Accents and Confidence Modulate Brain Activity during Speech Perception

Post by: Shireen Parimoo

What's the science?

In-group favoritism refers to people’s tendency to hold more positive views about members of their own social group compared to members of an out-group. Accents act as indicators of social belonging, and a speaker’s voice also conveys information about their trustworthiness; they are more likely to be believed when their tone is confident rather than doubtful. We don’t know how voice-based perception of a speaker is processed in the brain and how level of confidence may influence the perception of an out-group speaker. This week in NeuroImage, Jiang and colleagues investigated patterns of brain activity in participants listening to in-group and out-group speakers with different accents and varying degrees of confidence.

How did they do it?

Twenty-six young adults listened to and rated the believability of English statements spoken in their native accent (Canadian-English; in-group), in a regional accent (Québécois-French; out-group/regional), and in a foreign accent (Australian; out-group/foreign). The statements also varied in whether they sounded confident, neutral, or doubtful. Participants rated how intelligible each accent sounded to them and how much they liked each accent. Neural activity was recorded using functional magnetic resonance imaging (fMRI) to understand whether in-group and out-group accents differentially activated the brain while participants judged believability. The authors used psycho-physiological interaction (PPI) analysis to determine if activity in regions involved in confidence judgments, such as the right superior temporal gyrus and the inferior frontal gyrus, was correlated with activity in other brain regions while participants made believability judgments. Finally, they examined whether these functional connections in the brain were modulated by the speaker’s accent.

What did they find?

Overall, participants were more likely to believe statements spoken in their native accent than those spoken in a regional or foreign accent. Listening to speakers with out-group accents activated temporal regions of the brain (e.g. superior temporal gyrus), whereas listening to in-group accents activated frontal regions (e.g. superior frontal gyrus). Participants also rated neutral and confidently spoken statements as more believable than doubtful statements; statement confidence was related to increased activity in the superior temporal gyrus, while statements made in a doubtful voice were associated with greater activation of temporal areas. Although confident statements were rated as equally believable across all accents, brain activity was greater in the caudate, cuneus, and fusiform regions when confident statements were heard in out-group accents. This could be because judging the believability of out-group speakers requires more in-depth processing of the vocal and acoustic characteristics of speech. PPI analysis revealed that listening to out-group accents resulted in increased connectivity between regions involved in decoding confidence – such as the superior temporal gyrus – and regions involved in inferring meaning of sentences, such as the inferior frontal gyrus. Statement believability was associated with greater connectivity between the superior temporal gyrus and the middle temporal gyrus and between the superior temporal gyrus and the lingual gyrus/middle occipital gyrus when listening to out-group speakers. These findings suggest that neural activity associated with processing voice characteristics and associated biases towards out-group speakers can be modified by the level of confidence of the speaker.

                                     Brain, Servier Medical Art, image by BrainPost, CC BY-SA 3.0

What's the impact?

The study demonstrates how distinct neural mechanisms are involved in carrying out the same decision-making process in speech perception depending on the speaker’s accent and degree of confidence. These results provide a deeper understanding of how different regions of the brain are involved in categorizing speakers based on group membership, and the effect this has on social inference from speech.

Jiang et al. Neural architecture underlying person perception from in-group and out-group voices. NeuroImage. 2018.  Access the original scientific publication here.

The Effects of Maternal Cortisol on the Amygdala and Internalizing Behaviours

What's the science?

Cortisol is a hormone involved in the body’s physical and psychological stress response. During pregnancy, the hormone can reach the neonate either directly or via fetal corticotropin-releasing hormone. Some cortisol is critical for fetal brain development, but abnormal levels are associated with psychiatric disorders in offspring. The amygdala is a brain region that has many cortisol receptors, and in animal models, high levels of maternal cortisol have been found to result in high negative emotion and stress reactivity in offspring. Sex differences in the effects of maternal cortisol have also been found; negative emotionality may be more likely to be present in female offspring. This week in Biological Psychiatry, Graham and colleagues assessed the effects of in utero cortisol exposure on the amygdala shortly after birth.

How did they do it?

A total of 70 mother-infant dyads participated in the study. Each mother collected 5 saliva samples of cortisol over the course of a day for a 4 day period during each of her 3 trimesters of pregnancy (60 samples per mother total). The area under the curve (similar to assessing overall cortisol output) was calculated for each trimester, resulting in reliable indicators of cortisol levels representative of each of the three trimesters. These values were also log-transformed for normalization purposes. Infants underwent brain functional magnetic resonance imaging (fMRI) at 4 weeks of age. Resting state functional connectivity (a measure of the synchrony of brain activity at rest) was calculated between the right and left amygdala and the rest of the brain, and the relationship between maternal cortisol and these connections was assessed. At 24 months of age, mothers reported on their child's internalizing behavior (e.g. depression or anxiety symptoms) using the Internalizing Behavior Scale of the Children's Behavioral Checklist.

What did they find?

There was an interaction between sex and maternal cortisol in predicting connectivity between the bilateral amygdala and the left supramarginal gyrus and superior temporal gyrus. Probing the interaction revealed that in females, amygdala connectivity with the aforementioned cortical regions was generally stronger with higher maternal cortisol, while it was weaker in males. The results suggest that the relationships between cortisol and connectivity of the amygdala to various regions of the cortex were opposite for males versus females. Further, connectivity between the right amygdala and the supramarginal gyrus was positively correlated with internalizing behaviour in children (not dependent on sex). This association remained even after considering levels of maternal depressive symptoms, another important potential influence on child internalizing behavior. Upon mediation analysis, the authors found that connectivity between the right amygdala and supramarginal gyrus mediated the relationship between maternal cortisol and child internalizing. Therefore, cortisol exposure during pregnancy is associated with higher internalizing behaviors in females through a pathway involving stronger right amygdala connectivity.

What's the impact?

Cortisol levels have been assessed in utero in animals models and at single time points during pregnancy in humans. However, this is the first study to demonstrate a relationship between connectivity of amygdala and maternal cortisol (which differs by sex) using a robust measure for cortisol levels over multiple key time points. The results suggest that this hormone involved in the stress response may alter integration of the amygdala with cortical brain regions during an early phase of brain development.

Graham et al., Maternal Cortisol Concentrations During Pregnancy and Sex Specific Associations with Neonatal Amygdala Connectivity and Emerging Internalizing Behaviors. Biological Psychiatry (2018). Access the original scientific publication here.

Autoregulatory Gene Therapy as a Treatment for Focal Epilepsy

What's the science?

Patients with epilepsy often do not respond to anti-epileptic drugs and continue to experience seizures. Drug-resistance is especially common when seizures arise from a specific region of the brain (focal epilepsy). Further, anti-epileptic drugs are not selective for the neurons which cause seizures. Viral mediated gene therapy, where new DNA is carried by a viral vector and inserted into cells, could potentially be used to selectively modify neuron populations that cause seizures. Gene therapy has shown promise in animal models; however, most therapies have been irreversible. This week in Nature Medicine, Lieb and colleagues use an autoregulating viral-mediated gene therapy treatment in rats to test whether it is tolerated and reduces seizures.

How did they do it?

They designed a viral plasmid containing a gene encoding a glutamate-gated chloride channel that detects excessive glutamate (an excitatory neurotransmitter) release from neurons and inhibits neurons in a self-regulating manner. Glutamate release is increased in epilepsy resulting in heightened neural activity, so inhibiting this process can reduce seizures. Adult rats were injected with pilocarpine, a seizure inducing drug, before injection of the viral vector containing the glutamate sensitive channel or a control vector, and then again two weeks later. Both of these were administered to the primary motor cortex of the rats. An electrode was also placed in the motor cortex to record the electroencephalogram (EEG) to detect seizure activity. Comparing the effect of pilocarpine before and after treatment revealed the effect of gene therapy on seizure activity. They then tested the effect of gene therapy on a model of chronic focal epilepsy where seizures occur spontaneously for several weeks after injecting tetanus toxin into the visual cortex of rats. They did this by comparing the frequency of seizures before and after treatment. Finally, they performed a series of behavioral experiments to test whether motor coordination was altered by the gene therapy treatment administered to the primary motor cortex (i.e. whether it was well tolerated).

What did they find?

Rats injected with the viral DNA encoding the glutamate sensitive channel showed a reduction in frequency and amplitude of seizure-related activity (induced by pilocarpine in the motor cortex), when compared to rats injected with the control virus. The frequency of spontaneous seizures was also reduced after introducing the glutamate sensitive channel in a chronic model of focal epilepsy. However, there was no effect on seizure duration or intensity in the chronic epilepsy model, or on the background EEG. These results suggest that the gene therapy was effective in inhibiting both pilocarpine-evoked seizure-related activity and the number of spontaneous seizures in a chronic focal seizure model. After testing for effects of gene therapy on motor coordination, there was no difference between control rats and those rats treated with the viral injection of the glutamate sensitive channel, demonstrating that the gene therapy was well tolerated.

What's the impact?

This is the first study to demonstrate how gene therapy can be used to express an autoregulating channel that responds to excessive glutamate release to reduce seizures. This gene therapy was well-tolerated and able to inhibit neurons to reduce seizure related activity and reduce the number of seizures in a chronic model of focal epilepsy. This study shows that gene therapy could potentially be used to apply selective treatment to specific brain regions causing seizures. Further research will be needed to ensure that this gene therapy can be well tolerated in humans.

Lieb et al., Biochemical autoregulatory gene therapy for focal epilepsy. Nature Medicine (2018). Access the original scientific publication here.