Austin Coley, Ph.D.

Postdoctoral Fellow, Salk Institute

Austin Coley is a postdoctoral fellow in Kay Tye’s laboratory at the Salk Institute for Biological Studies. He received his bachelor’s degree in biology from North Carolina Central University and a master’s degree in cell physiology from Case Western Reserve University. He then received his Ph.D. in neuroscience from Drexel University under the mentorship of Wen-Jun Gao studying the synaptic proteins and mechanisms involved in schizophrenia. As a postdoctoral fellow in the Tye Lab he studies the effect of neural circuits on behavior and state-dependent and region-specific cellular aberrations implicated in neuropsychiatric conditions.

Project: Isolating condition-specific changes in mental health disorders

A critical issue within the mental health field is the lack of granularity in diagnostic practices. For example, a patient that is sleeping and eating too much may be prescribed the same antidepressant as a patient who is sleeping and eating too little. This may explain the low rates of efficacy for first-line antidepressants and begs further dissection. It also underscores the need to find more granularity within mental health conditions, which is the scientific vision of my research program.

As a scientific investigator, Coley applies integrative approaches such as in vivo two-photon calcium imaging to measure neural activity and population dynamics, and ex vivo electrophysiology to record synaptic properties. He utilizes optogenetics techniques to selectively activate neural circuits and assess the response within specific neurons. He also uses computer-based tracking systems to monitor behavioral tasks and apply machine learning methods to uncover the relationship between neural activity and behavior. Additionally, Coley uses theoretical and neurocomputational models to further understand neuronal population function in higher-order processing regions.

Currently, Coley studies anhedonia, described as the inability to experience pleasure or hedonic feelings. Anhedonia is linked to a dysregulation within the brain reward pathways that include the prefrontal cortex which is highly involved in emotional and valence processing, critical for encoding hedonic values. It remains unknown how specific neural substrates modulate mPFC valence-specific neuronal population activity during anhedonia.

Key questions remain that would elucidate how dysregulation in synaptic activity within select brain regions contributes to anhedonia. For instance, what are the specific neuronal populations and cortical circuits involved in anhedonia? Isolating individual neuronal cell types and pathways are a critical step for targeted therapeutic options. Also, how does a dysregulation of synaptic proteins affect synaptic plasticity during anhedonia? Identifying the synaptic proteins of interest would help understand the neuropathophysiological implications within these disorders. Finally, what are the biomarkers that lead to the onset of schizophrenia vs. major depressive disorder? Providing early intervention in both schizophrenia and major depressive disorder have shown to dramatically reduce psychotic symptoms and suicidal rates, respectively.

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