Open AccessPhenotypic profiling of mGlu 7 knockout mice reveals new implications for neurodevelopmental disorders
Author(s) -
Fisher Nicole M.,
Gould Robert W.,
Gogliotti Rocco G.,
McDonald Annalise J.,
Badivuku Hana,
Chennareddy Susmita,
Buch Aditi B.,
Moore Annah M.,
Jenkins Matthew T.,
Robb W. Hudson,
Lindsley Craig W.,
Jones Carrie K.,
Conn P. Jeffrey,
Niswender Colleen M.
Publication year - 2020
Publication title -
genes, brain and behavior
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.315
H-Index - 91
eISSN - 1601-183X
pISSN - 1601-1848
DOI - 10.1111/gbb.12654
Subject(s) - neurodevelopmental disorder , autism , rett syndrome , neuroscience , knockout mouse , metabotropic glutamate receptor , metabotropic receptor , glutamate receptor , epilepsy , context (archaeology) , phenotype , biology , psychology , genetics , psychiatry , receptor , gene , paleontology
Neurodevelopmental disorders are characterized by deficits in communication, cognition, attention, social behavior and/or motor control. Previous studies have pointed to the involvement of genes that regulate synaptic structure and function in the pathogenesis of these disorders. One such gene, GRM7 , encodes the metabotropic glutamate receptor 7 (mGlu 7 ), a G protein‐coupled receptor that regulates presynaptic neurotransmitter release. Mutations and polymorphisms in GRM7 have been associated with neurodevelopmental disorders in clinical populations; however, limited preclinical studies have evaluated mGlu 7 in the context of this specific disease class. Here, we show that the absence of mGlu 7 in mice is sufficient to alter phenotypes within the domains of social behavior, associative learning, motor function, epilepsy and sleep. Moreover, Grm7 knockout mice exhibit an attenuated response to amphetamine. These findings provide rationale for further investigation of mGlu 7 as a potential therapeutic target for neurodevelopmental disorders such as idiopathic autism, attention deficit hyperactivity disorder and Rett syndrome.