JAX Mouse Strain Datasheet - 002633

B6;129S4-Nos1^tm1Plh/J

Stock No:: 002633 |; nNos KO

Targeted Mutation

Cryo Recovery

Overview

Also Known As: nNos KO

Nos1 KO mice may useful when studying structure and function of neurons and their synaptic connections in the brain and periphery.

Donating Investigator

Dr. Paul Huang, Mass General Hospital, Harvard Med Sch

Genetic overview

Genetic Background	Generation

Nos1^tm1Plh

Allele Type	Gene Symbol	Gene Name
Targeted (Null/Knockout)	Nos1	nitric oxide synthase 1, neuronal

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Research Applications

Diabetes and Obesity Research
Neurobiology Research

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Base Price

Starting at:

$2,595.00 Domestic price Cryo Recovery

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Details

Important Note

This is the incipient stock for the congenic strain B6.129S4-Nos1^tm1Plh /J (#002986) that was backcrossed to C57BL/6J more than 10 generations.

Detailed Description

The nitric oxide signaling molecule produced by the neuronal Nos1 gene is widely expressed, affecting diverse systems. The knockout of this gene has been shown to affect such normal characteristics as cognition and behavior, long-term memory, cortical development, colonic motility, skeletal muscle contraction, ovarian cycle regulation, cardiac/cardiovascular function, and even sensitivity to Anthrax lethal toxin. Heterozygous mice are viable and fertile, while some lethality is seen in homozygotes due to stomach hypertrophy. Homozygotes have enlarged stomachs with hypertrophy of the pyloric sphincter and the circular muscle layer (Huang et al., 1993). Western blots of brain homogenates from homozygous mutant mice showed no detectable protein. However, splice variants are expressed and variable low levels of NOS activity are seen in the brain. Homozygous males are reported to be more aggressive than normal wildtype siblings although this has not been confirmed in The Jackson Laboratory colony.

Development

A targeting vector was designed to replace exon 1 of the nitric oxide synthase 1, neuronal (Nos1) gene with a neomycin cassette. This exon encodes the initiation site and amino acids 1 - 159 of the protein. The targeting vector was electroporated into 129S4/SvJae-derived Jl ES cells that were injected into C57BL/6 blastocysts. Injected blastocysts were implanted in (C57BL/6 x DBA/2)F1 mice. Chimeric progeny were backcrossed to C57BL/6 mice. Some mice were further backcrossed to C57BL/6J mice (Stock No. 000664) for more than 10 generations to produce Stock No. 002986.

Control Suggestions

Wild-type from the colony

Approximate Controls

101045 B6129SF2/J

Additional Information

Considerations for Choosing Controls

Selected References

Huang PL; Dawson TM; Bredt DS; Snyder SH; Fishman MC. 1993. Targeted disruption of the neuronal nitric oxide synthase gene. Cell 75(7):1273-86. PubMed: 7505721 MGI: J:16390

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Genetics

Nos1^tm1Plh

Allele Symbol: Nos1^tm1Plh

Allele Name	targeted mutation 1, Paul L Huang
Allele Type	Targeted (Null/Knockout)
Allele Synonym(s)	Kn; N2KO; NOS^delta; alphaNOS1; nNOS KO; nNOS-; nNOS^-
Gene Symbol and Name	Nos1, nitric oxide synthase 1, neuronal
Gene Synonym(s)	2310005C01Rik; 2310005C01Rik; IHPS1; N-NOS; NC-NOS; NO; NOS; Nos-1; Nos-1; RIKEN cDNA 2310005C01 gene; bNOS; nNOS; nitric oxide synthase 1 (macrophage)
Strain of Origin	129S4/SvJae
Chromosome	5
Molecular Note	A neomycin cassette replaced exon 1. This exon encodes the initiation site and amino acids 1 - 159 of the protein. Northern blots of brain homogenates from homozygous mutant mice showed no detectable mRNA. Western blots of brain homogenates from homozygous mutant mice showed no detectable protein. However, splice variants are expressed and variable low levels of NOS activity are seen in the brain.
Mutations Made By	Dr. Paul Huang, Mass General Hospital, Harvard Med Sch

Disease/Phenotype

Disease Terms

Research Areas By Genotype

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

Genotype: Nos1^tm1Plh related

Diabetes and Obesity Research
- Insulin Resistance
Neurobiology Research
- Neurotransmitter Receptor and Synaptic Vesicle Defects

Mammalian Phenotype Terms by Genotype

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae * C57BL/6J

renal/urinary system phenotype

abnormal renal reabsorbtion
- the rate of bicarbonate absorption is reduced in the proximal tubules

abnormal renal water reabsorbtion
- the rate of net fluid absorption is reduced in the proximal tubules

increased urine bicarbonate level
- increase in urine bicarbonate concentration

increased urine pH
- increase in urine pH

cardiovascular system phenotype

decreased mean systemic arterial blood pressure

increased heart rate
- atria display higher baseline heart rates
- decrease in heart rate in response to vagal nerve stimulation is slower

homeostasis/metabolism phenotype

abnormal renal water reabsorbtion
- the rate of net fluid absorption is reduced in the proximal tubules

acidosis
- arterial blood pH and bicarbonate concentrations are reduced resulting in a modest but significant metabolic acidosis

homeostasis/metabolism phenotype
- despite differences in behavioral responses to alcohol, no differences in blood alcohol elimination are detected

increased urine bicarbonate level
- increase in urine bicarbonate concentration

increased urine pH
- increase in urine pH

behavior/neurological phenotype

abnormal behavioral response to addictive substance
- following dosing with 2.5 or 4.5 gm/kg mice regain their righting reflex faster compared to similarly treated wild-type controls

abnormal liquid preference
- however, the concentration dependent aversion to quinine is not significantly different from controls
- the concentration dependent increase in sucrose preference is more pronounced in mutants compared to wild-type controls

abnormal spatial learning
- however, performance in the less stressful multiple T maze is improved compared to controls
- impaired performance during memory recall trials in a Morris water maze

enhanced behavioral response to addictive substance
- mice fail to develop tolerance to alcohol induced hypothermia following multiple ethanol injection

enhanced coordination
- in the last trial mice spend more time on the rotarod compared to wild-type controls

increased aggression towards males
- Background Sensitivity - mice display increased aggression compared to C57BL/6J mice but not compared to 129S2/SvPas mice
- Background Sensitivity - unlike mice on a congenic C57BL/6J background, male mice display increased aggression

increased alcohol consumption
- however, when presented with dilute solutions of alcohol (2 - 4%), alcohol consumption does not differ from controls
- mice consume more alcohol when presented with solutions containing high concentrations of alcohol (greater than 8% alcohol) compared to wild-type controls

increased anxiety-related response
- increase in grooming behavior is seen in mice in an open field and during an elevated plus maze assay suggesting an increase in the amount of stress mice experience under these conditions

increased coping response
- in a forced swim test mice spend more time actively swimming and less time immobile compared to wild-type controls

increased grooming behavior
- seen in mice in an open field and during an elevated plus maze assay suggesting an increase in the amount of stress mice experience under these conditions

digestive/alimentary phenotype

abnormal digestion
- stomachs often contain bezoars even after 2 days of fasting

digestive/alimentary phenotype
- unlike in human patients with Infantile Hypertrophic Pyloric Stenosis, the luminal aperture of the pyloric sphincter is not significantly smaller in relaxed tissues compared to wild type controls

enlarged duodenum
- diffuse enlargement

enlarged esophagus
- diffuse enlargement

enlarged stomach
- diffuse enlargement
- weight and volume are increased

gastric hypertrophy
- muscular thickening is seen throughout the stomach

impaired gastric peristalsis
- gastric emptying of solids and liquids is delayed

pyloric sphincter hypertrophy
- pyloric sphincter thickness is increased by 17% compared to controls

muscle phenotype

pyloric sphincter hypertrophy
- pyloric sphincter thickness is increased by 17% compared to controls

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
B6;129S4-Nos1^tm1Plh/J

behavior/neurological phenotype

abnormal sleep pattern
- however, there is no significant difference in the amount of time spent in non-REM sleep and mice display normal diurnal variation in sleep patterns
- mice spend less time in REM sleep as a result of fewer REM episodes and lengthened duration of the inter REM intervals

behavior/neurological phenotype
- increased aggressive behavior is not seen in males unlike in other reports

nervous system phenotype

abnormal brain wave pattern
- during non-REM sleep the absolute value of slow wave activity is increased

skeleton phenotype

abnormal osteoclast differentiation
- in culture RANKL and M-CSF induced osteoclast formation are increased

abnormal skeleton development
- indices of bone formation and resorption are lower

abnormal trabecular bone morphology
- trabecular bone tends to extend deeper into the metaphysis

increased bone mineral content
- bone mineral content is increased

increased bone mineral density
- bone mineral density is increased

increased trabecular bone thickness

increased trabecular bone volume

hematopoietic system phenotype

abnormal osteoclast differentiation
- in culture RANKL and M-CSF induced osteoclast formation are increased

immune system phenotype

abnormal osteoclast differentiation
- in culture RANKL and M-CSF induced osteoclast formation are increased

cellular phenotype

abnormal osteoclast differentiation
- in culture RANKL and M-CSF induced osteoclast formation are increased

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae * C57BL/6

mortality/aging

decreased sensitivity to induced morbidity/mortality
- in anesthetized mice under 12% oxygen all mutant mice survived while 4 of 14 wild-type mice died

decreased survivor rate
- survival at 20 months is reduced compared to Nos3 null mice

premature death
- slight increase in premature death
- survival at 20 months is reduced compared to Nos3 null mice
- the relative risk of death by 20 months of age is 2.5 times higher than in Nos3 null mice

cellular phenotype

abnormal mitochondrial physiology
- despite similar ratios of mitochondrial to nuclear DNA the amount of citrate synthase is significantly increased in homogenates from the heart, kidney and liver

liver/biliary system phenotype

abnormal hepatocyte morphology
- fat droplets are absent from the cytosol of hepatocytes

abnormal liver morphology
- lipid content of the liver is increased
- unlike in wild-type livers, glycogen content is increased in zone 3 relative to zone 1 of the liver

renal/urinary system phenotype

abnormal renal tubule morphology
- electron microscopy analysis indicates a lower density of mitochondria in tubule cells of the kidney
- however, the ratio of mitochondrial to nuclear DNA is similar to controls

growth/size/body region phenotype

growth/size/body region phenotype
- no difference in body weight is detected at 1 year of age

digestive/alimentary phenotype

abnormal stomach wall morphology
- hypertrophy of the pyloric sphincter and the circular muscle layer
- with age, the stomachs lose their interior folds and undergo thinning of the walls, however the intestine appears normal

enlarged stomach
- stomach dilation, however architecture of the stomach layers is preserved

pyloric sphincter hypertrophy

pyloric stenosis

stomach smooth muscle circular layer hypertrophy

reproductive system phenotype

abnormal ovulation
- ovulatory efficiency (number oocytes recovered divided by the number of ovarian rupture sites) is reduced in homozygotes
- significantly fewer oocytes are recovered following gonadotropin-stimulated ovulation in homozygous mutant females compared to wild-type females

nervous system phenotype

abnormal brain morphology
- electron microscopy analysis indicates a lower density of mitochondria in the cortex of the brain
- however, the ratio of mitochondrial to nuclear DNA is similar to controls

abnormal dendrite morphology
- decrease in the number of branches is first detected at about 100 um from the cell body with a peak in the decrease between about 160 - 260 um
- difference in branch number is limited to third and fourth order branches
- however, the number of primary dendrites and the longest dendritic path from a cell are not different from wild-type controls
- motor neurons display a significant decrease in the number of dendritic branches

abnormal motor neuron morphology
- however, the number of primary dendrites, the longest dendritic path from a cell, and cell body size are not different from wild-type controls
- motor neurons display a significant decrease in the number of dendritic branches

abnormal nervous system physiology
- delay in Wallerian degeneration following transection of the sciatic nerve in the right hindlimb

abnormal peripheral nervous system regeneration
- following transection of the sciatic nerve in the right hindlimb time to recovery of motor function is delayed
- following transection of the sciatic nerve in the right hindlimb uncontrolled sprouting is increased
- however, myelination following transection is not significantly different from controls

nervous system phenotype
- homozygous mice do not exhibit defects in brain structure or neuron degeneration

muscle phenotype

abnormal cardiac muscle relaxation
- time to 50% relaxation is increased

abnormal muscle physiology
- muscle atrophy induced by transection of the sciatic nerve in the right hindlimb is reduced

decreased cardiac muscle contractility
- attenuation of the beta-adrenergic inotropic responses indicating a decrease in myocardial contractile reserve

increased ventricle muscle contractility
- isolated ventricular myocytes display greater overall shortening at all stimulation frequencies between 0.2 and 10 Hz
- shortening in response to beta-adrenergic stimulation is greatly enhanced

pyloric sphincter hypertrophy

stomach smooth muscle circular layer hypertrophy

behavior/neurological phenotype

abnormal mating frequency
- by 7 to 8 h after introduction of a female, the number of mounts made by males is 2 to 3 times greater compared to wild-type males
- the number of mounts fails to decrease significantly 1 h after the introduction of an anestrus female to the cage
- when placed with females in estrus males display excessive and inappropriate mounting

increased aggression towards females
- when placed with females in estrus males display excessive and inappropriate mounting

increased aggression towards males
- for males latency to first attack is reduced to about 1/5 that of wild-type mice
- for males the duration of aggressive encounters is increased
- in a resident intruder assay males display more aggressive encounters and initiate more of the aggressive encounters compared to wild-type mice
- male mice display submissive postures about 1/10 as frequently as wild-type controls
- no increase in aggression is seen in females

homeostasis/metabolism phenotype

abnormal carbon dioxide production
- in awake mice carbon dioxide production is significantly decreased during 12% oxygen compared to 100% oxygen in mutant but not in wild-type mice

abnormal oxygen consumption
- in awake mice the magnitude of the decrease in oxygen consumption under 21% or 12% oxygen is greater than that in wild-type controls

homeostasis/metabolism phenotype
- despite the increase in aggressive and sexual behaviors, no significant difference is detected in blood testosterone levels compared to wild-type males

increased oxygen consumption

increased physiological sensitivity to xenobiotic
- sodium cyanide induced respiratory stimulation is increased in mutants compared to wild-type mice

respiratory system phenotype

abnormal breathing pattern
- anesthetized mice under 21% or 12% oxygen show period increases in respiratory rate not seen in wild-type mice

abnormal pulmonary respiratory rate
- in awake mice, the magnitude of the decrease in respiratory rate following brief exposure to 100% oxygen was greater than that in wild-type mice

increased pulmonary respiratory rate
- anesthetized mice do not display respiratory depression under 12% oxygen, unlike wild-type controls
- in anesthetized mutant mice the increase in ventilation under 21% oxygen results from an increase in both respiratory rate and tidal phrenic activity, unlike in wild-type mice where only tidal phrenic activity is increased
- in awake and anesthetized mice the magnitude of the increases in respiratory rate at 21% and 12% oxygen are greater than in wild-type controls
- sodium cyanide induced respiratory stimulation is increased in mutants compared to wild-type mice

increased pulmonary ventilation
- in awake and anesthetized mice the magnitude of the increase in minute ventilation is greater at both 21% and 12% oxygen compared to wild-type controls
- in awake mice the significant increases are seen in minute ventilation at both 21% and 12% oxygen unlike in wild-type controls where increases are seen only at 12% oxygen

increased tidal volume
- in awake mice the magnitude of the increases in tidal volume at 21% and 12% oxygen are greater than in wild-type controls

cardiovascular system phenotype

abnormal cardiac muscle relaxation
- time to 50% relaxation is increased

decreased cardiac muscle contractility
- attenuation of the beta-adrenergic inotropic responses indicating a decrease in myocardial contractile reserve

heart left ventricle hypertrophy
- age related

increased ventricle muscle contractility
- isolated ventricular myocytes display greater overall shortening at all stimulation frequencies between 0.2 and 10 Hz
- shortening in response to beta-adrenergic stimulation is greatly enhanced

The following phenotype information is associated with a similar, but not exact match to this JAX^® Mice strain

Genotype: Nos1^tm1Plh/Nos1⁺
B6.129S4-Nos1^tm1Plh

cardiovascular system phenotype

abnormal cardiovascular system physiology
- exercise training fails to augment the phenylephrine induced pulse interval response

abnormal heart rate
- exercise training fails to augment the phenylephrine induced or vagal nerve stimulation bradycardia responses
- no differences in heart rate responses are detected in the absence of exercise training

homeostasis/metabolism phenotype

abnormal physiological response to xenobiotic
- exercise training fails to augment the phenylephrine induced bradycardia and pulse interval responses
- no differences in phenylephrine induced responses are seen in untrained mice

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
B6.129S4-Nos1^tm1Plh

cardiovascular system phenotype

abnormal blood-brain barrier function
- kainic acid injection of hippocampi does not cause blood-brain barrier breakdown

cardiovascular system phenotype
- unlike mice null for Nos3, ischemia induced retinal neovascularization is not significantly different from controls

decreased susceptibility to induced choroidal neovascularization
- knockouts show a 58% decrease in neovascularization at sites of laser-induced Bruch's membrane rupture compared to heterozygous littermates

behavior/neurological phenotype

abnormal maternal behavior
- about a 90% decrease in the amount of time lactating females spend actively attacking or biting an intruder male
- in contrast to the decrease in maternal aggression, no defect in pup retrieval is detected
- lactating females display decreased aggression towards intruder males

abnormal seizure response to inducing agent
- when exposed to hyperbaric oxygen (greater than 99% oxygen) at 5 ATA for 60 min the time to first seizure in freely moving mice is significantly longer compared to similarly treated wild-type mice

behavior/neurological phenotype
- Background Sensitivity - unlike mice on a mixed 129S4/SvJae and C57BL/6J background, congenic male mice do not display significantly increased aggression compared to wild-type controls

decreased aggression towards males
- about a 90% decrease in the amount of time lactating females spend actively attacking or biting an intruder male
- lactating females display decreased aggression towards intruder males

increased aggression towards males
- increase in the number and duration of attacks and decrease in the latency to attack in a resident intruder assay
- significantly higher concentrations of serotonin receptor agonists are required to reduce aggressive behavior than in wild-type controls
- treatment with a serotonin precursor dramatically reduces aggressive behavior

homeostasis/metabolism phenotype

abnormal serotonin level
- as no change is seen on the concentration of the serotonin metabolite, 5-HIAA, the 5-HIAA to serotonin (5-HT) ratio is reduced in the cortex, hypothalamus, midbrain, and cerebellum indicating a decrease in serotonin turnover
- total serotonin content is increased in the cerebral cortex, hypothalamus, hippocampus, midbrain and cerebellum

decreased adiponectin level

decreased cerebral infarction size
- however, infarct size is increased compared to mice hemizygous for Tg(SOD1)76Dpr
- infarction sized induced by middle cerebral artery obstruction is reduced in males, but not in females, compared to wild-type controls

decreased susceptibility to ischemic brain injury
- functional deficits following middle cerebral artery obstruction are reduced compared to wild-type controls

decreased susceptibility to neuronal excitotoxicity
- kainic acid does not cause the hippocampal neurons to degenerate

increased circulating triglyceride level
- elevated plasma triglycerides

vision/eye phenotype

decreased susceptibility to induced choroidal neovascularization
- knockouts show a 58% decrease in neovascularization at sites of laser-induced Bruch's membrane rupture compared to heterozygous littermates

nervous system phenotype

abnormal blood-brain barrier function
- kainic acid injection of hippocampi does not cause blood-brain barrier breakdown

abnormal nervous system physiology
- in anesthetized mice the latency to hyperbaric oxygen (greater than 99% oxygen) at 5 ATA induced EEG seizure is increased compared to similarly treated wild-type mice
- striatal accumulation of 3-nitrotyrosine during hyperbaric oxygen exposure is decreased compared to similarly treated wild-type mice

abnormal seizure response to inducing agent
- when exposed to hyperbaric oxygen (greater than 99% oxygen) at 5 ATA for 60 min the time to first seizure in freely moving mice is significantly longer compared to similarly treated wild-type mice

decreased cerebral infarction size
- however, infarct size is increased compared to mice hemizygous for Tg(SOD1)76Dpr
- infarction sized induced by middle cerebral artery obstruction is reduced in males, but not in females, compared to wild-type controls

decreased susceptibility to ischemic brain injury
- functional deficits following middle cerebral artery obstruction are reduced compared to wild-type controls

decreased susceptibility to neuronal excitotoxicity
- kainic acid does not cause the hippocampal neurons to degenerate

cellular phenotype

decreased susceptibility to neuronal excitotoxicity
- kainic acid does not cause the hippocampal neurons to degenerate

maternal effect
- pups of homozygous females weigh more than pups of wild-type females

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
B6.129S4-Nos1^tm1Plh/J

growth/size/body region phenotype

decreased body weight
- in males only

muscle phenotype

decreased skeletal muscle weight
- decrease in skeletal muscle weight in males

impaired skeletal muscle contractility
- decrease in the maximal tetanic force generating capacity of the tibialis anterior muscle in males
- however, when normalized to muscle size the force generating capacity is not significantly different from wild-type controls
- peak twitch force is decreased in the tibialis anterior muscle of male mice

muscle fatigue
- tibialis anterior muscle displays an increase in the susceptibility to contraction induced fatigue in both males and females

immune system phenotype

decreased inflammatory response
- fever in response to LPS injection is partially reduced compared to wild-type controls
- however, fever in response to turpentine injection is not different from controls
- reduction in fever response mainly occurs during the early phase of fever response

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae

mortality/aging

decreased survivor rate
- about 80% survival rate at 10 months of age

premature death
- about 20% die before 10 months of age

reproductive system phenotype

reproductive system phenotype
- unlike in Nos3 null mice, the increase in maximal penile intracavernous pressure induced by papaverine is not significantly different from wild-type controls

growth/size/body region phenotype

decreased body weight

cellular phenotype

abnormal leukocyte adhesion
- dramatic increase in baseline leukocyte adherence
- treatment with an anti-P-selectin antibody significantly reduces the adhesion response in mutant but not in wild-type mice

decreased susceptibility to neuronal excitotoxicity
- the size of striatal lesions induced by malonate are significantly reduced compared to similarly treated controls

enhanced leukocyte tethering or rolling
- increase in baseline rolling
- treatment with a low dose of thrombin significantly increases rolling in mutant but not in wild-type mice
- treatment with an anti-P-selectin antibody significantly reduces the rolling response in mutant but not in wild-type mice

hematopoietic system phenotype

abnormal leukocyte adhesion
- dramatic increase in baseline leukocyte adherence
- treatment with an anti-P-selectin antibody significantly reduces the adhesion response in mutant but not in wild-type mice

abnormal neutrophil physiology
- following thioglycollate injection neutrophil accumulation in the peritoneum is significantly enhanced compared to wild-type mice

enhanced leukocyte tethering or rolling
- increase in baseline rolling
- treatment with a low dose of thrombin significantly increases rolling in mutant but not in wild-type mice
- treatment with an anti-P-selectin antibody significantly reduces the rolling response in mutant but not in wild-type mice

homeostasis/metabolism phenotype

abnormal vascular wound healing
- following carotid artery ligation the extent of neointimal formation is increased and luminal narrowing is worsened compared to wild-type controls

altered response of heart to induced stress
- myocardial infarct size following 30 min of global ischemia is increased compared to controls

decreased cerebral infarction size
- following occlusion of the middle cerebral artery infarct size is decreased

decreased susceptibility to injury
- 24 h after aspiration bulbectomy the number of apoptotic cells in the piriform cortex is reduced compared to similarly treated wild-type mice

decreased susceptibility to neuronal excitotoxicity
- the size of striatal lesions induced by malonate are significantly reduced compared to similarly treated controls

insulin resistance
- insulin resistance in peripheral tissues

nervous system phenotype

abnormal long term potentiation
- following a theta burst protocol at a weak intensity enhancement of EPSPs during the first 3 minutes after stimulation is significantly small compared to controls
- however, no significant differences are detected when a stronger intensity stimulation is used

abnormal nervous system physiology
- 24 h after aspiration bulbectomy the number of apoptotic cells in the piriform cortex is reduced compared to similarly treated wild-type mice

absent long term depression
- addition of uncaged NO or photoreleased cGMP to the stimulation protocol also fails to induce long term depression in Purkinje cells, unlike in wild-type mice
- stimulation of parallel fibers with a 50 msec postsynaptic depolarizations fails to induce long term depression in Purkinje cells

decreased cerebral infarction size
- following occlusion of the middle cerebral artery infarct size is decreased

decreased susceptibility to neuronal excitotoxicity
- the size of striatal lesions induced by malonate are significantly reduced compared to similarly treated controls

decreased synaptic glutamate release
- glutamate release after NMDA stimulation is significantly attenuated in the cerebral cortex, partially reduced in the striatum but unaffected in the hippocampus

nervous system phenotype
- despite the ability of NOS inhibitors to decrease long term potentiation, no significant decrease in long term potentiation is detected at 1 h after tetanus
- unlike cerebral blood flow, the intensity of neural activation induced by perioral stimulation is not significantly different from controls

behavior/neurological phenotype

behavior/neurological phenotype
- no defects in circadian rhythms are detected in a wheel running assay either under entrained or free running conditions
- unlike in earlier reports males show no signs of increased aggression

impaired balance
- mice show no improvement in their latency to fall off a pole or plank in the dark versus the light phase, unlike in wild-type controls resulting in deficits in balance compared to wild-type mice during the dark phase

digestive/alimentary phenotype

abnormal gastroesophageal sphincter physiology
- efferent vagal stimulation induced lower esophageal sphincter relaxation is significantly attenuated
- lower esophageal sphincters fail to display electrical field stimulation (60 V, 5 Hz) induced relaxation or rebound contraction
- mice show a range of responses to pharyngeal stimulation including no relaxation, partial relaxation , and sporadic near complete relaxation of the lower esophageal sphincter
- swallowing induced lower esophageal sphincter relaxation is significantly attenuated
- the mean resting lower esophageal sphincter pressure is significantly higher

immune system phenotype

abnormal leukocyte adhesion
- dramatic increase in baseline leukocyte adherence
- treatment with an anti-P-selectin antibody significantly reduces the adhesion response in mutant but not in wild-type mice

abnormal neutrophil physiology
- following thioglycollate injection neutrophil accumulation in the peritoneum is significantly enhanced compared to wild-type mice

enhanced leukocyte tethering or rolling
- increase in baseline rolling
- treatment with a low dose of thrombin significantly increases rolling in mutant but not in wild-type mice
- treatment with an anti-P-selectin antibody significantly reduces the rolling response in mutant but not in wild-type mice

muscle phenotype

abnormal gastroesophageal sphincter physiology
- efferent vagal stimulation induced lower esophageal sphincter relaxation is significantly attenuated
- lower esophageal sphincters fail to display electrical field stimulation (60 V, 5 Hz) induced relaxation or rebound contraction
- mice show a range of responses to pharyngeal stimulation including no relaxation, partial relaxation , and sporadic near complete relaxation of the lower esophageal sphincter
- swallowing induced lower esophageal sphincter relaxation is significantly attenuated
- the mean resting lower esophageal sphincter pressure is significantly higher

abnormal muscle physiology
- hyperpolarization and induction of an inhibitory junction potential in response to electrical field stimulation under nonadrenergic noncholinergic conditions in jejunal muscle strips are markedly reduced
- the resting membrane potential of jejunal smooth muscle cells is depolarized about 5 mV compared to wild type cells

abnormal muscle relaxation
- lower esophageal sphincters fail to display electrical field stimulation (60 V, 5 Hz) induced relaxation or rebound contraction
- the decrease in muscle contractions in jejunal muscle strips in response to electrical field stimulation is markedly reduced

cardiovascular system phenotype

abnormal blood circulation
- the increase in cerebral blood flow induced by glutamate, perioral stimulation, or harmaline is significantly attenuated

abnormal vascular wound healing
- following carotid artery ligation the extent of neointimal formation is increased and luminal narrowing is worsened compared to wild-type controls

altered response of heart to induced stress
- myocardial infarct size following 30 min of global ischemia is increased compared to controls

cardiovascular system phenotype
- unlike in mice null for Nos3 no significant abnormalities in hypoxic pulmonary vasoconstriction, vasodilation in response to bradykinin, or right ventricle systolic pressure are detected

decreased coronary flow rate
- however, coronary flow per beat is not significantly different from controls
- in isolated perfused hearts

decreased heart weight

vision/eye phenotype

vision/eye phenotype
- no defects are detected in visual acuity

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae * C57BL/10ScSn

muscle phenotype

muscle phenotype
- no abnormalities in muscle morphology are detected

References

Huang PL; Dawson TM; Bredt DS; Snyder SH; Fishman MC. 1993. Targeted disruption of the neuronal nitric oxide synthase gene. Cell 75(7):1273-86. PubMed: 7505721 MGI: J:16390

Additional References

Bonthius DJ; Tzouras G; Karacay B; Mahoney J; Hutton A; McKim R; Pantazis NJ. 2002. Deficiency of neuronal nitric oxide synthase (nNOS) worsens alcohol-induced microencephaly and neuronal loss in developing mice. Brain Res Dev Brain Res 138(1):45-59. PubMed: 12234657 MGI: J:79331
Chen L; Majde JA; Krueger JM. 2003. Spontaneous sleep in mice with targeted disruptions of neuronal or inducible nitric oxide synthase genes. Brain Res 973(2):214-22. PubMed: 12738065 MGI: J:83571
Chen L; Toth M. 2001. Fragile X mice develop sensory hyperreactivity to auditory stimuli. Neuroscience 103(4):1043-50. PubMed: 11301211 MGI: J:85912
Le Roy I; Pothion S; Mortaud S; Chabert C; Nicolas L; Cherfouh A; Roubertoux PL. 2000. Loss of aggression, after transfer onto a C57BL/6J background, in mice carrying a targeted disruption of the neuronal nitric oxide synthase gene. Behav Genet 30(5):367-73. PubMed: 11235982 MGI: J:67776
Nelson RJ; Demas GE; Huang PL; Fishman MC; Dawson VL; Dawson TM; Snyder SH. 1995. Behavioural abnormalities in male mice lacking neuronal nitric oxide synthase [see comments] Nature 378(6555):383-6. PubMed: 7477374 MGI: J:29970
Shankar RR; Wu Y; Shen HQ; Zhu JS; Baron AD. 2000. Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. Diabetes 49(5):684-7. PubMed: 10905473 MGI: J:62229
Tranguch S; Huet-Hudson Y. 2003. Decreased viability of nitric oxide synthase double knockout mice. Mol Reprod Dev 65(2):175-9. PubMed: 12704728 MGI: J:83112

Additional - Nos1^tm1Plh related

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Tsui AK; Marsden PA; Mazer CD; Adamson SL; Henkelman RM; Ho JJ; Wilson DF; Heximer SP; Connelly KA; Bolz SS; Lidington D; El-Beheiry MH; Dattani ND; Chen KM; Hare GM. 2011. Priming of hypoxia-inducible factor by neuronal nitric oxide synthase is essential for adaptive responses to severe anemia. Proc Natl Acad Sci U S A 108(42):17544-9. PubMed: 21976486 MGI: J:177441
Vallance BA; Dijkstra G; Qiu B; van der Waaij LA; van Goor H; Jansen PL; Mashimo H; Collins SM. 2004. Relative contributions of NOS isoforms during experimental colitis: endothelial-derived NOS maintains mucosal integrity. Am J Physiol Gastrointest Liver Physiol 287(4):G865-74. PubMed: 15217783 MGI: J:96074
Vandsburger MH; French BA; Kramer CM; Zhong X; Epstein FH. 2012. Displacement-encoded and manganese-enhanced cardiac MRI reveal that nNOS, not eNOS, plays a dominant role in modulating contraction and calcium influx in the mammalian heart. Am J Physiol Heart Circ Physiol 302(2):H412-9. PubMed: 22058155 MGI: J:181655
Wagner C; Godecke A; Ford M; Schnermann J; Schrader J; Kurtz A. 2000. Regulation of renin gene expression in kidneys of eNOS- and nNOS-deficient mice Pflugers Arch 439(5):567-72. PubMed: 10764216 MGI: J:62375
Walton JC; Selvakumar B; Weil ZM; Snyder SH; Nelson RJ. 2013. Neuronal nitric oxide synthase and NADPH oxidase interact to affect cognitive, affective, and social behaviors in mice. Behav Brain Res 256:320-7. PubMed: 23948215 MGI: J:202345
Wang H; Kohr MJ; Traynham CJ; Wheeler DG; Janssen PM; Ziolo MT. 2008. Neuronal nitric oxide synthase signaling within cardiac myocytes targets phospholamban. Am J Physiol Cell Physiol 294(6):C1566-75. PubMed: 18400986 MGI: J:136639
Wang H; Viatchenko-Karpinski S; Sun J; Gyorke I; Benkusky NA; Kohr MJ; Valdivia HH; Murphy E; Gyorke S; Ziolo MT. 2010. Regulation of myocyte contraction via neuronal nitric oxide synthase: role of ryanodine receptor S-nitrosylation. J Physiol 588(Pt 15):2905-17. PubMed: 20530114 MGI: J:176763
Wang T; Inglis FM; Kalb RG. 2000. Defective fluid and HCO(3)(-) absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice. Am J Physiol Renal Physiol 279(3):F518-24. PubMed: 10966931 MGI: J:64896
Watkins CC; Boehning D; Kaplin AI; Rao M; Ferris CD; Snyder SH. 2004. Carbon monoxide mediates vasoactive intestinal polypeptide-associated nonadrenergic/noncholinergic neurotransmission. Proc Natl Acad Sci U S A 101(8):2631-5. PubMed: 14983060 MGI: J:88640
Watkins CC; Sawa A; Jaffrey S; Blackshaw S; Barrow RK; Snyder SH; Ferris CD. 2000. Insulin restores neuronal nitric oxide synthase expression and function that is lost in diabetic gastropathy. J Clin Invest 106(3):373-84. PubMed: 10930440 MGI: J:63749
Wehling-Henricks M; Oltmann M; Rinaldi C; Myung KH; Tidball JG. 2009. Loss of positive allosteric interactions between neuronal nitric oxide synthase and phosphofructokinase contributes to defects in glycolysis and increased fatigability in muscular dystrophy. Hum Mol Genet 18(18):3439-51. PubMed: 19542095 MGI: J:151716
Weitzdoerfer R; Hoeger H; Engidawork E; Engelmann M; Singewald N; Lubec G; Lubec B. 2004. Neuronal nitric oxide synthase knock-out mice show impaired cognitive performance. Nitric Oxide 10(3):130-40. PubMed: 15158692 MGI: J:101815
Whiteus C; Freitas C; Grutzendler J. 2014. Perturbed neural activity disrupts cerebral angiogenesis during a postnatal critical period. Nature 505(7483):407-11. PubMed: 24305053 MGI: J:207919
Workman JL; Trainor BC; Finy MS; Nelson RJ. 2008. Inhibition of neuronal nitric oxide reduces anxiety-like responses to pair housing. Behav Brain Res 187(1):109-15. PubMed: 17928072 MGI: J:145099
Wu HH; Cork RJ; Huang PL; Shuman DL; Mize RR. 2000. Refinement of the ipsilateral retinocollicular projection is disrupted in double endothelial and neuronal nitric oxide synthase gene knockout mice. Brain Res Dev Brain Res 120(1):105-11. PubMed: 10727738 MGI: J:61144
Wu HH; Cork RJ; Mize RR. 2000. Normal development of the ipsilateral retinocollicular pathway and its disruption in double endothelial and neuronal nitric oxide synthase gene knockout mice J Comp Neurol 426(4):651-65. PubMed: 11027405 MGI: J:64999
Xu L; Okuda-Ashitaka E; Matsumura S; Mabuchi T; Okamoto S; Sakimura K; Mishina M; Ito S. 2007. Signal pathways coupled to activation of neuronal nitric oxide synthase in the spinal cord by nociceptin/orphanin FQ. Neuropharmacology 52(5):1318-25. PubMed: 17350656 MGI: J:122321
Xu R; Serritella AV; Sen T; Farook JM; Sedlak TW; Baraban J; Snyder SH; Sen N. 2013. Behavioral effects of cocaine mediated by nitric oxide-GAPDH transcriptional signaling. Neuron 78(4):623-30. PubMed: 23719162 MGI: J:201545
Xue L; Farrugia G; Miller SM; Ferris CD; Snyder SH; Szurszewski JH. 2000. Carbon monoxide and nitric oxide as coneurotransmitters in the enteric nervous system: evidence from genomic deletion of biosynthetic enzymes. Proc Natl Acad Sci U S A 97(4):1851-5. PubMed: 10677545 MGI: J:89581
Yang G; Zhang Y; Ross ME; Iadecola C. 2003. Attenuation of activity-induced increases in cerebellar blood flow in mice lacking neuronal nitric oxide synthase. Am J Physiol Heart Circ Physiol 285(1):H298-304. PubMed: 12623792 MGI: J:84255
Yang JZ; Ajonuma LC; Rowlands DK; Tsang LL; Ho LS; Lam SY; Chen WY; Zhou CX; Chung YW; Cho CY; Tse JY; James AE; Chan HC. 2005. The role of inducible nitric oxide synthase in gamete interaction and fertilization: a comparative study on knockout mice of three NOS isoforms. Cell Biol Int 29(9):785-91. PubMed: 16087361 MGI: J:112824
Yatera Y; Shibata K; Furuno Y; Sabanai K; Morisada N; Nakata S; Morishita T; Toyohira Y; Wang KY; Tanimoto A; Sasaguri Y; Tasaki H; Nakashima Y; Shimokawa H; Yanagihara N; Otsuji Y; Tsutsui M. 2010. Severe dyslipidaemia, atherosclerosis, and sudden cardiac death in mice lacking all NO synthases fed a high-fat diet. Cardiovasc Res 87(4):675-82. PubMed: 20304785 MGI: J:176098
Yemisci M; Gursoy-Ozdemir Y; Vural A; Can A; Topalkara K; Dalkara T. 2009. Pericyte contraction induced by oxidative-nitrative stress impairs capillary reflow despite successful opening of an occluded cerebral artery. Nat Med 15(9):1031-7. PubMed: 19718040 MGI: J:154320
Zaharchuk G; Hara H; Huang PL; Fishman MC; Moskowitz MA; Jenkins BG ; Rosen BR. 1997. Neuronal nitric oxide synthase mutant mice show smaller infarcts and attenuated apparent diffusion coefficient changes in the peri-infarct zone during focal cerebral ischemia. Magn Reson Med 37(2):170-5. PubMed: 9001139 MGI: J:40122
Zakhary R; Poss KD; Jaffrey SR; Ferris CD; Tonegawa S; Snyder SH. 1997. Targeted gene deletion of heme oxygenase 2 reveals neural role for carbon monoxide. Proc Natl Acad Sci U S A 94(26):14848-53. PubMed: 9405702 MGI: J:89562
Zhang J; Huang XY; Ye ML; Luo CX; Wu HY; Hu Y; Zhou QG; Wu DL; Zhu LJ; Zhu DY. 2010. Neuronal nitric oxide synthase alteration accounts for the role of 5-HT1A receptor in modulating anxiety-related behaviors. J Neurosci 30(7):2433-41. PubMed: 20164327 MGI: J:157840
Zhang P; Fu WY; Fu AK; Ip NY. 2015. S-nitrosylation-dependent proteasomal degradation restrains Cdk5 activity to regulate hippocampal synaptic strength. Nat Commun 6:8665. PubMed: 26503494 MGI: J:227913
Zhang YH; Zhang MH; Sears CE; Emanuel K; Redwood C; El-Armouche A; Kranias EG; Casadei B. 2008. Reduced phospholamban phosphorylation is associated with impaired relaxation in left ventricular myocytes from neuronal NO synthase-deficient mice. Circ Res 102(2):242-9. PubMed: 18007024 MGI: J:141557
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Also Known As: nNos KO

Donating Investigator

Genetic overview

Research Applications

Base Price

Important Note

Detailed Description

Development

Control Suggestions

Approximate Controls

Additional Information

Selected References

Nos1tm1Plh

Allele Symbol: Nos1tm1Plh

Disease Terms

Research Areas By Genotype

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

Genotype: Nos1tm1Plh related

Mammalian Phenotype Terms by Genotype

Genotype: Nos1tm1Plh/Nos1tm1Plhinvolves: 129S4/SvJae * C57BL/6J

renal/urinary system phenotype

cardiovascular system phenotype

homeostasis/metabolism phenotype

behavior/neurological phenotype

digestive/alimentary phenotype

muscle phenotype

Genotype: Nos1tm1Plh/Nos1tm1PlhB6;129S4-Nos1tm1Plh/J

behavior/neurological phenotype

nervous system phenotype

skeleton phenotype

hematopoietic system phenotype

immune system phenotype

cellular phenotype

Genotype: Nos1tm1Plh/Nos1tm1Plhinvolves: 129S4/SvJae * C57BL/6

mortality/aging

cellular phenotype

liver/biliary system phenotype

renal/urinary system phenotype

growth/size/body region phenotype

digestive/alimentary phenotype

reproductive system phenotype

nervous system phenotype

muscle phenotype

behavior/neurological phenotype

homeostasis/metabolism phenotype

respiratory system phenotype

cardiovascular system phenotype

Genotype: Nos1tm1Plh/Nos1+B6.129S4-Nos1tm1Plh

cardiovascular system phenotype

homeostasis/metabolism phenotype

Genotype: Nos1tm1Plh/Nos1tm1PlhB6.129S4-Nos1tm1Plh

cardiovascular system phenotype

behavior/neurological phenotype

homeostasis/metabolism phenotype

vision/eye phenotype

nervous system phenotype

cellular phenotype

Genotype: Nos1tm1Plh/Nos1tm1PlhB6.129S4-Nos1tm1Plh/J

growth/size/body region phenotype

muscle phenotype

immune system phenotype

Genotype: Nos1tm1Plh/Nos1tm1Plhinvolves: 129S4/SvJae

mortality/aging

reproductive system phenotype

growth/size/body region phenotype

cellular phenotype

hematopoietic system phenotype

homeostasis/metabolism phenotype

nervous system phenotype

behavior/neurological phenotype

digestive/alimentary phenotype

immune system phenotype

muscle phenotype

cardiovascular system phenotype

vision/eye phenotype

Genotype: Nos1tm1Plh/Nos1tm1Plhinvolves: 129S4/SvJae * C57BL/10ScSn

muscle phenotype

References

Additional References

Additional - Nos1tm1Plh related

Nos1^tm1Plh

Allele Symbol: Nos1^tm1Plh

Genotype: Nos1^tm1Plh related

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae * C57BL/6J

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
B6;129S4-Nos1^tm1Plh/J

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae * C57BL/6

Genotype: Nos1^tm1Plh/Nos1⁺
B6.129S4-Nos1^tm1Plh

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
B6.129S4-Nos1^tm1Plh

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
B6.129S4-Nos1^tm1Plh/J

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae

Genotype: Nos1^tm1Plh/Nos1^tm1Plh
involves: 129S4/SvJae * C57BL/10ScSn

Additional - Nos1^tm1Plh related