From the social-emotional brain session: how the word ‘fear’ can be misleading, the role of oxytocin in bonding, and frontotemporal dementia.
Coming to Terms with Fear - Joseph LeDoux, New York University, New York, NY
At the Annual Meeting of the American Neurological Association, Joseph LeDoux, PhD opened Tuesday morning’s session, The Social-Emotional Brain: from Neurobiology to Neurological Disease, by discussing the importance of terminology, specifically fear, when presenting research. “As a neuroscientist I try to understand how a structure, like the amygdala itself with synapses, connects a threat to a bodily response without having to introduce the concept of ‘fear’ at all. . .Rather than thinking of the amygdala circuitry being involved with fear, we can instead talk about it more neutrally, in terms of threat detection and response. . .this doesn’t mean fear is an irrelevant construct, it’s just not what’s causing the behavioral or physiological responses in so-called nerve conditioning.”
“While mechanisms that detect and respond to threats contribute indirectly to conscious feelings of fear, they are not the same as those that give rise to conscious fear. This is an important distinction since symptoms based on conscious and non-conscious processes may be vulnerable to different predisposing factors and may also be treatable with different therapeutic approaches in people who suffer from uncontrolled fear or anxiety.”
LeDoux cited studies on anti-anxiety drugs as an example. “If mice are given the drug and spend more time in the open area of an open field test, the idea is that the animal is less timid and therefore less anxious and therefore people should be less anxious when you give them the drug. But this isn’t working very well. The drugs are not making people less anxious, but what are they doing? If you give a patient with social anxiety disorder an SSRI, the patient might be more likely to go to a party, but still feel anxious while they’re there. So, the drug is actually a success. It’s doing exactly what it did in the animals – making the person less timid, but just not making them less anxious.”
“So we need a concept in fear and anxiety that recognizes these innate circuits but actually doesn’t confuse these circuits. . .The anti-anxiety medications are having their effects on behavioral timidity by working subcortically, but not having their effects on fear and anxiety because they’re not targeting the right circuits.”
Neuroscience of Social Bonding & Empathy - Larry Young, Emory University School of Medicine, Atlanta, GA
Larry Young, PhD spoke about the role of oxytocin in social bonding and empathy. He studied prairie voles, which are monogamous animals, to look at the neurobiology and genetic mechanisms of social behaviors like pair bonding and empathy behaviors.
Compared to rats, prairie voles have a much more precise response to social clues. For mating, male rats show a preference for female rats, but prairie voles bond with a specific partner. “In prairie voles, oxytocin links the neural encoding of the social signature of the partner with the rewarding aspects of mating through interactions with dopamine and by coordinating communication across a neural network linking social information with reward.”
Young discussed a study where pups were placed in isolation for a period of time. When the pups became adults, those with more oxytocin receptors in the striatum were able to form bonds, but those with naturally lower levels of receptors were not.
In a study, Young and his group removed a female and subjected her to mild stress before returning her to the group. “Prairie voles show a very robust response to a familiar individual being in distress. They go up to that individual and engage in a lot of grooming behavior. We’ve seen that that grooming behavior reduces cortisol, or anxiety, in the individual.” They show this response to a mate or a sibling, but not to an unfamiliar vole, which suggests this response is related to empathy. If an oxytocin antagonist was injected into the anterior cingulate cortex of the animals, they did not engage in this consoling behavior.
“In humans, intranasal oxytocin enhances eye gaze into the eyes of others, the ability to infer the emotions of others from facial clues, empathy, and socially reinforced learning. Thus the oxytocin system may be a viable target for drugs to improve social functioning in autism.”
Socioemotional Disruption in Frontotemporal Dementia - Virginia Sturm, University of California, San Francisco, San Francisco, CA
Virginia Sturm, PhD presented her research on behavioral variant frontotemporal dementia (bvFTD). A clinical subtype of frontotemporal dementia, bvFTD, targets brain regions that support emotion generation and resting autonomic physiology. “Two of the symptoms, apathy and loss of sincere empathy, really highlight the emotional changes that are hallmark features of this disease.”
“In our research, we use a laboratory-based approach to assess emotional reactivity, empathy, and emotion regulation in patients with FTD and Alzheimer disease.”
“As you heard earlier from Dr. LeDoux’s talk, there’s a lot of discussion about what emotions are and what they are not. In our perspective, in humans we think it’s helpful to think of emotions as multisystem responses that include both psychological and physiological components. When you experience an emotion, certain thoughts become more salient in your mind, certain actions may become more readily available, and physiologically there are certain kinds of changes that occur and accompany an emotional response, both in facial expressions and in the body.”
Sturm and her group conducted a study, which they called the ‘karaoke test,’ where participants were asked to sing a song and then later, without warning, were shown a video of themselves singing. Coders unfamiliar with the trial noted the participants’ autonomic reactivity while watching themselves sing. Sturm showed clips of this and other studies to illustrate the emotional reactions of controls and patients with Alzheimer disease that could be seen through facial expressions versus the limited or non-existent facial expressions of patients with FTD.
“This was the general finding – patients with FTD don’t show lower negative emotions of other kinds on their face. They show sadness, anger, or disgust, but they really don’t show embarrassment – that self-conscious reaction – that controls do.”
“To summarize, I hope I’ve convinced you that you can measure emotion generation and emotion dysfunction objectively in a laboratory setting and that these measures do reflect measures of neural integrity. In bvFTD, it’s not that all emotions are equally vulnerable, it seems to be that certain emotions are more vulnerable than others. Embarrassment and disgust seem to be two of those emotions and emotional empathy also seems to be inherent. This reflects the fact that these kinds of responses do depend on key hubs in the emotion generation system. In the case of bvFTD, in order to make progress in this field, we might need to use less standard approaches like laboratory methods from affective science in order to really hone in on the areas of impairment in the patients. I think this is important not only for understanding the circuitry of bvFTD but also for really understanding the neurological basis of affective symptoms that are shared across numerous psychiatric and neurologic disorders.”
From the Annual Meeting of the American Neurological Association. The Social-Emotional Brain: from Neurobiology to Neurological Disease session. Baltimore, MD. October 18, 2016.