Strain Name:

B6;129-Nrxn3tm1Sud Nrxn1tm1Sud Nrxn2tm1Sud/J

Stock Number:

006377

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Mice that are homozygous for neurexin I, II and III gene mutations die within 24 hours of birth. Although newborn mice are initially capable of directed movements and react to tactile stimuli, the integrative brain functions required for breathing are impaired.

Description

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Strain Information

Type Mutant Stock; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
Visit our online Nomenclature tutorial.
Specieslaboratory mouse
Generation?+F8pN1
Generation Definitions
 
Donating InvestigatorDr. Thomas C. Sudhof,   Stanford University School of Medicine

Description
Mice that are homozygous for all three targeted mutations die within 24 hours of birth. Although newborn mice are initially capable of directed movements and react to tactile stimuli, the integrative brain functions required for breathing are impaired. At birth, the body and brain weights of triple targeted mutation mice are indistinguishable. Assymetric type I and symmetric type II synapses in triple homozygotes are ultrastructurally normal. The density of symmetric (presumptive inhibitory) synapses are reduced whereas the density of asymmetric (presumptive excitatory) synapses are not. Neurotransmitter release is generally impaired due to reduced Ca2+ channel function. No protein product from any of the targeted genes is detected in brain tissue. Quantification of the levels of 22 other neuronal proteins detected no major changes. This mutant mouse strain represents a model that may be useful in studies of synaptic vesicle exocytosis mechanisms in neurons.

Development
A targeting vector containing a neomycin resistance gene was used to replace the first coding exons of the three targeted genes. The construct was electroporated into 129/Sv-derived embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. Chimeric animals were crossed with C57BL/6 mice.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls

Related Strains

Strains carrying other alleles of Nrxn1
008416   B6;129-Nrxn3tm2Sud Nrxn1tm2Sud Nrxn2tm2Sud/J
View Strains carrying other alleles of Nrxn1     (1 strain)

Strains carrying other alleles of Nrxn2
008416   B6;129-Nrxn3tm2Sud Nrxn1tm2Sud Nrxn2tm2Sud/J
View Strains carrying other alleles of Nrxn2     (1 strain)

Strains carrying other alleles of Nrxn3
008416   B6;129-Nrxn3tm2Sud Nrxn1tm2Sud Nrxn2tm2Sud/J
014157   B6;129-Nrxn3tm3Sud/J
016194   B6;129-Nrxn3tm4.1Sud/J
View Strains carrying other alleles of Nrxn3     (3 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Chromosome 2p16.3 Deletion Syndrome   (NRXN1)
Pitt-Hopkins-Like Syndrome 2; PTHSL2   (NRXN1)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Nrxn1tm1Sud/Nrxn1tm1Sud Nrxn2tm1Sud/Nrxn2tm1Sud Nrxn3tm1Sud/Nrxn3tm1Sud

        involves: 129 * C57BL/6
  • mortality/aging
  • complete neonatal lethality
    • all mice die within a day of birth putatively due to dysfunction of essential neural networks involved in breathing   (MGI Ref ID J:89452)
  • respiratory system phenotype
  • respiratory distress
    • mutants have difficulty breathing with a highly irregular respiratory rhythm and reduced ventilation activity due to a dysfunctional output of rhythm generating network in the brainstem   (MGI Ref ID J:89452)
  • nervous system phenotype
  • abnormal CNS synaptic transmission
    • decrease in spontaneous miniature postsynaptic current frequency, decrease in evoked response, increase in failure rates, and lack of noticeable changes in postsynaptic receptor activity shows a primary pre-synaptic defect involving impaired neurotransmitter release   (MGI Ref ID J:89452)
    • post-synaptic defects involving impaired NMDA receptor function   (MGI Ref ID J:88641)
    • impaired evoked synaptic transmission in neocortex   (MGI Ref ID J:89452)
    • abnormal GABA-mediated receptor currents
      • large decrease in the frequency of GABA(A)-receptor mediated spontaneous miniature postsynaptic currents in the neocortex and the brainstem   (MGI Ref ID J:89452)
      • density of GABA-releasing terminals is reduced by about 2-fold, whereas the density of glutamatergic terminals is unchanged   (MGI Ref ID J:89452)
    • abnormal synaptic depression
      • aggravation of short-term synaptic depression within individual stimulus trains and increased synaptic depression during multiple stimulus trains   (MGI Ref ID J:89452)
    • decreased excitatory postsynaptic current amplitude
      • impaired evoked synaptic transmission in brainstem; even at high stimulation strengths, the amplitudes of excitatory postsynaptic currents are smaller than in controls   (MGI Ref ID J:89452)
    • reduced AMPA-mediated synaptic currents
      • large decrease in the frequency of AMPA-receptor mediated spontaneous miniature postsynaptic currents in the neocortex and the brainstem   (MGI Ref ID J:89452)
    • reduced NMDA-mediated synaptic currents
      • the NMDA-receptor-dependent component of spontaneous synaptic miniature responses is reduced about 50%, while the AMPA-receptor-dependent component is unaffected   (MGI Ref ID J:88641)
      • selective decrease in NMDA-receptor-mediated currents affecting evoked synaptic responses   (MGI Ref ID J:88641)
  • abnormal paired-pulse inhibition
    • within a stimulus train, paired-pulse depression is normal in response to the second stimulus but responses to the 3rd and 4th stimulus are lower in synapses   (MGI Ref ID J:89452)
  • decreased CNS synapse formation
    • density of symmetric (presumptive inhibitory) synapses are reduced in the brainstem but density of asymmetric (presumptive excitatory) are not   (MGI Ref ID J:89452)
  • decreased neurotransmitter release
    • spontaneous and evoked neurotransmitter release is impaired as measured in excitatory and inhibitory synapses in the brainstem and neocortex, partly due to a decrease in presynaptic calcium currents, especially N-type calcium currents   (MGI Ref ID J:89452)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Neurobiology Research
Neurotransmitter Receptor and Synaptic Vesicle Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Nrxn1tm1Sud
Allele Name targeted mutation 1, Thomas C Sudhof
Allele Type Targeted (knock-out)
Common Name(s) Nrxn1alphaKO; SKO2;
Strain of Origin129
Gene Symbol and Name Nrxn1, neurexin I
Chromosome 17
Gene Common Name(s) 1700062G21Rik; 9330127H16Rik; A230068P09Rik; Hs.22998; Nrxn1b; PTHSL2; RIKEN cDNA 1700062G21 gene; RIKEN cDNA 9330127H16 gene; RIKEN cDNA A230068P09 gene; SCZD17; alpha-latrotoxin receptor (calcium-dependent); mKIAA0578; neurexin I alpha; neurexin I beta;
Molecular Note A neo cassette replaced the first exon, which contains the complete 5' UTR, start codon, signal peptide and the first LNS domain. Protein was undetected by Western blot analysis of mutant mice. [MGI Ref ID J:45298]
 
Allele Symbol Nrxn2tm1Sud
Allele Name targeted mutation 1, Thomas C Sudhof
Allele Type Targeted (knock-out)
Mutation Made ByDr. Thomas Sudhof,   Stanford University School of Medicine
Strain of Origin129
Gene Symbol and Name Nrxn2, neurexin II
Chromosome 19
Gene Common Name(s) 6430591O13Rik; RIKEN cDNA 6430591O13 gene; mKIAA0921; neurexin II alpha; neurexin II beta;
Molecular Note A neo cassette replaced the first exon, which contains the complete 5' UTR, start codon, signal peptide and the first LNS domain. Immunoblotting of mutant brain confirmed lack of protein expression. [MGI Ref ID J:89452]
 
Allele Symbol Nrxn3tm1Sud
Allele Name targeted mutation 1, Thomas C Sudhof
Allele Type Targeted (knock-out)
Mutation Made ByDr. Thomas Sudhof,   Stanford University School of Medicine
Strain of Origin129
Gene Symbol and Name Nrxn3, neurexin III
Chromosome 12
Gene Common Name(s) 4933401A11Rik; 9330112C09Rik; D12Bwg0831e; DNA segment, Chr 12, Brigham & Women's Genetics 0831 expressed; RIKEN cDNA 4933401A11 gene; RIKEN cDNA 9330112C09 gene; neurexin III alpha; neurexin III beta;
Molecular Note A neo cassette replaced the first exon, which contains the complete 5' UTR, start codon, signal peptide and the first LNS domain. Immunoblotting of mutant brain confirmed lack of protein expression. [MGI Ref ID J:89452]

Genotyping

Genotyping Information

Genotyping Protocols

Nrxn1tm1Sud, Separated PCR
Nrxn3tm1Sud, Separated PCR
Nrxn2tm1Sud, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Missler M; Zhang W; Rohlmann A; Kattenstroth G; Hammer RE; Gottmann K; Sudhof TC. 2003. Alpha-neurexins couple Ca2+ channels to synaptic vesicle exocytosis. Nature 423(6943):939-48. [PubMed: 12827191]  [MGI Ref ID J:89452]

Additional References

Nrxn1tm1Sud related

Dudanova I; Sedej S; Ahmad M; Masius H; Sargsyan V; Zhang W; Riedel D; Angenstein F; Schild D; Rupnik M; Missler M. 2006. Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules. J Neurosci 26(41):10599-613. [PubMed: 17035546]  [MGI Ref ID J:113228]

Dudanova I; Tabuchi K; Rohlmann A; Sudhof TC; Missler M. 2007. Deletion of alpha-neurexins does not cause a major impairment of axonal pathfinding or synapse formation. J Comp Neurol 502(2):261-74. [PubMed: 17347997]  [MGI Ref ID J:132844]

Etherton MR; Blaiss CA; Powell CM; Sudhof TC. 2009. Mouse neurexin-1alpha deletion causes correlated electrophysiological and behavioral changes consistent with cognitive impairments. Proc Natl Acad Sci U S A 106(42):17998-8003. [PubMed: 19822762]  [MGI Ref ID J:153748]

Geppert M; Khvotchev M; Krasnoperov V; Goda Y; Missler M; Hammer RE; Ichtchenko K; Petrenko AG; Sudhof TC. 1998. Neurexin I alpha is a major alpha-latrotoxin receptor that cooperates in alpha-latrotoxin action. J Biol Chem 273(3):1705-10. [PubMed: 9430716]  [MGI Ref ID J:45298]

Grayton HM; Missler M; Collier DA; Fernandes C. 2013. Altered social behaviours in neurexin 1alpha knockout mice resemble core symptoms in neurodevelopmental disorders. PLoS One 8(6):e67114. [PubMed: 23840597]  [MGI Ref ID J:203721]

Kattenstroth G; Tantalaki E; Sudhof TC; Gottmann K; Missler M. 2004. Postsynaptic N-methyl-D-aspartate receptor function requires alpha-neurexins. Proc Natl Acad Sci U S A 101(8):2607-12. [PubMed: 14983056]  [MGI Ref ID J:88641]

Laarakker MC; Reinders NR; Bruining H; Ophoff RA; Kas MJ. 2012. Sex-dependent novelty response in neurexin-1alpha mutant mice. PLoS One 7(2):e31503. [PubMed: 22348092]  [MGI Ref ID J:185327]

Mosedale M; Egodage S; Calma RC; Chi NW; Chessler SD. 2012. Neurexin-1alpha contributes to insulin-containing secretory granule docking. J Biol Chem 287(9):6350-61. [PubMed: 22235116]  [MGI Ref ID J:182555]

Reichelt AC; Rodgers RJ; Clapcote SJ. 2012. The role of neurexins in schizophrenia and autistic spectrum disorder. Neuropharmacology 62(3):1519-26. [PubMed: 21262241]  [MGI Ref ID J:183601]

Sons MS; Busche N; Strenzke N; Moser T; Ernsberger U; Mooren FC; Zhang W; Ahmad M; Steffens H; Schomburg ED; Plomp JJ; Missler M. 2006. alpha-Neurexins are required for efficient transmitter release and synaptic homeostasis at the mouse neuromuscular junction. Neuroscience 138(2):433-46. [PubMed: 16406382]  [MGI Ref ID J:107025]

Tobaben S; Sudhof TC; Stahl B. 2002. Genetic analysis of alpha-latrotoxin receptors reveals functional interdependence of CIRL/latrophilin 1 and neurexin 1 alpha. J Biol Chem 277(8):6359-65. [PubMed: 11741895]  [MGI Ref ID J:115214]

Zhang W; Rohlmann A; Sargsyan V; Aramuni G; Hammer RE; Sudhof TC; Missler M. 2005. Extracellular domains of alpha-neurexins participate in regulating synaptic transmission by selectively affecting N- and P/Q-type Ca2+ channels. J Neurosci 25(17):4330-42. [PubMed: 15858059]  [MGI Ref ID J:98345]

Nrxn2tm1Sud related

Dudanova I; Sedej S; Ahmad M; Masius H; Sargsyan V; Zhang W; Riedel D; Angenstein F; Schild D; Rupnik M; Missler M. 2006. Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules. J Neurosci 26(41):10599-613. [PubMed: 17035546]  [MGI Ref ID J:113228]

Dudanova I; Tabuchi K; Rohlmann A; Sudhof TC; Missler M. 2007. Deletion of alpha-neurexins does not cause a major impairment of axonal pathfinding or synapse formation. J Comp Neurol 502(2):261-74. [PubMed: 17347997]  [MGI Ref ID J:132844]

Kattenstroth G; Tantalaki E; Sudhof TC; Gottmann K; Missler M. 2004. Postsynaptic N-methyl-D-aspartate receptor function requires alpha-neurexins. Proc Natl Acad Sci U S A 101(8):2607-12. [PubMed: 14983056]  [MGI Ref ID J:88641]

Sons MS; Busche N; Strenzke N; Moser T; Ernsberger U; Mooren FC; Zhang W; Ahmad M; Steffens H; Schomburg ED; Plomp JJ; Missler M. 2006. alpha-Neurexins are required for efficient transmitter release and synaptic homeostasis at the mouse neuromuscular junction. Neuroscience 138(2):433-46. [PubMed: 16406382]  [MGI Ref ID J:107025]

Nrxn3tm1Sud related

Dudanova I; Sedej S; Ahmad M; Masius H; Sargsyan V; Zhang W; Riedel D; Angenstein F; Schild D; Rupnik M; Missler M. 2006. Important contribution of alpha-neurexins to Ca2+-triggered exocytosis of secretory granules. J Neurosci 26(41):10599-613. [PubMed: 17035546]  [MGI Ref ID J:113228]

Dudanova I; Tabuchi K; Rohlmann A; Sudhof TC; Missler M. 2007. Deletion of alpha-neurexins does not cause a major impairment of axonal pathfinding or synapse formation. J Comp Neurol 502(2):261-74. [PubMed: 17347997]  [MGI Ref ID J:132844]

Kattenstroth G; Tantalaki E; Sudhof TC; Gottmann K; Missler M. 2004. Postsynaptic N-methyl-D-aspartate receptor function requires alpha-neurexins. Proc Natl Acad Sci U S A 101(8):2607-12. [PubMed: 14983056]  [MGI Ref ID J:88641]

Sons MS; Busche N; Strenzke N; Moser T; Ernsberger U; Mooren FC; Zhang W; Ahmad M; Steffens H; Schomburg ED; Plomp JJ; Missler M. 2006. alpha-Neurexins are required for efficient transmitter release and synaptic homeostasis at the mouse neuromuscular junction. Neuroscience 138(2):433-46. [PubMed: 16406382]  [MGI Ref ID J:107025]

Health & husbandry

The genotypes of the animals provided may not reflect those discussed in the strain description or the mating scheme utilized by The Jackson Laboratory prior to cryopreservation. Please inquire for possible genotypes for this specific strain.

Health & Colony Maintenance Information

Animal Health Reports

Production of mice from cryopreserved embryos or sperm occurs in a maximum barrier room, G200.

Colony Maintenance

Breeding & HusbandryWhen maintained as a live colony, animals homozygous for Nrxn2 and heterozygous for Nrxn1 and Nrxn3 are intercrossed.

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2085.00
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Cryopreserved

Cryopreserved Mice - Ready for Recovery

Price (US dollars $)
Cryorecovery* $2710.50
Animals Provided

At least two mice that carry the mutation (if it is a mutant strain) will be provided. Their genotypes may not reflect those discussed in the strain description. Please inquire for possible genotypes and see additional details below.

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Supply Notes

  • Cryorecovery - Standard.
    Progeny testing is not required.
    The average number of mice provided from recovery of our cryopreserved strains is 10. The total number of animals provided, their gender and genotype will vary. We will fulfill your order by providing at least two pair of mice, at least one animal of each pair carrying the mutation of interest. Please inquire if larger numbers of animals with specific genotype and genders are needed. Animals typically ship between 11 and 14 weeks from the date of your order. If a second cryorecovery is needed in order to provide the minimum number of animals, animals will ship within 25 weeks. IMPORTANT NOTE: The genotypes of animals provided may not reflect the mating scheme utilized by The Jackson Laboratory prior to cryopreservation, or that discussed in the strain description. Please inquire about possible genotypes which will be recovered for this specific strain. The Jackson Laboratory cannot guarantee the reproductive success of mice shipped to your facility. If the mice are lost after the first three days (post-arrival) or do not produce progeny at your facility, a new order and fee will be necessary.

    Cryorecovery to establish a Dedicated Supply for greater quantities of mice
    Mice recovered can be used to establish a dedicated colony to contractually supply you mice according to your requirements. Price by quotation. For more information on Dedicated Supply, please contact JAX® Services, Tel: 1-800-422-6423 (from U.S.A., Canada or Puerto Rico only) or 1-207-288-5845 (from any location).

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Cryopreserved. Ready for recovery. Please refer to pricing and supply notes on the strain data sheet for further information.

Control Information

  Control
   None Available
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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