Alexei Morozov, PhD
Assistant Professor, Virginia Tech Carilion Research Institute
Assistant Professor, Virginia Tech-Wake Forest University School of Biomedical Engineering and Sciences
Assistant Professor of Psychiatry and Behavioral Medicine, Virginia Tech Carilion School of Medicine
The Morozov Laboratory reseachers are interested in neuronal substrates of social behaviors. Empathy is an evolutional hallmark that has shaped human civilization by influencing social behaviors. Animals can also express empathy, so the goal of the research program is, by using rodent models, to identify neuronal circuits that underlie empathy and determine how these circuits become altered in pathological conditions relevant to post-traumatic stress disorder, depression, psychopathy, autism, and schizophrenia. Morozov and his team address this by 1) developing genetic and behavioral mouse models that involve empathy; 2) identifying changes in neuronal circuits during transition to pathological states; and 3) establishing a causal link between the circuit and behavior through optogenetic manipulation of circuit elements in behaving animals. The scientists focus on communications between the anterior cingulate cortex (ACC), the primary hub of empathy in humans, and the amygdala, the emotional center of the brain, and on their modulation by the rest of the limbic system. Currently Morozov and his team employ two mouse models in which empathy is involved: a model of emotional trauma, induced by observation of suffering in a cage-mate and a genetically induced model of psychopathy, in which empathy-like behaviors are attenuated. A unique feature of the emotional trauma model is lack of physical pain or distress, which is similar to emotional trauma in humans undergoing psychological rather than physical suffering. By using channelrhodopsin-mediated selective stimulation of amygdala afferents, the scientists found that emotional distress selectively increases NMDA-receptor function in the amygdala input from the ACC. Currently the researchers are testing a hypothesis that the increased NMDA receptor function is causally linked to behavioral symptoms of emotional trauma. The genetic model of antisocial behaviors is mice with hippocampal CA3-restricted knockout of BDNF. These animals are highly aggressive, dominant, and lacking empathy-like behavior, but have normal cognition, which are the traits of psychopathy. Morozov and his team found that oscillatory activity in the hippocampus is altered in the model, and the cause is a decreased activity of 5-HT3 receptor positive interneurons. Currently the scientists are testing a hypothesis that the suppression of 5-HT3 interneurons in the hippocampus is causally linked to the traits of psychopathy. By investigating how brain circuits and molecules control normal and pathological behavior in mice, researchers in the Morozov Laboratory generate knowledge that will help relieve the burden of mental disease on human society.
For a more complete listing of Alexei Morozov's publications, visit PubMed.
Education and Training
- Columbia University: Postdoctoral fellowship, Neurobiology and behavior
- University of Illinois at Chicago: PhD, Biochemistry
- Lomonosov Moscow State University: BS, Bioorganic chemistry
- National Institute of Mental Health
Investigator, Neural mechanisms of emotions
- Institute of Molecular Biology, Russian Academy of Sciences
Researcher, Genes regulation
- Institute of Medical Enzymology, Russian Academy of Medical Health Sciences
Researcher, Genes regulation
Awards and Honors
- Graduate College Fellowship, University of Illinois at Chicago, 1993-1996
- Dorothea H. Fleming Student Research Fund Award, University of Illinois at Chicago, 1993-1995
- Certificate of Merit for Outstanding Student Research Presentation, Eleventh Annual Molecular Biology Retreat, University of Illinois at Chicago, 1994
- Huang Y, Yoon K, Ko H, Jiao S, Ito W, Wu JY, Yung WH, Lu B, Morozov A. (2016). 5-HT3a Receptors Modulate Hippocampal Gamma Oscillations by Regulating Synchrony of Parvalbumin-Positive Interneurons. Cerebral Cortex 26(2), 576-85.
- Ito W, Erisir A, Morozov A. (2015). Observation of Distressed Conspecific as a Model of Emotional Trauma Generates Silent Synapses in the Prefrontal-Amygdala Pathway and Enhances Fear Learning, but Ketamine Abolishes those Effects. Neuropsychopharmacology 40(22), 2536-45.
- Subramanian J, Dye L, Morozov A. (2013). Rap1 signaling prevents L-type calcium channel-dependent neurotransmitter release. J Neurosci 33(17), 7245-52.
- Zou W, Izawa T, Zhu T, Chappel J, Otero K, Monkley SJ, Critchley DR, Petrich BG, Morozov A, Ginsberg MH, Teitelbaum SL. (2013). Talin1 and Rap1 are critical for osteoclast function. Mol Cell Biol 33(4), 830-44.
- Chu HY, Ito W, Li J, Morozov A. (2012). Target-specific suppression of GABA release from parvalbumin interneurons in the basolateral amygdala by dopamine. J Neurosci 32(42), 14815-20.
- Huang Y, Ko H, Cheung ZH, Yung KK, Yao T, Wang JJ, Morozov A, Ke Y, Ip NY, Yung WH. (2012). Dual actions of brain-derived neurotrophic factor on GABAergic transmission in cerebellar Purkinje neurons. Exp Neurol 233(2), 791-8.
- Ito W, Chehab M, Thakur S, Li J, Morozov A. (2011). BDNF-restricted knockout mice as an animal model for aggression. Genes, Brain and Behavior 10(3), 365-74.
- Subramanian J, Morozov A. (2011). Erk1/2 inhibit synaptic vesicle exocytosis through L-type calcium channels. The Journal of Neuroscience 31(12), 4755-64.
- Huang Y, Morozov A. (2011). Hippocampal deletion of BDNF gene attenuates gamma oscillations in area CA1 by up-regulating 5-HT3 receptor. PLoS One 6(1), e16480.
- Morozov A, Sukato D, Ito W. (2011). Selective suppression of plasticity in amygdala inputs from temporal association cortex by the external capsule. The Journal of Neuroscience 5(31), 339-45.