Phenotypes associated with this allele

• Allele Symbol: Chrm5^tm1Jwe
• Allele Name: targeted mutation 1, Jurgen Wess
• Allele ID: MGI:2155599
• Summary: 2 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Chrm5^tm1Jwe/Chrm5^tm1Jwe	B6.129S6-Chrm5^tm1Jwe	MGI:4830248
hm2	Chrm5^tm1Jwe/Chrm5^tm1Jwe	involves: 129S6/SvEvTac * CF-1	MGI:2662638

Genotype
MGI:4830248

hm1

• Allelic Composition: Chrm5^tm1Jwe/Chrm5^tm1Jwe
• Genetic Background: B6.129S6-Chrm5^tm1Jwe

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

nervous system

abnormal synaptic dopamine release ( J:163596 )

• stimulated release of dopamine in the dorsolateral striatum is reduced as compared with wild-type controls

• non-selective muscarinic agonist oxotremorine-M failed to potentiate the release of dopamine

• the bath application of oxotremorine-M to striatal brain slices results in an enhanced decrease in evoked dopamine release as measured by CV

Genotype
MGI:2662638

hm2

• Allelic Composition: Chrm5^tm1Jwe/Chrm5^tm1Jwe
• Genetic Background: involves: 129S6/SvEvTac * CF-1

cardiovascular system

abnormal vasodilation ( J:72953 )

• under basal conditions, homozygotes show no differences in cerebral arteriole diameter, mean arterial pressure, or arterial pH and blood gasses relative to wild-type mice

• however, acetylcholine-induced vasodilation responses of cerebral (pial) arterioles are abolished in mutant mice, whereas ADP-dependent vasodilator effects remain largely unaffected

• similarly, acetylcholine-induced vasodilation of large cerebral (basilar) arteries is almost completely abolished, whereas papaverine-induced vasodilator effects remain largely unaffected

• in contrast, acetylcholine-induced dilation of extra-cerebral (coronary and carotid) arteries is largely normal, indicating that only cerebral blood vessels are affected

nervous system

nervous system phenotype ( J:112505 )

N • facilitation of cortical synaptic transmission induced by 200 micromolar acetylcholine, measured the changes in amplitude of extracellular field potentials (FPs) evoked by stimulation of white matter (WM) and recording in cortical layer II/III, is similar to controls

N • depression of cortical synaptic transmission induced by 1.5mm acetylcholine is not affected

behavior/neurological

behavior/neurological phenotype ( J:72953 )

N • no overt behavioral abnormalities and no significant differences in oxotremorine-induced tremor, salivation, and hypothermia responses relative to wild-type mice

N • in addition, homozygotes show normal locomotor coordination and do not differ from wild-type littermates in spontaneous locomotor activity and in the magnitude of stimulatory locomotor responses induced by administration of direct and indirect dopamine receptor agonists

muscle

abnormal vasodilation ( J:72953 )

• under basal conditions, homozygotes show no differences in cerebral arteriole diameter, mean arterial pressure, or arterial pH and blood gasses relative to wild-type mice

• however, acetylcholine-induced vasodilation responses of cerebral (pial) arterioles are abolished in mutant mice, whereas ADP-dependent vasodilator effects remain largely unaffected

• similarly, acetylcholine-induced vasodilation of large cerebral (basilar) arteries is almost completely abolished, whereas papaverine-induced vasodilator effects remain largely unaffected

• in contrast, acetylcholine-induced dilation of extra-cerebral (coronary and carotid) arteries is largely normal, indicating that only cerebral blood vessels are affected

homeostasis/metabolism

abnormal dopamine level ( J:72953 )

• striatal slices from homozygotes exhibit a >50% reduction in muscarinic agonist-induced dopamine release at an intermediate agonist (oxotremorine) dose; however, maximum dopamine release remains unaltered