Phenotypes associated with this allele

• Allele Symbol: Clstn1^tm1.1Uge
• Allele Name: targeted mutation 1.1, Urs Gerber
• Allele ID: MGI:5637427
• Summary: 1 genotype

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Clstn1^tm1.1Uge/Clstn1^tm1.1Uge	involves: C57BL/6 * C57BL/6NTac	MGI:5689346

Genotype
MGI:5689346

hm1

• Allelic Composition: Clstn1^tm1.1Uge/Clstn1^tm1.1Uge
• Genetic Background: involves: C57BL/6 * C57BL/6NTac

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

nervous system

nervous system phenotype ( J:212386 )

N • homozygotes show normal gross hippocampus and cortex morphology

abnormal dendrite morphology ( J:212386 )

• juvenile homozygotes show decreased dendritic arborization in CA1 pyramidal cells

• however, no structural modification of the dendritic tree is noted in adulthood

abnormal dendritic spine morphology ( J:212386 )

• juvenile homozygotes display an altered spine-type distribution in CA1 pyramidal cells, with fewer thin spines and more filopodia-like structures, indicating a more immature state of the dendritic tree

• however, no difference in spine structure is noted in adulthood

abnormal CNS synaptic transmission ( J:212386 )

• juvenile (P15-P21) homozygotes exhibit reduced basal excitatory synaptic transmission relative to wild-type controls

• however, juvenile presynaptic function is unaffected, as shown by normal dendritic spine density in CA1 pyramidal cells, and no significant changes in paired-pulse facilitation (PPF) or short-term plasticity

• adult homozygotes show no differences in synaptic function or structure relative to wild-type controls

decreased excitatory postsynaptic current frequency ( J:212386 )

• the frequency of spontaneous EPSCs recorded in CA1 pyramidal cells voltage clamped at -70 mV is reduced in acute hippocampal slices from juvenile (P15-P21) homozygotes relative to that seen in wild-type slices

• no significant change in the amplitudes of spontaneous EPSCs is observed in juvenile homozygotes

• adult homozygotes exhibit normal basal synaptic transmission, as shown in recordings of spontaneous EPSC amplitude and frequency

prolonged excitatory postsynaptic current decay time ( J:212386 )

• juvenile (P15-P21) homozygotes exhibit a slowing in the decay kinetics of the NMDA but not the AMPA receptor-mediated responses

abnormal excitatory postsynaptic potential ( J:212386 )

• evoked synaptic activity induced by Schaffer collateral stimulation is decreased in field recordings of CA1 pyramidal cells from juvenile (P15-P21) homozygotes relative to wild-type controls

• the input/output curve obtained from field recordings showed a significant decrease in EPSP slope

• data normalized to the amplitude of the input volley confirmed a significant decrease in the fEPSP

abnormal glutamate-mediated receptor currents ( J:212386 )

• juvenile (P15-P21) homozygotes exhibit increased levels of GluN2B subunit-containing NMDA receptors relative to wild-type controls

• evoked AMPA and NMDA receptor-mediated responses recorded in the same CA1 pyramidal cell at -70 mV (inward currents) and at +30 mV (outward currents) revealed that the AMPA/NMDA response ratio is lower than in wild-type controls

abnormal NMDA-mediated synaptic currents ( J:212386 )

• juvenile (P15-P21) homozygotes exhibit a slowing in the decay kinetics of the NMDA but not the AMPA receptor-mediated responses

enhanced long-term potentiation ( J:212386 )

• juvenile (P15-P21) homozygotes show enhanced NMDA receptor (NMDAR)-dependent LTP at Schaffer collateral-CA1 pyramidal cell synapses

• LTP in CA1 pyramidal cells elicited by HFS (100 Hz) of Schaffer collaterals is greater in mutant than in wild-type slices

• a similar enhancement is noted for LTP induced by TBS

• LTP enhancement is prevented in the presence of an antagonist for GluN2B subunit-containing NMDARs; in contrast, the increased LTP observed in mutant slices persists after blocking GluN2A subunit-containing NMDA receptors

• paired-pulse analysis revealed that presynaptic release properties are not altered after LTP induction

• LTD at Schaffer collateral-CA1 pyramidal cell synapses induced by LFS is normal

behavior/neurological

behavior/neurological phenotype ( J:212386 )

N • homozygotes are viable and fertile and do not display any overt behavioral phenotypes