Open AccessMouse knockout of guanylyl cyclase C: Recognition memory deficits in the absence of activity changes
Author(s) -
Mann Elizabeth A.,
Sugimoto Chiho,
Williams Michael T.,
Vorhees Charles V.
Publication year - 2019
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.12573
Subject(s) - neurochemical , prepulse inhibition , startle reaction , phenotype , startle response , endocrinology , soluble guanylyl cyclase , medicine , hippocampal formation , dopamine , knockout mouse , monoamine neurotransmitter , neuroscience , psychology , biology , reflex , psychiatry , biochemistry , schizophrenia (object oriented programming) , receptor , nitric oxide , guanylate cyclase , serotonin , gene
Guanylyl cyclase C (GC‐C) is found in brain regions where dopamine is expressed. We characterized a mouse in which GC‐C was knocked out (KO) that was reported to be a model of attention deficit hyperactivity disorder (ADHD). We re‐examined this model and controlled for litter effects, used 16 to 23 mice per genotype per sex and assessed an array of behavioral and neurochemical outcomes. GC‐C KO mice showed no phenotypic differences from wild‐type mice on most behavioral tests, or on striatal or hippocampal monoamines, and notably no evidence of an ADHD‐like phenotype. KO mice were impaired on novel object recognition, had decreased tactile startle but not acoustic startle, and females had increased latency on cued training trials in the Morris water maze, but not hidden platform spatial learning trials. Open‐field activity showed small differences in females but not males. The data indicate that the GC‐C KO mouse with proper controls and sample sizes has a moderate cognitive and startle phenotype but has no ADHD‐like phenotype.