Genetic basis of behavior, neural circuit formation and function
- 213 Zoology Research Building
- Ph.D. University of Wisconsin-Madison
- Lab Website
- Integrative Biology
- Research Interests
- Genetic basis of behavior, neural circuit formation and function
- Research Fields
- Behavior, Cognition and Emotion, Development, Plasticity, and Repair, Molecular Neuroscience, Neuronal Circuits
Animals constantly update their behavior by integrating current sensory input with information stored from previous experience. Therefore, appropriate behavior is contingent upon the nervous system’s ability to learn and recall memory. All animals exploit a fundamental mechanism of learning, called habituation, to filter irrelevant sensory input and prioritize attention. Habituation is observed by a progressive response decline to repeatedly experienced, yet inconsequential stimuli. Habituation deficits represent hallmark features of human behavioral disorders, including schizophrenia, addiction, and attention deficit hyperactivity disorder. Despite habituation’s biological conservation and clinical relevance, our understanding of the genetic mechanisms underlying habituation is limited. The goals of our research are to identify and understand the genes that govern how neural circuits regulate habituation.
To identify genes critical for habituation, I performed a forward genetic screen in zebrafish and identified mutants with specific defects in habituation of the highly conserved acoustic startle response. These mutants represent the first vertebrate mutants isolated based solely on a learning deficiency and provide unique inroads to the genetic basis of habituation learning. Our current work combines mutant analysis with genetic and pharmacological manipulations, imaging of neural circuits, and high throughput behavioral analyses to dissect the genetic and neural basis of habituation learning. This work will provide unique insight into the genetic mechanisms underlying learning so that we may better understand cognitive disorders marked by habituation deficits.
Search PubMed for more publications by Marc Wolman
Hao L, Phan D, Jontes J, Wolman M, Granato M, Beattie C. 2013. Temporal requirement for SMN in motoneuron development. Human Molecular Genetics 22(13):2612-25.
Wolman MA*, Gyda M*, Lorent K, Granato M. 2012. The tumor suppressor gene Retinoblastoma-1 controls visual connectivity and function. PLoS Genetics (8)11: e1003106.
Shin J, Padmanabhan A, de Groh ED, Lee JS, Haidar S, Dahlberg S, Guo F, Wolman MA, Granato M, Lawson ND, Wolfe SA, Kim SH, Solnica-Krezel L, Kanki JP, Ligon KL, Epstein JA, and Look AT. 2012. Zebrafish neurofibromatosis type 1 genes have redundant functions in tumorigenesis and embryonic development. Disease Models and Mechanisms 5(6):881-94.
Hao L, Wolman MA, Granato M, Beattie CE. 2012. Survival motor neuron (SMN) affects plastin 3 protein levels leading to motor defects. J Neurosci. 32(15):5074-84.
Rosenberg AF, Wolman MA, Franzini-Armstrong C, Granato M. 2012. In vivo nerve-macrophage interactions following peripheral nerve injury. J Neurosci. 32(11):3898-909.
Wolman MA, Granato M. 2012. Behavioral genetics in larval zebrafish: Learning from the young. Dev Neurobiol. 72(3):366-72.
Jain RA*, Wolman MA*, Schmidt LA, Burgess HA, Granato M. 2011. Molecular-genetic mapping of zebrafish mutants with variable phenotypic penetrance. PLoS One. 6(10):e26510.
Wolman MA, Jain RA, Liss L, Granato M. 2011. Chemical modulation of memory formation in larval zebrafish. Proc Natl Acad Sci. 108(37):15468-73.