Our social interactions are a large determinant of our quality of life.  Yet understanding how our brain produces social behaviors is a difficult feat.  Social behaviors require a panoply of different brain regions -- one key structure is the amygdala.  In my research, I use neurophysiological recordings to probe how the amygdala gives rise to social behaviors using naturalistic paradigms in a laboratory setting (Mosher et al. 2011).  Through this approach, we have discovered that neurons in the human and monkey amygdala preferentially respond when we see a face in a crowded scene (Minxha et al., 2017) or when we make eye-contact with another individual (Mosher et al., 2014).  In addition, the amygdala processes somatosensory feedback during the production of facial expressions, possibly to monitor the social signals we broadcast to the world (Mosher et al., 2016).  

How do we find a friend in a crowd?  How do we decide to make eye-contact with someone?   How does a smile communicate a feeling?


When we experience emotions, we often feel changes in our body -- our throats clench up, our mouths gets dry, our hearts beat faster.  But are these changes in our body necessary to feel emotions?  What if we didn't have bodies and were just brains floating in a jar, could we still feel happy?  This is a long outstanding question in neuroscience.  In my research I explore brain-body connections by recording neural activity simultaneously with the activity of the body.  While we have shown that emotional centers of the brain can trigger physical changes in the body (like making our palms sweat, Laine et al., 2009), identifying how the body might influence the brain is a more difficult challenge.  In my current work I'm examining how feedback from the heart influences cognition and emotional perception.

Why do our palms sweat when we're nervous?  Why do our hearts race when we're angry?  Can I feel emotions if I don't have a heart?


In my research on social interactions and emotions, I have the unique opportunity to record the activity of individual brain cells from neurosurgical patients.  In patients with epilepsy, we record electrophysiological signals to help identify the source of their seizures.  During surgery for Deep Brain Stimulation we record neurons of patients with Parkinson's Disease and other motor disorders.  In these cases, we are sometimes able to probe how changes in neural activity might be involved in neurological symptoms.  Recently we showed that, in patients with epilepsy, inter-ictal discharges disrupt the activity of neurons in the hippocampus and interfere with a patients ability to remember things (Reed et al., 2020).  In my current work, I'm probing how neurons in the subthalamic nucleus of patients with Parkinson's Disease stop ongoing motor plans.

Why do patients with epilepsy experience memory lapses? What causes sudden-unexpected-death-in-epilepsy?  How does a patient with Parkinson's Disease start and stop a movement?


© 2020 by Clayton P. Mosher