Peter Perrino

Peter Perrino is currently a graduate student in the Behavioral Neuroscience program at the University of Connecticut under the mentorship of Dr. Holly Fitch.  After receiving his Bachelors of Science degree in Physiology and Neurobiology with a minor in Molecular Cell Biology, Peter worked with Dr. Fitch as the Murine Behavioral Neurogenetics Facility (MBNF) Research Assistant where he developed new behavioral paradigms to evaluate how genetic and environmental manipulations can effect behavioral outcomes.

Specifically, Peter gained experience behaviorally phenotyping various mouse models, which include how maternal immune activation may produce an autism-like phenotype in offspring, as well as NG2 cell ablation influence on sensory processing and fear-related behavior. While the Research Assistant of the MBNF, Peter assisted Fitch Lab graduate students, gaining further insight into phenotyping of transgenic mouse models of neurodevelopmental disorders.

After his time spent as the MBNF Research Assistant, Peter transitioned to the Behavioral Neuroscience program where his research has been directed towards the behavioral and neuroanatomical characterization of transgenic mouse models targeting genes implicated in neurodevelopmental disorders, particularly those with a language communicative component (e.g. SLI, autism, Usher Syndrome). Understanding the genetic mechanisms behind behavior is instrumental in developing future screening and interventions for individuals with neurodevelopmental disorders, as well as providing basic insight into the genetics and neurocircuitry subserving these processes in typical cognition.

Currently Peter is working on a project which aims to further investigate the underlying genetic mechanisms of Usher Syndrome — an autosomal recessive form of congenital deafness and blindness that results from a mutation in both USH2A gene alleles.  Interestingly, heterozygous individuals are believed to be phenotype-free, yet recent evidence suggests carriers may have a specific language deficit.  Novel findings from this work indicate that mice with a heterozygous deletion of Ush2a exhibit auditory processing deficits at low frequencies, but show normal processing at ultrasonic frequencies.  These results shed new light on how the USH2A gene may lead to auditory processing impairments and subsequent language impairments in affected humans.

Peter plans on defending his Master’s in the spring of 2018 and hopes to continue studying neurodevelopmental disorders for his dissertation work.