Analysis Tools|
Allele Symbol Allele Name Allele ID |
Chrm4tm1Jwe targeted mutation 1, Jurgen Wess MGI:2155567 |
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| Summary |
4 genotypes
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• flat ultrasonic vocalizations exhibit a small increase compared to in wild-type mice
• however, frequency-modulated ultrasonic vocalizations are normal
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• homozygotes display a 30% increase in basal locomotor activity in an open-field test relative to wild-type mice
• in addition, homozygotes show significantly enhanced locomotor activity in response to dopamine receptor agonists apomorphine (nonselective) and SKF 38393 (D1-type selective), with no significant changes in inhibitory locomotor responses induced by D2-type agonist, quinpirole
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• homozygotes are viable, fertile and healthy and exhibit no postural abnormalities, ataxia, tremor, or catalepsy
• however, adult homozygotes weigh ~5% less than wild-type littermates
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| N |
• homozygotes display normal tremorogenic, hypothermic, sialagogic, and analgesic responses to the centrally acting, nonselective muscarinic agonist oxotremorine relative to wild-type mice
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• spontaneously beating atria derived from mutant mice display a normal basal atrial rate relative to wild-type atria
• however, at low concentrations, bradycardic effects of muscarinic agonist carbamylcholine are significantly reduced in mutant atrial preparations
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| N |
• homozygotes display normal carbamylcholine-dependent smooth muscle contractile responses in stomach fundus, urinary bladder, and tracheal smooth muscle preparations
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• carbamylcholine-induced contraction in gallbladder from (M4) homozygous mutant mice is dextrally shifted compared with the response in gallbladder from wild-type mice, but antagonism of carbamylcholine-induced contraction by AF-DX 116 or pirenzepine is not consistent with an interaction with M4 receptors, suggesting that gallbladder contractility to carbamylcholine is dependent on the presence of the M4 receptor for optimal efficacy
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• carbamylcholine-induced contraction in gallbladder from (M4) homozygous mutant mice is dextrally shifted compared with the response in gallbladder from wild-type mice, but antagonism of carbamylcholine-induced contraction by AF-DX 116 or pirenzepine is not consistent with an interaction with M4 receptors, suggesting that gallbladder contractility to carbamylcholine is dependent on the presence of the M4 receptor for optimal efficacy
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• 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 absent or significantly reduced
• depression of cortical synaptic transmission induced by 1.5mm acetylcholine is not affected
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• fast Fourier transform (FFT) analysis shows that the paradoxical sleep-theta peak frequency (TPF) values in double homozygous mice are spectrally distinct during the dark phase, with a frequency increase in mutants
• the cumulative theta power is significantly decreased during the light phase for paradoxical sleep in mutant vs. control mice
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• the cumulative theta power is significantly decreased during the light phase for paradoxical sleep in mutant vs. control mice
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• 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 absent or significantly reduced
• depression of cortical synaptic transmission induced by 1.5mm acetylcholine is not affected
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| N |
• no differences regarding the sleep vigilance states, including paradoxical sleep, are seen in double homozygous mice
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| ♀ | phenotype observed in females |
| ♂ | phenotype observed in males |
| N | normal phenotype |
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• 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 absent
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• depression of cortical synaptic transmission induced by 1.5mm acetylcholine, is significantly reduced in double homozygous mice
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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 09/30/2025 MGI 6.24 |
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