Matching the survey data, university counseling centers have been reporting increases in the students’ utilization of campus mental health services. However, it is impossible to know if this was driven by more students in need seeking help or actual increases in the number of students with poor mental health. The study was not designed to determine the causes of increasing mental health issues but instead to just make public the prevalence of this issue.

            Data demonstrating the increasing frequency of young adults with depression being placed alongside the possible moral implications that come with serotonin depletion lay the groundwork for a quite harmful epidemic. Both articles highlight just how crucial mental health reform is now. With more individuals diagnosed with depression every year, the influence on societal morality will likely follow the same trend. Crockett’s work coupled with Duffy’s survey analysis point toward the necessity of continued research. Duffy’s work outlines the size of the issue while Crockett’s research highlights the influence depression can have on the individual. Connecting the individual burden with the large-scale numbers exemplifies the societal burden. Comprehending the societal consequences of depression is the first step of finding the solution. Crockett and Duffy’s work provide a necessary move in the right direction.

Works Cited

Crockett, Molly J. “Morphing Morals.” Moral Brains, 2016, pp. 237–245.,

doi:10.1093/acprof:oso/9780199357666.003.0011.

Duffy, Mary E., et al. “Trends in Mood and Anxiety Symptoms and Suicide-Related Outcomes

Among U.S. Undergraduates, 2007–2018: Evidence From Two National Surveys.”

Journal of Adolescent Health, vol. 65, no. 5, 2019, pp. 590–598.,

doi:10.1016/j.jadohealth.2019.04.033.

Vulnerability to Depression in Youth: Advances From Affective Neuroscience

Depression is one of the most common psychiatric disorders to date. In the U.S. alone rates of depression have risen from 6.6 percent in 2005 to 7.3 percent in 2015. The Most significant findings of this increase over the span of those 10 years is the rise in adolescents and young adults. People aged 12 to 17 saw an increase from 8.7 percent to 12.7 percent from 2005 to 2015. With this knowledge in mind Kujawa and Burkhouse began to investigate further about the vulnerability of adolescents to depression and tried to find tests to find attributes that were present in youth that increased the development of depression. 

This study took into account family history, child’s temperament, as well as different affective neuroscience tests to identify what attributes made youth higher at risk and what increased their likelihood of developing depression. In order to get the best results they used both high and low risk youth. They deemed that children with a history of depression in their family we’re at higher risk than those whose family had no prior history of depression. Other indicators of depression development in youth are negative and positive emotionality. It is found that for negative emotionality which is characterized by sadness,irritability and anxiety tends to be the greater indicator of the two. While positive emotionality which is characterized by positive affect, sociability and appetitive behavior was shown to be less indicative of depression development. This study found that high risk youth demonstrated an altered neural response to both negative and positive stimuli. It is important to note that these were observed prior to the onset of the disorder. In addition evidence showed that youth’s depression risk was defined by deficits in approach motivation and positive valence systems, which includes reduced ERP and striatal responses to reward. This in combination with blunted emotional responses may act as a vulnerability for depression especially when in combination with life stress, increased tendency to withdraw and failure to readjust behavior in order to increase positive reinforcement.

Lastly it was observed that those at higher risk showed blunted reactivity to negative images and emotional disengagement. In addition to this, those at high risk showed greater amygdala activity when presented with threatening emotional faces. 

While there is an exorbitant amount of research into what may be a predictor of depression onset there has not been many efficacious studies into preventions or treatments of depression. Currently, even the drug therapies on the market are not as efficacious in the treatment of depression. This becomes especially true in regards to youth and young adults. Dr. Lauren Shapiro who presented her research on the possibility of inhibiting ROCK as a form of antidepressant treatment in yout, discussed this fact in greater detail. She mentioned that most if not all current drug therapies (especially SSRIs) are cautiously given to youth and young adults, anyone under the age of 25, because they have been shown to increase the symptoms of depression such as suicidal ideations and negative mood. This is one of the reasons she listed as to why she began doing research into ROCK inhibition in adolescent mice. Although her research was only founded on efficacy in mice there was evidence that suggests it may have similar effects in humans. 

It is important to be aware of what may predispose adolescents to the onset of depression as demonstrated by the research done by Kujawa and Burkhouse. But as Dr. Shapiro said we need to use this research to conduct more research into the development of efficacious prevention and drug therapies. Now that adolescent depression is on the rise, preventative measures should be included in youth health. It is pertinent that medical doctors include at risk questionnaires/intakes as well as provide information to the child’s parents on what signs to watch for and what they can do to help their child develop emotionally healthy behaviors. Along with giving young adults resources and access to screenings for the presence of depression. While neurological clinical trials have not been invested in as of late because of their low efficacy it is important that something be done to reduce the rate of depression. Especially because of the proportional relationship between depression and suicide. As the depression rates rise in the youth and young adult so does that of the suicide rates.

Works Cited 

Kujawa, A., & Burkhouse, K. (2017). Vulnerability to Depression in Youth: Advances from Affective Neuroscience. Biological Psychiatry. Cognitive Neuroscience and Neuroimaging, 2(1), 28-37.

Shapiro, L., Kietzman, H., Guo, J., Rainnie, D., & Gourley, S. (2018). Rho-kinase inhibition has antidepressant-like efficacy and expedites dendritic spine pruning in adolescent mice. Neurobiology of Disease, 124, 520-530.

Antidepressants and Age: How Depression Medication Works Differently for Adolescents

The article “Teen Depression Treatment Is an Increasingly Thorny Issue” describes the use of antidepressants and how their impact on children and adolescents is not always beneficial. Depression is quite common in teens, with about 11% of Americans ages 12-17 having had a major depressive episode in the past year. However, the Food and Drug Administration (FDA) has issued warnings for individuals under 25 years of age which state that antidepressants could increase suicidal ideations.

In the article, the author discusses the research done by Dr. Andrea Cipriani and her team at the University of Oxford. They tested 5,000 children and teens who were taking antidepressants. They found that only one medication, fluoxetine (commonly referred to as Prozac), improved their symptoms. As a result, the researchers believe that children and teens should begin depression treatment with quality psychotherapy rather than prescriptions right away. Their recommendations align with those of the American Psychological Association, which shows that this team is not the only one that has taken notice of the effects of antidepressants.

In her lecture on November 19, 2019, Dr. Lauren Shapiro spoke about the treatment struggle for adolescents experiencing depression. The reason that antidepressants work differently in children and in adults is due to the development of a brain area known as the prefrontal cortex. The prefrontal cortex is responsible for areas like personality, cognitive functioning, mood, social behavior, and decision-making. However, this important and complex brain area does not fully develop until 25 years of age – the exact age targeted in the FDA’s antidepressant warnings.

Dr. Shapiro’s research focuses on finding new ways to treat depression that stray away from antidepressants. She has found that a drug that inhibits a regulatory factor called Rho-kinase (ROCK) can lead to antidepressant-like effects in adolescent mice. This drug could be a step in the right direction towards future medications which might treat depression in those under 25 more effectively than common antidepressants.

Looking at the research of both Dr. Cipriani and Dr. Shapiro, one thing is clear: more work needs to be done in order to understand the impact of antidepressants on adolescent health and mental wellbeing. Before that work is done, it is critical that psychologists and psychiatrists take heed of the FDA’s warnings and strive to do what is best for their patients with the most updated research they can find.

Links

https://time.com/4361897/teen-depression-treatment-antidepressants/ https://www.dropbox.com/sh/13j3ka06799we8d/AACN7USeByJriNdkAoq8pHiNa/(11.19.19)%20-%20Lauren%20Shapiro?dl=0&preview=Shapiro+et+al+2019.pdf&subfolder_nav_tracking=1

References

Park, A. (2016, June 8). Antidepressants May Not Work Well Among Children and Teens. Retrieved from https://time.com/4361897/teen-depression-treatment-antidepressants/.

Shapiro, L. "A cytoskeletal based approach to understanding antidepressant-like mechanisms and depression-related behaviors." Neuroscience Seminar. Loyola University Chicago. 19 Nov. 2019.