Cell Biology - all faculty and staff

Mohiuddin Ahmad, M.B.B.S., Ph.D.

Mohiuddin Ahmad, M.B.B.S., Ph.D.

Assistant Professor, Department of Cell Biology


Education:

Ph.D., Neuroscience, Georg-August University, Goettingen, Germany
M.B.B.S., J.N. Medical College, Aligarh Muslim University, India


Post-doctoral Fellowship:

Postdoctoral Fellowship, Stanford University, Palo Alto, California


Contact Information:

Office Phone: (405) 271-8001 ext. 47964
Fax Number: (405) 271-3548

 

Email: mohiuddin-ahmad@ouhsc.edu  

 

University of Oklahoma Health Sciences Center
Department of Cell Biology
940 Stanton L. Young Blvd. BMSB 538
Oklahoma City, OK 73104


Research Interests:

 

Synaptic plasticity involves activity dependent changes in the strength of synaptic transmission and is critical for information processing and storage in the brain. The primary goal of my laboratory is to elucidate the cellular and molecular mechanisms that mediate various forms of synaptic plasticity in the mouse brain. We use a combination of cutting edge techniques of patch-clamp electrophysiology,  optogenetics, in-vivo & in-vitro molecular manipulations and confocal imaging to investigate synapses. One focus of the lab is to study the trafficking mechanisms of AMPA-type of glutamate receptors that lead to long-term synaptic plasticity. It is widely accepted that trafficking of AMPA receptors in the dendrites and their incorporation into synapses mediates long-term potentiation (LTP), a prototypic form of synaptic plasticity. Using a variety of knockout and knockdown approaches, we are investigating the role of transmembrane interaction partners of AMPA receptors and proteins involved in exocytosis in synaptic plasticity.

 

Another focus of the lab is to investigate how different cells and circuits in the mouse brain utilize synaptic plasticity events to regulate behavior. Long-term synaptic plasticity is believed to mediate many forms of experience dependent plasticity including learning and memory. We are using in-vivo virus based molecular manipulations, optogenetics and behavioral assays to link synaptic plasticity events in specific circuits to behavior.

 

It is being increasingly appreciated that synaptic dysfunction underlies many forms of neurologic and psychiatric diseases such as autism spectrum disorders,  Alzheimer’s disease, schizophrenia and depression. The knowledge gained through research into synaptic physiology will help us unravel how brain circuits generate normal behaviors as well as their disturbances in brain disorders.


Selected Publications:

 

Troyano-Rodriguez E, Mann S, Ullah R, and Ahmad M (2019). PRRT1 regulates basal and plasticity-induced AMPA receptor trafficking. Molecular and Cellular Neuroscience. 2019 Jun 16;98:155-163.

 

Troyano-Rodriguez E, Wirsig-Wiechmann CR, and Ahmad M (2019). Neuroligin-2 Determines Inhibitory Synaptic Transmission in the Lateral Septum to Optimize Stress-Induced Neuronal Activation and Avoidance Behavior. Biological Psychiatry. 2019 Jun 15;85(12):1046-1055.

 

Zhang D, Marlin MC, Liang Z, Ahmad M, Ashpole NM, Sonntag WE, Zhao ZJ, Li G (2016). The Protein Tyrosine Phosphatase MEG2 Regulates the Transport and Signal Transduction of Tropomyosin Receptor Kinase A. The Journal of Biological Chemistry, 291(46):23895-23905.

 

Bacaj T*, Ahmad M*, Jurado S*, Malenka RC and Südhof TC (2015). Synaptic function of Rab11Fip5: selective requirement for hippocampal long-term depression. The Journal of Neuroscience, 35(19):7460-7474. *contributed equally to the study

 

Soler-Llavina GJ, Arstikaitis P, Morishita W, Ahmad M, Südhof TC and Malenka RC (2013). Leucine-rich repeat transmembrane proteins are essential for maintenance of long-term potentiation. Neuron 79, 439-446.

 

Ahmad M, Polepalli JS, Goswami D, Yang X, Kaeser-Woo YJ, Südhof TC and Malenka RC (2012). Postsynaptic complexin controls AMPA receptor exocytosis during LTP. Neuron 73, 260-267.

 

Fairless R,  Masius H, Rohlmann A, Heupel K, Ahmad M, Reissner C, Dresbach T, Müller M, and Missler M (2008). Polarized targeting of Neurexins to synapses is regulated by their C-terminal sequences. The Journal of Neuroscience, 28(48), 12969-81.

 

Dudanova I*, Sedej S*, Ahmad M*, Masius H, Sargsyan V, Zhang W, Riedl D, Angenstein F, Schild D, Rupnik M, Missler M (2006). Important contribution of α-neurexins to Ca2+-triggered exocytosis of secretory granules. The Journal of Neuroscience, 26, 10599-10613. *contributed equally to the study​

 

Complete List of Published Work in My Bibliography

http://www.ncbi.nlm.nih.gov/myncbi/1ZI7myh13SrQa/bibliography/44175599/public/?sort=date&direction=ascending

 

Profile Last Edited:  July 1, 2019