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Behavioral Neuroscience

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The Behavioral Neuroscience Program is largely focused on studying the mammalian neocortex and the complex behaviors that arise from its function. We use different animal models to understand the development of cortical circuits and their function as well as the mechanisms involved in neural plasticity. To this effect, we study a range of neuro-behavioral processes such as those involved in sensory systems and perception, neurodevelopmental disorders, distractor attenuation, cortical map plasticity as well as learning and memory. Across our program, we engage in multiple levels of analysis which range from genetics and biochemistry to synaptic plasticity, to electrophysiological mapping, population imaging, and behavior. Faculty in the area are experts in a range of fields related to psychology and neuroscience. These include the neurobiology of memory, cortical network dynamics, neocortical reorganization, neocortical mechanisms underlying attention and prediction, and developmental disorders such as Autism Spectrum Disorders stemming from disruptions in Fragile X Messenger Ribonucleoprotein 1  and Fetal Alcohol Spectrum Disorders. Graduate students in the Behavioral Neuroscience Program are a part of the Graduate Program in Psychology but also participate in the Interdepartmental Neuroscience Graduate Program and are well integrated with the students there. The synthesis of the two graduate programs provides a strong breadth of experience from faculty across the campus with interests that range from molecular neuroscience to systems biology and human brain imaging as well as behavioral neuroscience.

Grant title: Circuit Mechanisms of Hypersensitivity to Sensory Distractors in Fragile X Syndrome. 

Principal Investigator: Anubhuti Goel

Source: Brain and Behavior Foundation

Summary:  The goal of this project is to study the dysfunctional long-range neural dynamics from frontal cortical brain areas and subcortical inputs from the nucleus basalis, to primary visual cortex in a mouse model of Fragile X Syndrome. 


Grant title: Targeting of Serotonin 1A receptors during development to reverse neurobehavioral phenotypes in Fmr1 KO mice.

Co-Principal Investigator: Khaleel Razak

Source: FRAXA Research Foundation.

Summary: The goal of the project is to determine whether biased and selective serotonin-1A receptor agonists can reduce auditory hypersensitivity in Fmr1 knockout mice.


Grant title: Sensory plasticity in fathers.

Co-Principal Investigator: Khaleel Razak

Source: National Science Foundation 

Summary: This study examines auditory processing in biparental rodent fathers. The goal of the project is to determine whether the auditory cortex shows plasticity for enhanced processing of pup vocalizations, and if responses are also altered by pup specific odor. 


Grant title: Using nicotine to reverse age-related auditory processing deficit. 

Co-Principal Investigator: Khaleel Razak

Source: National Institutes of Health; National Institute on Aging. 

Summary: To test the hypothesis that age-related changes in central auditory processing can be reversed with nicotinergic acetylcholine receptor activation. 


Grant title: Translational medicine and mechanistic studies of brain neurophysiology in Fragile X Syndrome. 

Co-Principal Investigator: Khaleel Razak

Source: National Institutes of Health; National Institute of Child Health and Human Development; Center for research on FXS 

Summary: To identify mechanisms and biomarkers of sensory hypersensitivity in FXS.


Grant title: Sex-specific mechanisms of cortical circuit dysfunction in a mouse ASD model.

Co-Principal Investigator: Khaleel Razak

Source: National Institutes of Health

Summary: To identify mechanisms of sex and genotype differences in sensory processing in a PTEN mouse model of ASD


Grant title: Cortical plasticity within and across lifetimes. 

Co-Principal Investigator: Khaleel Razak

Source: James S. McDonnell Foundation grant. 

Summary: Studies of Neocortical Evolution in model systems. 


Grant title: Conquering fear and its generalization through synthesis of artificial memory traces.

Principal Investigator: Ed Korzus

Source: Department Of Army Research

Summary: To investigate prefrontal circuit dynamics guiding fear modulation using calcium imaging in freely behaving animals.


Grant title: Prefrontal network dynamics associated with learning to control fear.

Principal Investigator: Ed Korzus

Summary: To investigate prefrontal network biomarkers of fear generalization.


Grant title: The role of prefrontal circuitry in fear discrimination learning

Principal Investigator: Ed Korzus

Source: Brain & Behavior Research Foundation

Summary: To provide insights into how the prefrontal circuit supports fear modulation.


Grant title: Cortical Feedback Modulation of Sensory Processing During Selective Detection

Principal Investigator: Edward Zagha

Source: National Institutes of Health; National Institute of Neurological Disorders and Stroke

Summary: To understand the neural mechanisms by which cortical feedback pathways modulate sensory signals according to task demands.

Fragile X Syndrome: Fragile X Syndrome (FXS), the leading known inherited cause of atypical behaviors associated with autism spectrum disorders (ASD) arises due to the reduced expression or absence of the Fragile X Messenger Ribonucleoprotein 1 (FMRP). Individuals with ASD and FXS experience atypical sensory processing, in sensory modalities such as touch, hearing, and/or vision. The consequence of altered sensory processing is debilitating, resulting in impairment in sensory discrimination and an inability to ignore irrelevant sensory stimuli such as innocuous sounds, smells, sights, or touches. Currently, the field of FXS has a knowledge gap in the understanding of circuit mechanisms that result in atypical sensory processing and how this contributes to hypersensitivity and learning impairments. Animal models of FXS capture many of the sensory hypersensitivity issues observed in humans and exhibit excess anxiety, learning, and social impairments. Using Fmr1-/- mouse model, the Goel and Razak laboratories have designed novel behavior paradigms for probing sensory atypicalities in FXS, across visual and auditory modalities and elucidating the underlying neural dysfunction. Both labs have pioneered the use of comparable methodologies across mice and humans to improve the translational potential of this work and to guide therapies in humans.


Fetal Alcohol Syndrome: Huffman Laboratory: Prenatal ethanol exposure (PrEE) represents the leading preventable cause of intellectual disability worldwide and disproportionately affects people of lower SES (WHO, 2012). Our research investigates how ethanol impacts brain and behavioral development, the heritability of PrEE-related outcomes, and how ethanol-related phenotypes in exposed offspring may be reversed. Prior work from my laboratory was groundbreaking as it described a novel murine phenotype stemming from maternal consumption of alcohol during the prenatal period. PrEE results in abnormal neural connectivity, ectopic gene expression patterns in the newborn neocortex, and abnormal weanling behavior. Moreover, our most prominent discovery revealed how prenatal alcohol exposure can result in heritable, transgenerational phenotypes that span at least three generations and we have identified some epigenetic mechanisms that underlie the transgenerational transfer (Abbott et al., 2018).  It is important to study animal models of human conditions as this is the best way to understand the development of the condition and the mechanisms that drive it. Translational research such as this can lead to treatments that will improve human health and wellness.

Where have BN PhD graduates landed? 

Huffman Lab: 

  • Olga Kozanian Ph.D. Global Scientific Publications.
  • Sarah Santiago Ph.D., Sony Corporation
  • David Rohac, Bakersfield Community College

Zagha lab:

  • Behzad Zareian Ph.D. Yale School of Medicine (postdoc)

Razak lab:

  • Sarah Reinhard Ph.D. Cabrillo College

Media

Razak Lab: 

Huffman Lab: 

Zagha lab: