Julie G. Hensler
Selected Publications

Julie G. Hensler

Professor of Pharmacology
Ph.D., Northwestern University

Office: 210-567-4236



serotonin, brain derived neurotrophic factor (BDNF), depression, anxiety, behavior, stress


Research Summary

We study the cellular and molecular mechanisms by which serotonin receptor systems compensate or change in disease states (e.g. major depressive disorder, alcoholism) or in response to repeated drug treatment. Because the treatment of many psychiatric disorders involves long-term pharmacological intervention, compensatory changes in the sensitivity of these receptor systems may be involved in the mechanism by which drugs produce their therapeutic or side effects. To date there have been identified some fourteen subtypes of receptor for serotonin which are targets for a wide variety of drugs (e.g. hallucinogens, and drugs used to treat schizophrenia, anxiety, migraine). Serotonergic neurotransmission is also altered by several classes of antidepressant drugs. In my laboratory we have taken both in vivo and in vitro approaches to examine the processes underlying the regulation of serotonin receptor function and expression. In vitro systems (i.e. cells in culture) allow us to examine the regulation of serotonin receptors in more mechanistic studies. Our findings from these studies are compared to what has been observed to occur in the brain. Receptor function in the brain is assessed using biochemical, physiological and behavioral assays.


Changes or abnormalities in the serotonergic system have been implicated in many psychiatric disorders, substance abuse and addiction. Neurotrophins, such as brain derived neurotrophic factor (BDNF), are essential to the function and survival of neurons in the adult brain. BDNF has profound effects on the functional architecture of neurons and has a fundamental role in promoting serotonergic neurotransmission. As chronic stress decreases BDNF in frontal cortex and hippocampus, stress-related psychiatric disorders, such as major depression, may be due to diminished function or atrophy of neurons in these brain regions. We are using mice deficient in BDNF to explore the neurochemical and behavioral effects of decreases in BDNF expression, and how the interaction of stress with this BDNF deficiency alters brain function and behavior.


flow chart of Reciprocal BDNF-serotonin interactions

• Appointments, Boards, Committees and Memberships •

Leadership Texas - Class of 2012 - Leadership Texas

President - Serotonin Club -

• Research Group •

Wenrui Ye
Wenrui Ye
Graduate Student
Michael Pitlock
Michael Pitlock
Student Associate II