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Alexei Morozov, Ph.D.

Alexei Morozov, Ph.D.

Assistant Professor

Alexei Morozov, Ph.D. headshot

“Negative emotional experience leaves a trace in the brain, which makes us more vulnerable. Observational fear physically redistributes the flow of information, and this redistribution is achieved by stress, not just observed, but communicated through social cues, such as body language, sound, and smell.”

Uncovering the neural basis of social behavior, empathy, and fear

How and why do we share the feelings of others? 

The Morozov Laboratory studies the 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.

Dr. Morozov and his team address this by developing genetic and behavioral mouse models that involve empathy, identifying changes in neuronal circuits during transition to pathological states, and by establishing a causal link between the circuit and behavior through optogenetic manipulation of circuit elements in behaving animals. The Morozov Lab focuses 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.

  • Assistant Professor, Fralin Biomedical Research Institute at VTC
  • Assistant Professor, Department of Psychiatry and Behavioral Medicine, School of Medicine

Prefrontal-amygdala plasticity enabled by observational fear. Ito W, Morozov A. Neuropsychopharmacology. 2019 Feb 13. doi: 10.1038/s41386-019-0342-7. [Epub ahead of print] PMID: 30759453

Social modulation of fear: facilitation versus buffering. A. Morozov and W. Ito. Genes Genes Brain Behav. 2019 Jan;18(1):e12491. doi: 10.1111/gbb.12491. Published online June 13, 2018.

Disinhibition-assisted long-term potentiation in the prefrontal-amygdala pathway via suppression of somatostatin-expressing interneurons. Ito W., Fusco B., Morozov A. Neurophoton. 7(1), 015007 (2020), doi: 10.1117/1.NPh.7.1.015007

W. Ito, A. Erisir, A. Morozov. 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 2015 Oct;40(11):2536-45. doi: 10.1038/npp.2015.100. PMID: 25865929

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

  • Columbia University: Postdoctoral fellowship, Neurobiology and behavior
  • University of Illinois at Chicago: Ph.D., Biochemistry
  • Lomonosov Moscow State University: B.S., Bioorganic chemistry
  • 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


News about Alexei Morozov, Ph.D.