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Phenotypes associated with this allele
Allele Symbol
Allele Name
Allele ID
Ntn3tm1(KOMP)Mbp
targeted mutation 1, Mouse Biology Program, UC Davis
MGI:4456545
Summary 1 genotype
Jump to Allelic Composition Genetic Background Genotype ID
hm1
Ntn3tm1(KOMP)Mbp/Ntn3tm1(KOMP)Mbp involves: C57BL/6J * C57BL/6N MGI:7524367


Genotype
MGI:7524367
hm1
Allelic
Composition
Ntn3tm1(KOMP)Mbp/Ntn3tm1(KOMP)Mbp
Genetic
Background
involves: C57BL/6J * C57BL/6N
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Ntn3tm1(KOMP)Mbp mutation (0 available); any Ntn3 mutation (13 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
integument
• STZ-induced diabetic mice exhibit significantly increased epidermal innervation of GAP43+ axons in hind paw skin, with a higher axon density than in diabetic wild-type controls, suggesting aberrant intraepidermal sprouting of sensory axons; a retrograde labeling experiment identified the sensory neuronal subtype of aberrant sprouting axons as CGRP+ sensory neurons in dorsal root ganglia (DRGs)

mortality/aging
N
• mice exhibit normal viability at birth

growth/size/body
N
• mice exhibit normal body weights relative to wild-type controls

behavior/neurological
N
• mice show normal anxiety-like behaviors, spontaneous motor activity, and motor-sensory coordination; no sensory dysfunction is detected by measuring mechanical and cold allodynia or thermal hyperalgesia
• after streptozotocin (STZ) administration, diabetic mice exhibit thermal pain levels similar to those in diabetic wild-type controls in the thermal hyperalgesia test
• starting at 3 weeks after STZ administration, diabetic mice show a significantly lower mechanical pain threshold than diabetic wild-type controls in the von Frey test, indicating aggravated mechanical allodynia
• at 4 weeks after STZ administration, diabetic mice develop more severe cold allodynia than diabetic wild-type controls in the acetone test

nervous system
N
• at 4 weeks after STZ administration, diabetic mice show normal progression of axon damage in the sciatic nerves, as indicated by the axon degeneration ratio and the g-ratio (an indicator of demyelination); moreover, analysis of PGP9.5+ intraepidermal nerve fiber (IENF) density showed normal epidermal axon loss relative to diabetic wild-type controls
• STZ-induced diabetic mice exhibit normal activation of astrogliosis and microgliosis in the spinal cord and show similar increases in mRNA expression of cytokines related to neuropathic pain
• STZ-induced diabetic mice exhibit significantly increased epidermal innervation of GAP43+ axons in hind paw skin, with a higher axon density than in diabetic wild-type controls, suggesting aberrant intraepidermal sprouting of sensory axons; a retrograde labeling experiment identified the sensory neuronal subtype of aberrant sprouting axons as CGRP+ sensory neurons in dorsal root ganglia (DRGs)

homeostasis/metabolism
N
• mice exhibit normal glucose metabolism in the glucose challenge test relative to wild-type controls
• after STZ administration, mice show normal progression of STZ-induced diabetes with significantly increased concentrations of blood glucose and decreased body weights, similar to those in diabetic wild-type controls





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last database update
12/10/2024
MGI 6.24
The Jackson Laboratory