All Phenotypes Tg(Gfap-cre)73.12Mvs MGI Mouse

abnormal synaptic vesicle number ( J:363787 )

• at P28, thalamocortical synapses show a significant decrease in the number of synaptic vesicles within multisynaptic boutons, with no change at monosynaptic connections

abnormal CNS synapse formation ( J:363787 )

• mice show abnormal glutamatergic synapse maturation and stabilization in the developing visual cortex (VC) during the critical period of synapse maturation

• at P28 (peak of the critical period), thalamocortical synapses within the primary VC show structural immaturity whereas intracortical synapses show functional immaturity with reduced incorporation of GLUA2 subunits into AMPA-type glutamate receptors (AMPARs)

delayed CNS synapse formation ( J:363787 )

• by P120, intracortical synapses exhibit normalized VGLUT1and GLUA2 puncta numbers and colocalization of VGLUT1 and GLUA2 in L1 and L2/3, while thalamocortical synapses show restored VGLUT2 puncta volume in L1 and L4, indicating recovery from the synaptic alterations detected at P28

abnormal synaptic bouton morphology ( J:363787 )

• at P28, thalamocortical synapses show a ~40% decrease in the volume of VGLUT2 puncta in layers L1 and L4 of the VC, indicating smaller presynaptic terminals

• analysis of thalamocortical axons in L4 shows that the average terminal volume of presynaptic boutons is significantly reduced, driven by a significant decrease in the volume of multisynaptic boutons, with no change in the volume of monosynaptic connections

• moreover, both the average number of postsynaptic partners at a multisynaptic bouton and the maximum number of synapses observed at a single bouton are increased

abnormal dendritic spine morphology ( J:363787 )

• at P28, L4 thalamocortical synapses show a shift in dendritic spine morphology toward a more immature state at monosynaptic, but not at multisynaptic, connections

• in contrast, L2/3 pyramidal neurons consisting of predominantly intracortical synapses show no gross abnormalities in dendritic spine structure at P28

abnormal dendritic mushroom spine morphology ( J:363787 )

• at P28, L4 thalamocortical synapses show a significant decrease in the % of mushroom dendritic spines at monosynaptic connections

abnormal dendritic thin spine morphology ( J:363787 )

• at P28, L4 thalamocortical synapses show a significant increase in the % of thin dendritic spines at monosynaptic connections

abnormal postsynaptic density morphology ( J:363787 )

• at P28, thalamocortical synapses in L4 show a decreased postsynaptic density (PSD) surface area and more postsynaptic partners at multisynaptic connections

• decrease in PSD surface area is seen at dendritic spines opposed to both monosynaptic and multisynaptic boutons

abnormal excitatory synapse morphology ( J:363787 )

• at P28, intracortical excitatory synapses within the VC show a deceased protein level of GLUA2 (a postsynaptic marker for mature synapses) specifically in layers L2/3: colocalization of GLUA2 and VGLUT1 (a presynaptic marker for intracortical synapses) in L2/3 is reduced by ~30%, driven by a decrease in GLUA2 puncta in L2/3 but not in L1; however, no change is noted in the number of presynaptic VGLUT1 terminals, number of postsynaptic GLUA1 puncta (immature synapses) in L1 or L2/3, or in the colocalization of GLUA1 and VGLUT1 in either layer

• at P28, thalamocortical excitatory synapses within the VC exhibit a ~40% decrease in the volume of VGLUT2 puncta (a presynaptic marker for thalamocortical synapses) in both L1 and L4; however, no change is noted the number of presynaptic VGLUT2 terminals, colocalization of VGLUT2 with postsynaptic GLUA1 or GLUA2 in L1 or L4, or in the number of GLUA1, GLUA2 or VGLUT2 puncta in either layer

• analysis of thalamocortical axons in L4 indicates that thalamocortical synapses are structurally immature, with smaller presynaptic boutons, decreased postsynaptic density area, and more postsynaptic partners at multisynaptic connections

• AAV2/5 mediated HA-GPC5 overexpression in VC astrocytes is sufficient to increase the total level of GLUA2 in L2/3 intracortical synapses, without impacting VGLUT1 puncta number or colocalization of VGLUT1-GLUA2 in L2/3

• however, overexpression of GPC5 in L4 thalamocortical synapses has no impact on VGLUT2 terminal volume

abnormal synaptic plasticity ( J:363787 )

• mice show enhanced ocular dominance plasticity in response to visual deprivation in adulthood: when monocularly enucleated (ME) at P120, mice show a significant increase in the width of the Arc zone at 5 days after ME relative to 12 h after ME (baseline innervation); moreover, the width of the Arc zone after 5 days of ME is significantly larger than that in wild-type controls

• however, no change in large-scale ocular dominance plasticity is detected when ME is performed at P28 (during the critical period)

decreased excitatory postsynaptic current amplitude ( J:363787 )

• at P28, whole-cell patch clamp recordings from L2/3 pyramidal neurons in acute slices of the primary visual cortex show that AMPA-mediated spontaneous excitatory postsynaptic currents (sEPSCs) are significantly reduced in amplitude

• however, no major change is noted in the sEPSC interevent interval, 10%-90% rise time or decay time

abnormal synaptic vesicle number ( J:363787 )

• at P28, thalamocortical synapses show a significant decrease in the number of synaptic vesicles within multisynaptic boutons, with no change at monosynaptic connections

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

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

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

Contributing Projects: Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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