Phenotypes associated with this allele

• Allele Symbol: Lynx1^tm1Htz
• Allele Name: targeted mutation 1, Nathaniel Heintz
• Allele ID: MGI:3716630
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Lynx1^tm1Htz/Lynx1^tm1Htz	involves: 129X1/SvJ * C57BL/6J	MGI:3717402

Genotype
MGI:3717402

hm1

• Allelic Composition: Lynx1^tm1Htz/Lynx1^tm1Htz
• Genetic Background: involves: 129X1/SvJ * C57BL/6J

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

nervous system

abnormal forebrain morphology ( J:122965 )

abnormal corpus callosum morphology ( J:122965 )

• at 12 months, mice exhibit neurodegeneration in neurons of the striatum, corpus callosum and cerebellum

abnormal striatum morphology ( J:122965 )

• at 12 months, mice exhibit neurodegeneration in neurons of the striatum, corpus callosum and cerebellum

abnormal dorsal striatum morphology ( J:122965 )

• at 12 months, mice exhibit neurodegeneration in axons of the dorsal striatum and cerebellum associated with vacuolization

abnormal hindbrain morphology ( J:122965 )

abnormal cerebellum morphology ( J:122965 )

• at 12 months, mice exhibit neurodegeneration in axons of the dorsal striatum and cerebellum associated with vacuolization

• at 12 months, mice exhibit neurodegeneration in neurons of the striatum, corpus callosum and cerebellum

brain vacuoles ( J:122965 )

• beginning at 12 months and continuing through 15 and 18 month, mice exhibit an increase in vacuoles in the dorsal striatum and medial corpus callosum

• vacuolization is increased with exposure to nicotine

neuron degeneration ( J:122965 )

• at 12 months, mice exhibit neurodegeneration in neurons of the striatum, corpus callosum and cerebellum

• degeneration is worsened by nicotine treatment

axon degeneration ( J:122965 )

• at 12 months, mice exhibit neurodegeneration in axons of the dorsal striatum and cerebellum associated with vacuolization

• degeneration is worsened by nicotine treatment

abnormal nervous system physiology ( J:122965 )

increased susceptibility to neuronal excitotoxicity ( J:122965 )

• cultured neurons exposed to glutamate are more sensitive to glutamate-mediated excitotoxicity and the neuroprotective ability of nicotine is completely abolished

decreased paired-pulse facilitation ( J:122965 )

• paired-pulse ratios are reduced relative to wild-type mice responses at intervals of 50-70ms

behavior/neurological

abnormal cued conditioning behavior ( J:122965 )

• mice exhibit increased freezing in response to a shock-associated tone

abnormal motor coordination/balance ( J:122965 )

• mice show improved performance on a rotarod compared to controls when treated with nicotine and saccharin

homeostasis/metabolism

increased physiological sensitivity to xenobiotic ( J:122965 )

• mice exhibit a larger peak response in the medial habenula when exposed to 250ms nicotine pulse compared to wild-type mice

• half-maximal response is significantly prolonged

• calcium signaling following nicotine exposure is increased compared to in wild-type mice

increased susceptibility to neuronal excitotoxicity ( J:122965 )

• cultured neurons exposed to glutamate are more sensitive to glutamate-mediated excitotoxicity and the neuroprotective ability of nicotine is completely abolished

cellular

increased susceptibility to neuronal excitotoxicity ( J:122965 )

• cultured neurons exposed to glutamate are more sensitive to glutamate-mediated excitotoxicity and the neuroprotective ability of nicotine is completely abolished