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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Adora1tm1Bbf
targeted mutation 1, Bertil B Fredholm
MGI:2180136
Summary 4 genotypes
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Adora1tm1Bbf/Adora1tm1Bbf B6.129P2-Adora1tm1Bbf MGI:5007487
hm2
Adora1tm1Bbf/Adora1tm1Bbf involves: 129P2/OlaHsd * C57BL MGI:3613555
hm3
Adora1tm1Bbf/Adora1tm1Bbf involves: 129P2/OlaHsd * C57BL/6 MGI:3622796
cn4
Adktm2Bois/Adktm2Bois
Adora1tm1Bbf/Adora1tm1Bbf
Tg(Nes-cre)1Kln/0
involves: 129P2/OlaHsd * C57BL/6 * SJL MGI:5816716


Genotype
MGI:5007487
hm1
Allelic
Composition
Adora1tm1Bbf/Adora1tm1Bbf
Genetic
Background
B6.129P2-Adora1tm1Bbf
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora1tm1Bbf mutation (1 available); any Adora1 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• in the complete Freund's adjuvant model of chronic inflammatory pain or in the spared nerve injury model of neuropathic pain, mice injected with human ACPP exhibit increased mechanical allodynia compared with wild-type mice
• in mice injected with human ACPP
• in mice injected with human ACPP in the complete Freund's adjuvant model of chronic inflammatory pain or in the spared nerve injury model of neuropathic pain

integument
• in the complete Freund's adjuvant model of chronic inflammatory pain or in the spared nerve injury model of neuropathic pain, mice injected with human ACPP exhibit increased mechanical allodynia compared with wild-type mice
• in mice injected with human ACPP
• in mice injected with human ACPP in the complete Freund's adjuvant model of chronic inflammatory pain or in the spared nerve injury model of neuropathic pain




Genotype
MGI:3613555
hm2
Allelic
Composition
Adora1tm1Bbf/Adora1tm1Bbf
Genetic
Background
involves: 129P2/OlaHsd * C57BL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora1tm1Bbf mutation (1 available); any Adora1 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
• homozygotes exhibit normal body temperature; however, the hypothermia induced by i.p. administration of A1R agonist N6-cyclohexyladenosine (0.1 mg/kg) in wild-type controls (-3.4 +/- 0.16 degrees C) is abolished in mutant mice (-0.08 +/- 0.39 degrees C)

behavior/neurological
• homozygotes display increased anxiety in the dark-light box test, with a significantly reduced number of entries into as well as less total time spent in the lit compartment
• however, visual placing reflex, equilibrium, prehensility or total activity over a 24-h period are normal
• homozygotes exhibit thermal (but not mechanical) hyperalgesia relative to wild-type or heterozygous mice
• homozygotes react faster to thermal pain, as shown by significanlty reduced latencies under basal conditions or after intrathecal administration of adenosine analogue R-PIA in the tail-flick test
• i.p. administration of morphine (5 mg/kg) has no effect on thermal nociception

cardiovascular system
N
• homozygotes show no significant differences in heart rate or blood pressure relative to wild-type mice

nervous system
• homozygotes display complete loss of both adenosine-mediated inhibition and theophylline-mediated augmentation of excitatory glutamatergic neurotransmission
• electrophysiological recordings from hippocampal slices indicate that homozygotes fail to exhibit adenosine-mediated inhibition of EPSCs
• electrophysiological recordings from hippocampal slices indicate that homozygotes fail to exhibit adenosine-mediated inhibition of fEPSPs
• in response to hypoxia/anoxia, homozygotes show a significantly delayed and attenuated inhibition of fEPSP responses in hippocampal slices, with no recovery after 60 min of incubation in hypoxic buffer
• homozygotes exhibit a reduced response to hypoxia/anoxia, with mutant hippocampal slices exhibiting a delayed and attenuated decrease in synaptic transmission relative to wild-type slices

respiratory system
• in reponse to hypoxia, brainstem spinal cord preparations from wild-type mice show a decrease in respiratory output within 3 min after the onset of hypoxia, with full recovery of the respiratory rhythm and brainstem neuronal activity upon reintroduction of oxygenated medium; in mutant preparations, the depression in respiratory output is significantly delayed and full recovery is not attained

integument
• homozygotes exhibit thermal (but not mechanical) hyperalgesia relative to wild-type or heterozygous mice
• homozygotes react faster to thermal pain, as shown by significanlty reduced latencies under basal conditions or after intrathecal administration of adenosine analogue R-PIA in the tail-flick test
• i.p. administration of morphine (5 mg/kg) has no effect on thermal nociception




Genotype
MGI:3622796
hm3
Allelic
Composition
Adora1tm1Bbf/Adora1tm1Bbf
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adora1tm1Bbf mutation (1 available); any Adora1 mutation (3 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
homeostasis/metabolism
N
• response to caffeine induced wakefulness is similar to wild-type mice




Genotype
MGI:5816716
cn4
Allelic
Composition
Adktm2Bois/Adktm2Bois
Adora1tm1Bbf/Adora1tm1Bbf
Tg(Nes-cre)1Kln/0
Genetic
Background
involves: 129P2/OlaHsd * C57BL/6 * SJL
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Adktm2Bois mutation (0 available); any Adk mutation (19 available)
Adora1tm1Bbf mutation (1 available); any Adora1 mutation (3 available)
Tg(Nes-cre)1Kln mutation (4 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
behavior/neurological
• mice exhibit increased susceptibility to stress-induced (placement in novel environment) seizures

mortality/aging
• increase in mortality

nervous system
• mice exhibit increased susceptibility to stress-induced (placement in novel environment) seizures





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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
10/08/2019
MGI 6.14
The Jackson Laboratory