- B.A., University of California, Los Angeles, 1986
- Ph.D., University of California, Berkeley, 1994
- Postdoc, Northwestern University, 1994-1997
- Research Faculty, SUNY-Downstate Medical Center, 1997-2008
My research interest is to identify how various signaling pathways are affected by stress, fear, developmental insults, pharmacological challenges, neural stimulation and cognition. There are three projects that reflect these long-standing interests.
Long-Term Potentiation, Long-Term Depression and Memory
Long-term potentiation (LTP) and long-term depression (LTD) are electrophysiological models used to investigate neural mechanisms of synaptic plasticity in the rodent brain. Using an in vitro hippocampal slice preparation, we analyze the effects of various pharmacological and biochemical manipulations to isolate key neural functions important for maintaining LTP and LTD. These electrophysiology experiments allow us to develop stronger and more promising hypothesis for the neural mechanisms involved in learning and memory.
Developmental Psychobiology and Developmental Learning Disorders
The aim of this project is to investigate how highly regulated and influential developmentally regulated proteins affect synaptic plasticity and ultimately cognition. Using various environmental, electrophysiological and pharmacological challenges, we identify the critical time windows when the brain is most susceptible to damage or trauma. These experiments provide a functional understanding of brain development that is important for advancing treatment of developmental brain disorders.
Neural Mechanisms of Stress, Fear and Post-Traumatic Stress Disorder (PTSD)
The central hypothesis of this project is that elevated levels of fear, anxiety and stress alter various proteins affecting cognitive function. Given PKMƒê¡¦s fundamental role in the retention of long-term memories (see Science , 313, 1141-1144. 2006, below), my lab examines PKMƒê¡¦s function in PTSD genesis using a rodent model based on predatory scent stress. The objective is to ultimately develop better and more effective treatment regimens for PTSD.
- Schrott LM, Franklin LT & Serrano PA. (2008) Acquisition of radial arm maze is impaired following prenatal opiate exposure potential role of brain derived neurotrophic factor. Brain Research, 1198, 132-140.
- Yao Y, Kelly MT, Sakimura S, Serrano PA, Tian D, Bergold P, Frey J, Sacktor TC. (2008) PKM maintains late-LTP by enhancing NSF/GluR2-mediated trafficking of postsynaptic AMPARs. Journal of Neuroscience 28, 7820-7.
- Serrano P, Friedman EL, Kenney J, Taubenfeld SM, Zimmerman JM, et al. (2008) PKM? Maintains Spatial, Instrumental, and Classically Conditioned Long-Term Memories. PLoS Biol 6(12): e318. doi:10.1371/journal.pbio.0060318
- *Pastalkova E, *Serrano PA, Pinkhasova D, Wallace E, Fenton A & Sacktor TC (2006) Spatial information storage by the maintenance mechanism of LTP. Science , 313, 1141-1144. *authors contributed equally to this work.
- Serrano PA, Yao Y & Sacktor TC (2005) Persistent phosphorylation by protein kinase M maintains late phase long-term potentiation. Journal of Neuroscience 25, 1979-1984.
- Cracco J, Serrano PA, Moskowiz SI, Bergold PJ & Sacktor TC (2005) Protein synthesis-dependent LTP in isolated dendrites of CA1 pyramidal cells. Hippocampus, 15, 551-556.
- Hernandez IA, Blace N, Crary JF, Serrano PA, Leitges M, Libien J, Weinstein G, Tcherepanov A, & Sacktor TC (2003) PKM synthesis from a brain mRNA encoding an independent PKC catalytic domain: implications for the molecular mechanism of memory. Journal of Biological Chemistry, 278, 40305-40316.
- Ling, DS, Benard LS, Serrano PA, Blace N, Kelly MT, Crary JF & Sacktor T C (2002) Persistently active protein kinase M is both necessary and sufficient for maintaining long-term potentiation. Nature Neuroscience 5, 295-6.