Dilyan I. Dryanovski, Ph.D.
Research Associate
Education
Ph.D. in Neuroscience, Northwestern University, Chicago IL B.Sc. in Biology, the George Washington University, Washington DC Current Projects Using electrophysiology to examine rapid acting antidepressant-induced changes in synaptic plasticity. Research Interests Mechanisms of drug action in the treatment of depression, addiction, and neurodegeneration. Contact Information Email: ddryanovski[at]som.umaryland.edu Phone: (410) 706-6799 |
Research Description
I completed my PhD at Northwestern University in the laboratory of Dr. James Surmeier where I was involved in determining the mechanism of selective neuronal vulnerability of dopamine neurons in Parkinson’s disease. Using primary neuronal cell cultures, two-photon microscopy, calcium imaging and patch-clamp electrophysiology, I showed that activity-dependent calcium entry through L-type calcium channels increased mitochondrial oxidative stress in both the soma and dendrites of dopamine neurons. I also showed that formation of intracellular α-synuclein aggregates further increased oxidative stress independently of the mitochondria. My work showed that physiological and proteostatic stressors are additive and that both contribute independently to the death of midbrain dopamine neurons in Parkinson’s disease. After graduate school, I completed a postdoctoral fellowship at the National Institute on Drug Abuse (NIDA) in the laboratory of Dr. Carl Lupica where I was investigating the mechanism of cocaine-induced endocannabinoid synthesis and release in the mouse mesolimbic pathway. Using slice electrophysiology, I found that in response to cocaine, endocannabinoids are synthesized and released from dopamine neurons and travel retrogradely to activate endocannabinoid receptors on axon terminals of presynaptic cells to block the release of inhibitory neurotransmitters onto dopamine neurons. This results in increased activity of dopamine neurons by disinhibition and increased dopamine release in mesolimbic pathway target areas, thus leading to the addictive effect of cocaine.
I completed my PhD at Northwestern University in the laboratory of Dr. James Surmeier where I was involved in determining the mechanism of selective neuronal vulnerability of dopamine neurons in Parkinson’s disease. Using primary neuronal cell cultures, two-photon microscopy, calcium imaging and patch-clamp electrophysiology, I showed that activity-dependent calcium entry through L-type calcium channels increased mitochondrial oxidative stress in both the soma and dendrites of dopamine neurons. I also showed that formation of intracellular α-synuclein aggregates further increased oxidative stress independently of the mitochondria. My work showed that physiological and proteostatic stressors are additive and that both contribute independently to the death of midbrain dopamine neurons in Parkinson’s disease. After graduate school, I completed a postdoctoral fellowship at the National Institute on Drug Abuse (NIDA) in the laboratory of Dr. Carl Lupica where I was investigating the mechanism of cocaine-induced endocannabinoid synthesis and release in the mouse mesolimbic pathway. Using slice electrophysiology, I found that in response to cocaine, endocannabinoids are synthesized and released from dopamine neurons and travel retrogradely to activate endocannabinoid receptors on axon terminals of presynaptic cells to block the release of inhibitory neurotransmitters onto dopamine neurons. This results in increased activity of dopamine neurons by disinhibition and increased dopamine release in mesolimbic pathway target areas, thus leading to the addictive effect of cocaine.