Present Institution:

University of New Mexico

Location:

Albuquerque NM US

Career Status:

Professor
Assistant Professor

Bio

I received my BA and MA degrees in Turkey
then moved to the USA to get a PhD in neurosciences. I received my PhD from Northwestern University in 2017. I switched departments and stayed at Northwestern University as a postdoc until 2023. I started working as an Assistant professor in the Department of Neurosciences at the University of New Mexico in August 2023. Currently
I am training people in my lab and starting new experiments while setting up the lab. My research focuses on understanding how neural circuits and gene networks react to stressful experiences that produce lasting changes in the brain
how such changes can predict adaptive and maladaptive behaviors
and how to modulate these changes to prevent and reverse neuropsychiatric disease-like states.

Interested in presenting:

1.Scientific presentations in your area of expertise
Behavior
General Neuroscience
Motivation and emotion

Sample of a Science/Scholarship Abstract

Generally scientific talks. -Common mechanisms underlying antidepressant action. BrainExPo
Brown University
2023. -Hippocampal neuronal activity and BMP signaling in antidepressant action. Dr. Samuel M. Nabrit Conference
Brown University
2022. -Role of Hippocampal Neurogenesis and BMP Signaling on Aging Related Changes in Cognition and Affect. Mechanisms of Aging and Dementia Training Program
Northwestern University
2018.

What type of talks have you presented in the past?

The cellular and molecular mechanisms underlying the behavioral effects of antidepressants are not well defined. However
it is known that chronic antidepressant treatment prevents hippocampal volume reduction and increases neurogenesis
the production of new neurons in the hippocampus. Indeed
decreased neurogenesis
structural abnormalities
and functional deficits are common in depression and are normalized by antidepressant treatments
raising the possibility that newborn neurons have a part in depression. Reducing the number of newborn neurons leads to changes in affective behaviors and abolishes the effect of antidepressants. Therefore
increased neurogenesis may be necessary for antidepressant effects
although this remains controversial. To address this issue
we used chemogenetic technology in transgenic mice to selectively manipulate the activity of newborn neurons. Silencing of newborn neurons abolished the antidepressant effect. Remarkably
enhancing the excitability of these neurons
in the absence of an increase in neuronal number
was sufficient to alleviate depression-like behavior and reverse the adverse effects of unpredictable chronic mild stress. These findings indicate that the activity of newly generated DG neurons exerts profound effects on behavior. Further
activity of newborn neurons is necessary for the behavioral effects of fluoxetine. Cell-autonomous restriction of our experimental manipulations enabled us to establish this causal relationship.