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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Avpr1atm1Gzt
targeted mutation 1, Gozoh Tsujimoto
MGI:3623418
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Avpr1atm1Gzt/Avpr1atm1Gzt involves: 129 * C57BL/6J MGI:3665424


Genotype
MGI:3665424
hm1
Allelic
Composition
Avpr1atm1Gzt/Avpr1atm1Gzt
Genetic
Background
involves: 129 * C57BL/6J
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Avpr1atm1Gzt mutation (0 available); any Avpr1a mutation (35 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
cardiovascular system
• homozygotes exhibit a significant 9% reduction in circulating blood volume, although total body weight, hematocrit values, and red blood cell counts remain normal
• homozygotes display normal baseline heart rates relative to wild-type mice
• however, the bradycardiac response to electrical stimulation of the vagus nerve is significantly attenuated, indicating a CNS defect
• under basal conditions, homozygotes exhibit significantly reduced systolic, diastolic and mean arterial pressures relative to wild-type mice
• however, no significant changes in heart rate, heart size and histology, blood chemistry, blood cell counts, cardiac output or renal function are observed
• homozygotes show complete absence of AVP-induced vasopressor responses; instead, AVP causes a decrease in blood pressure, partly through V2 receptor-mediated release of nitric oxide from the vascular endothelium

nervous system
• homozygotes display significantly impaired arterial baroreceptor reflexes

homeostasis/metabolism
• homozygotes exhibit significantly reduced baseline atrial natriuretic peptide levels relative to wild-type mice
• homozygotes display normal baseline corticosterone levels relative to wild-type mice
• responses to vasoactive hormones including AVP remain mostly intact; however, the ACTH-stimulated corticosterone response is significantly reduced

endocrine/exocrine glands
• homozygotes show abnormal adrenal gland histology, with unclear adrenocortical zonation and enhanced depositions of lipofuscin in the reticular layer

muscle
• homozygotes show complete absence of AVP-induced vasopressor responses; instead, AVP causes a decrease in blood pressure, partly through V2 receptor-mediated release of nitric oxide from the vascular endothelium

behavior/neurological
• homozygotes display impaired spatial memory in an eight-arm radial maze task, with an increase in the number of errors after several days of training sessions compared to controls





Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
10/29/2024
MGI 6.24
The Jackson Laboratory