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Fig. 1, the figure shows that Grasp1 (GRIP-associated protein 1, GRIPAP1) KO Mice Have Reduced AMPA mEPSC frequency and dendritic spines.\n\nLiteral:\n\"However, mEPSC frequency in KO mice was significantly reduced compared to WT littermates (Figures 1A and 1C), suggesting that GRASP1 mediates neuronal connectivity and/or presynaptic glutamate release. To test whether the reduced mEPSC frequency reflects a decrease in glutamatergic synapse number, we crossed Grasp1 mice with Thy1-GFP transgenic mice to sparsely label CA1 neurons with a GFP-fill (Figure 1E). We found that the glutamatergic synapse density, quantified as the number of spines on secondary dendrites, was significantly lower in juvenile KO than WT littermates (Figures 1E and 1F), suggesting that GRASP1 regulates neuronal connectivity in the developing hippocampus.\"\n\nFig. 2, Grasp1 KO Mice show impaired NMDAR-dependent LTP but normal LTD\nand presynaptic function because GRASP1 is required for the appropriate delivery of synaptic AMPARs.\n\nLiteral:\n\"LTP induction resulted in an initially less potentiated field excitatory postsynaptic potential (fEPSP) and remained reduced for at least 1 hr in Grasp1 KO mice (Figures 2A-2C). Since this form of LTP results from an increase in postsynaptic AMPARs (Huganir and Nicoll, 2013), these results suggest that GRASP1 is required for the appropriate delivery of synaptic AMPARs in response to TBS. On the other hand, NMDAR-mediated LTD was not different between KO and WT mice (Figures 2D and 2E), suggesting a specific role of GRASP1 in activity-dependent incorporation, but not removal, of synaptic AMPARs. We further tested whether GRASP1 regulates presynaptic function by comparing paired-pulse ratios (PPRs), a standard approach to assess neurotransmitter release probability. Grasp1 KO mice showed comparable PPRs in a wide range of interstimulus intervals, suggesting that GRASP1 does not regulate presynaptic vesicle release (Figure 2F). Together with the observation that Grasp1 KO mice had fewer spines, we concluded that the attenuated mEPSC frequency reflects primarily a reduction in glutamatergic inputs onto hippocampal CA1 neurons.\"\n\nFig. 3, Grasp1 KO mice show impaired learning-induced synaptic AMPAR incorporation.\n\nLiteral:\n\"To test whether GRASP1 is required for learning-induced synaptic AMPAR delivery, we isolated the postsynaptic density (PSD) fraction, highly enriched in synaptic proteins, from the dorsal hippocampus of adult Grasp1 mice 30 min following IA training. Consistent with previous findings, we found that in WT animals, IA training increased the levels of GluA1, 2, and 3 AMPAR subunits compared to littermates that did not receive a foot shock (Figures 3F and 3G). The learning-induced increase in synaptic glutamate receptors is AMPAR specific because we did not detect changes in the NMDAR subunit GluN1 or the metabotropic glutamate receptor 5 (mGluR5). Remarkably, this learning-induced increase in AMPAR is completely abolished in KO mice (Figures 3F and 3G). AMPARs in the post-nuclear supernatant (S1) fraction remain comparable regardless of the genotype and IA training, indicating that GRASP1 is specifically required for synaptic delivery of AMPARs during IA learning (Figures 3H and 3I). Taken together, these data demonstrate a critical role for GRASP1 in spatial (MWM) and associative (IA) learning and memory, likely via regulation of activity-dependent AMPAR trafficking and synaptic potentiation.\"\n\n9/11/2017 Pim\n- GRASP1 KO --\u003e Literal: \"Our finding that Grasp1 KO mice have impaired LTP but normal mEPSC amplitude suggests that GRASP1 is selectively required for activity-dependent AMPAR trafficking and synaptic strengthening\"\n- GRASP1 ID mutant --\u003e Literal: \"These data further support our argument that the reduction in sGluA2 following AMPA stimulation in ID mutant-replaced neurons (Figures 5D and 5F) is a result of recycling effect, but not AMPAR degradation.\"\n- term: \u0027regulation of neurotransmitter receptor transport, endosome to postsynaptic membrane (GO:0099152)\u0027 was selected based on these conclusions. Experimental description: The KO mice for GRASP1 were used. In AMPAR work rat neurons were used. Overexpressed Grasp1 is of mouse species.\n\nLiteral form M\u0026M:\n- KO data: \"Animals ...Grasp1 KO mice were generated with a neomycin resistance gene cassette inserted into exon 6 of GRASP1, creating a premature stop codon (Figure S1A) on a 129 background but were backcrossed to C57BL/6 background for more than 10 generations.\"\n- Cell culture data: \"Hippocampal or cortical neurons from E18 rat pups were plated onto p\"\n- Overexpressed Grasp1 is of mouse species: \"HA:GRASP1 WT (from mouse) on pEGFP backbone\"\n\nantibody / target sequence:\nMouse anti-GRIP1, BD Biosciences, Cat# 611319, RRID: AB_398845\nRabbit anti-GRIP1 (JH2260), Dong et al., 1997, PMID:9069286\nshRNA targeting sequence: shGRASP1: 5\u0027-GCTAAGCTCTCTGAGAAAT-3\u0027\nNucleotide BLAST confirms this is gene \"Gripap1\""},{"key":"https://w3id.org/biolink/vocab/in_taxon","value":"http://purl.obolibrary.org/obo/NCBITaxon_10090"}]}