Autism Spectrum Disorder (ASD) is a heterogeneous group of disorders that is usually diagnosed in young children, characterized by a wide range of developmental symptoms including impairments in social communication and social interactions, restricted or repetitive behaviors, and increased comorbidity with many mental health disorders, particularly anxiety disorders. Many genes have been implicated in the susceptibility to ASD, including neural cell adhesion molecules such as PROTOCADHERIN 10 (PCDH10) and Neurexin1. A published study from the Brodkin Lab has demonstrated, in mice lacking one copy of Pcdh10 (Pcdh10+/- mice), reduced social approach behaviors; alterations in NMDA glutamate receptors; and rescue of the low social approach behavior by acute treatment with d-cycloserine, a co-agonist at the glycine binding site of NMDA receptors. To further test the role of glycine in this mouse model in this study, we tested the hypothesis that acute treatment with a glycine transporter inhibitor drug (GTI) would increase social approach behavior in juvenile Pcdh10+/- mice. Our results replicate the social approach deficits of juvenile male Pcdh10 +/- mice, and indicate that GTI caused increased social approach in some measures. Future studies will be conducted to determine whether this result can be replicated, and will further dissect the role of brain (especially amygdala) NMDA receptor signaling in social approach behaviors in Pcdh10 +/- mice, which may identify promising strategies for treatment of ASD.
As a rising senior majoring in Biological Basis of Behavior, my time spent researching PCDH10 mice in the Brodkin Lab has greatly enriched my educational experience. This upcoming year, I will complete my honors thesis for the Biological Basis of Behavior Program in the Brodkin Lab. My thesis project will have a similar focus as the one summer. The data from the glycine transporter inhibitor study is preliminary, and I hope to gather more conclusive results in the coming months. Going forward, the Brodkin Lab is moving toward human genetic studies on the Neurexin1 gene. I plan to have a career in either psychiatry or neurosurgery, so studying and researching neurocognitive disordered such as Autism Spectrum Disorder a critical component of reaching my career goals.
Autism Spectrum Disorder (ASD) is a heterogeneous group of disorders that is usually diagnosed in young children, characterized by a wide range of developmental symptoms including impairments in social communication and social interactions, restricted or repetitive behaviors, and increased comorbidity with many mental health disorders, particularly anxiety disorders. Many genes have been implicated in the susceptibility to ASD, including neural cell adhesion molecules such as PROTOCADHERIN 10 (PCDH10) and Neurexin1. A published study from the Brodkin Lab has demonstrated, in mice lacking one copy of Pcdh10 (Pcdh10+/- mice), reduced social approach behaviors; alterations in NMDA glutamate receptors; and rescue of the low social approach behavior by acute treatment with d-cycloserine, a co-agonist at the glycine binding site of NMDA receptors. To further test the role of glycine in this mouse model in this study, we tested the hypothesis that acute treatment with a glycine transporter inhibitor drug (GTI) would increase social approach behavior in juvenile Pcdh10+/- mice. Our results replicate the social approach deficits of juvenile male Pcdh10 +/- mice, and indicate that GTI caused increased social approach in some measures. Future studies will be conducted to determine whether this result can be replicated, and will further dissect the role of brain (especially amygdala) NMDA receptor signaling in social approach behaviors in Pcdh10 +/- mice, which may identify promising strategies for treatment of ASD.
As a rising senior majoring in Biological Basis of Behavior, my time spent researching PCDH10 mice in the Brodkin Lab has greatly enriched my educational experience. This upcoming year, I will complete my honors thesis for the Biological Basis of Behavior Program in the Brodkin Lab. My thesis project will have a similar focus as the one summer. The data from the glycine transporter inhibitor study is preliminary, and I hope to gather more conclusive results in the coming months. Going forward, the Brodkin Lab is moving toward human genetic studies on the Neurexin1 gene. I plan to have a career in either psychiatry or neurosurgery, so studying and researching neurocognitive disordered such as Autism Spectrum Disorder a critical component of reaching my career goals.