The Impact of Mechanisms on Stereotypes and Prejudice Formation

Social perception is complex and category processing occurs rapidly. Stereotypes are cognitive representations of various social groups. Prejudices are affective associations about these groups. A variety of mechanisms operating at different levels feed into the processes of racial perception, stereotyping and prejudice formation.

Intergroup bias is dynamically shaped through the interplay of multiple mechanisms that regulate perceived outgroup threats. The claims above will be explored through studying the effects of these different mechanisms on the processes underlying stereotyping and prejudice formation. The genetic mechanism that will be explored is the sensitivity of the serotonin transporter gene polymorphism 5-HTTLPR to threatening contexts.

The physiological mechanism of amygdala activation in response to viewing Black/White faces will also be examined. The environmental mechanisms that will be investigated are the contextual cues of outgroup threat such as negative prior contact with outgroups and other social cues such as attire. Finally, the interplay of these various mechanisms will be observed via the cyclical feedback effect of the environmental mechanism of stressful life events (SLES) on the genetic mechanism of 5-HTTLPR and on the physiological mechanism of the amygdala.

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5-HTTLPR is an important genetic mechanism that influences the process of stereotyping and prejudice formation. The experience of threat in intergroup bias is highly subjective. 5-HTTLPR is a functional polymorphism of the serotonin transporter gene SLC6A4 and is represented by two allele variants, short (S) or long (L), that reflect the length of the promoter region of SLC6A4.

The S-allele is less transcriptionally efficient and is associated with larger concentrations of serotonin remaining in the synaptic cleft as compared to the L-allele. The difference in the reuptake of serotonin is associated with variations in affective processing based on genotype. (Canli & Lesch, 2007).

Individuals with at least one S-allele (S/S or S/L) display a psychological phenotypic profile of heightened sensitivity to threatening contexts, supported by greater tendencies towards anxiety, vigilance and risk aversion. Thus, S-allele carriers are more likely to perceive higher levels of intergroup threat than L-allele carriers and consequently form stronger prejudices towards outgroups.

Significantly, polymorphic variations of 5-HTTLPR also affect neurodevelopment, which shapes the structure and function of brain regions critical for emotion processing such as the amygdala. Homberg, Schubert and Gaspar (2010) studied mice and rats that had been prenatally exposed to selective serotonin reuptake inhibitors (SSRIs), leading to increased extracellular serotonin levels, and found that the SSRIS caused alterations in the morphology of pyramidal neurons in the amygdala.

S-allele carriers of 5-HTTLPR show increased left amygdala activation in response to unpleasant stimuli compared to neutral stimuli. This is because S-allele carriers have smaller bilateral amygdala volumes and smaller volumes are associated with higher activations. Homberg et al. (2010) posit that 5-HTTLPR can exert an early neurodevelopmental influence on amygdala structure, which translates the polymorphic variations into endo-phenotypic amygdala reactivity. Thus, 5-HTTLPR influences the structure and functioning of the amygdala.

The amygdala furthermore influences the process of stereotyping. The perceived threat from outgroups is a consistent social-environmental antecedent of intergroup bias. Phelps, O'Connor, Cunningham, Funayama, Gatenby, Gore and Banaji (2000) used fMRI to observe amygdala activity in White American subjects in response to Black and White male faces with neutral expressions.

The experiments employed startle potentiation to indirectly indicate the emotional evaluation of the stimulus. The startle response is a defensive reflex, one component of which is an eye-blink response. (Lang, Bradley & Cuthbert, 1990) There was a strong correlation between amygdala activity and the potentiation of the eye-blink startle response to Black faces.

The implicit racial biases of the subjects were also evaluated using the Implicit Association Test (IAT) in which subjects had to categorize the faces as Black or White while simultaneously categorizing words as good or bad. The response time for the Black+good/White+bad pairing was longer compared to that for the Black+bad/White+good pairing.

There was also a significant correlation between bias in response time on the IAT and the strength of amygdala activation to Black-versus-White faces. Thus, we see how the physiological mechanism of the amygdala, influenced by the genetic mechanism of 5-HTTLPR, affects the process of stereotyping and prejudice formation.

Stereotyping and prejudice formation is also influenced by environmental mechanisms. One such mechanism is the quality of prior contact with outgroups. Pettigrew and Troop (2006) found that greater quality of prior outgroup contact is associated with higher levels of intergroup tolerance.

They defined intergroup contact as actual face-to-face interaction between members of clearly defined groups and performed meta-analyses on a number of such organized interactions. Results demonstrated that intergroup contact effects typically generalize beyond participants in the immediate contact situation. Not only do attitudes towards the immediate participants usually become more favorable but so do attitudes towards the entire outgroup, outgroup members in other situations and even outgroups not involved in the contact.

Social status cues shape race perception. A recent approach to person categorization views it as an ongoing process where both bottom-up facial cues and top-down stereotypical expectations interact over time to stabilize onto an ultimate categorization. (Freeman, Penner, Saperstein, Scheutz & Ambady 2011) One potential trigger of stereotypical expectations could be the contextual cues that often surround a face in the real world, such as attire. Freeman et al. (2011) designed experiments in which participants were instructed to categorize faces as White or Black as quickly and accurately as possible.

The faces varied along 13-point White-Black morph continua and were affixed to either high-status business attire or low-status janitor attire. Results demonstrated that low-status cues presented with a face increased the likelihood of Black categorization whereas high-status cues presented with a face increased the likelihood of White categorization. Further, such influences grew stronger as a face's race became more ambiguous. This work bolsters evidence that higher- order social cognition can constrain lower-order visual processes and furthers the perspective that social perception is driven by interplay between both biological (sensory) and environmental phenomena.

The different mechanisms outlined above do not operate independently of one another, but rather feed into and influence one another. Genotype predisposes individuals to experience more negative intergroup contact or have more dangerous perceptions of the environment, which may ultimately shape intergroup bias. S-allele carriers of 5-HTTLPR may be disposed to greater contextual sensitivity, tending to exhibit greater symptomatology of anxiety in response to stressful environments.

Conversely, this may also promote more positive affective and behavioral outcomes in the absence of stressful experiences or in the presence of positive experiences. (Pluess, Belsky, Way & Taylor, 2010) Thus, 5-HTTLPR reflects a differential susceptibility to the presence of environmental threats such that S-allele carriers exhibit higher or lower levels of threat-related psychological outcomes in response to negative or positive environments respectively, as compared to L-allele carriers. Not only do the allele variants of 5-HTTLPR influence social mechanisms, but are also in turn influenced by environmental factors.

Pluess et al. (2010) found that the magnitude of stressful life events (SLES) is positively correlated with higher levels of neuroticism between S-allele carriers, such that S-allele carriers display higher levels of neuroticism than L/L-allele carriers when experiencing high SLES, but also display lower levels of neuroticism than L/L-allele carriers when experiencing low SLES. Thus, exposure to negative intergroup contact is more likely to lead to bias against that outgroup in S-allele carriers than in L-allele carriers.

Such a loop exists in the case of the amygdala too. Vyas, Mitra, Shankaranarayana and Chattarji (2002) found that exposure to SLES caused the pyramidal and stellate neurons in the basolateral complex of the amygdala to exhibit enhanced dendritic arborization. Their findings point to the possibility that certain forms of chronic stress, by altering specific neuronal elements in the amygdala, may lead to behavioral manifestations of enhanced emotionality.

Essentially, stress-induced structural plasticity in the neurons of the amygdala may provide a candidate cellular substrate for heightened affective reactions triggered by SLES. This points to the possibility that certain individuals are more sensitive to social and contextual cues of stereotypes due to modified neuronal amygdaloidal components. Thus, environmental mechanisms influence the physiological mechanism of the amygdala and then subsequently environmental stimuli are processed differently as a result.

In conclusion, we see that the process of stereotyping and prejudice formation is influenced by various mechanisms such as 5-HTTLPR at the genetic level, the amygdala at the physiological level and mechanisms at the social level such as prior intergroup contact and contextual cues such as attire.

These mechanisms are not independent of each other but in fact dynamically interact with each other as seen through the cyclical way in which 5- HTTLPR and the amygdala and SLES influence each other. Future research should be directed towards examining how more primarily internal mechanisms at the genetic, physiological and neurological level interact with external mechanisms at the social and environmental level in order to contribute to the process of stereotyping and prejudice formation so that we can find external factors that can be controlled or manipulated to further reduce intergroup bias.

References

1. Canli, T. & Lesch, K.P. (2007) Long story short: the serotonin transporter in emotion regulation and social cognition. Nature Neuroscience, 10(9), 1103-1109.
2. Freeman, J.B., Penner, A.M., Saperstein, A., Scheutz, M. & Ambady, N. (2011) Looking the part: Social status cues shape race perception.
3. Public Library of Science, 6(9): e25107. Homberg, J.R., Schubert, D. & Gaspar, P. (2010) New perspectives on the neurodevelopmental effects of SSRIs.
4. Trends in Pharmacological Science, 31, 60-65. Lang, P.J., Bradley, M.M. & Cuthbert, B.N. (1990) Emotion, attention and the startle reflex.
5. Psychological Review, 97, 377-395.
6. Pettigrew, T.F. & Tropp, L.R. (2006) A meta-analytic test of intergroup contact theory. Journal of Personality and Social Psychology, 90(5), 751-783.
7. Phelps, E.A., O'Connor, K.J., Cunningham, W.A., Funayama, E.S., Gatenby, J.C., Gore, J.C. & Banaji, M.R. (2000) Performance on indirect measures of race evaluation predicts amygdala activation.
8. Journal of Cognitive Neuroscience, 12(5), 729-738. Pluess. M, Belsky, J., Way, B.M. & Taylor, S.E. (2010) 5-HTTLPR moderates effects of current life events on neuroticism: differential susceptibility to environmental influences.
9. Progress in Neuro-psychopharmacology & Biological Psychiatry, 34(6), 1070-1074. Vyas, A., Mitra, R., Shankaranarayana, R. & Chattarji, S. (2002) Chronic stress induces contrasting patterns of dendritic remodeling in hippocampal and amygdaloid neurons. Journal of Neuroscience, 22(15), 6810-6818.

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