Selected Publications
  • Pineda E.A., Hensler J.G., Sankar R., Shin D., Burke T.F., Mazarati A.M. Interleukin-1beta causes fluoxetine resistance in an animal model of epilepsy-associated depression. Neurotherapeutics 9:477-485, 2012
  • Burke T.F., Advani T., Adachi M., Monteggia L.M., and Hensler J.G. Sensitivity of hippocampal serotonin1A receptors to stress in mice deficient in brain-derived neurotrophic factor. Int. J. Neuropsychopharmacology 2012 May 10:1-15. [Epub ahead of print]
  • Pineda, E.A.,Hensler, J.G., Sankar, R., Shi, D., Burke, T.F., Mazarati, A.M. Plasticity of presynaptic and postsynaptic serotonin1A receptors in an animal model of epilepsy – associated depression. Neuropsychopharmacology 2011 36:1305-1316.
  • Hensler, J.G. Serotonin in Mood and Emotion. Handbook of Behavioral Neuroscience, The Behavioral Neurobiology of Serotonin 2011 C.P. Müller & B. Jacobs (eds.), pp. 367-378.
  • Gould GG, Hensler J.G., Burke TF, Benno RH, Onaivi ES, Daws LC. Density and function of central serotonin (5-HT) transporters, 5-HT1A and 5-HT2A receptors, and effects of their targeting on BTBR T+tf/J mouse social behavior. Journal of Neurochemistry 116:291-303, 2011.
  • Advani T., Koek W. and Hensler J.G.: Gender differences in the enhanced vulnerability of BDNF+/- mice to mild stress. Int. J. Neuropsychopharmacol 12:583-585, 2009.
  • Hensler, J.G., Vogt, M.A., and Gass, P. Regulation of cortical and hippocampal 5-HT1A receptor function by corticosterone in GR+/- mice. Psychoneuroendocrinology 2009 Sep 17. [Epub ahead of print].
  • Lapiz-Bluhm M.D.S., Soto-Piña A.E., Hensler J.G., and Morilak D.A.: Chronic intermittent cold stress and serotonin depletion induce deficits of reversal learning in an attentional set-shifting test in rats. Psychopharmacology [Epub 2008 Jun 30].
  • Rossi D.V., Burke T.F., and Hensler J.G.: Differential regulation of serotonin-1A receptor-stimulated [35S]GTPgammaS binding in the dorsal raphe nucleus by citalopram and escitalopram. Eur. J. Pharmacol. 583:103-107, 2008.
  • Rossi D.V., Burke T.F., McCasland M., and Hensler J.G.: Serotonin1A receptor function in the dorsal raphe nucleus following chronic administration of the selective serotonin reuptake inhibitor setraline. J. Neurochem. 105:1091-1099, 2008.
Julie G. Hensler

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 -

• Lab Personnel •

Alicia Avelar - IMGP Student