| Annotated protein: | Platelet-activating factor acetylhydrolase IB subunit beta (Lissencephaly-1 protein) (LIS-1) (PAF acetylhydrolase 45 kDa subunit) (PAF-AH 45 kDa subunit) (PAF-AH alpha) (PAFAH alpha). Gene symbol: PAFAH1B1. Taxonomy: Mus musculus (Mouse). Uniprot ID: P63005 |
| antibody wiki: | |
| SynGO gene info: | SynGO data @ PAFAH1B1 |
| Ontology domain: | Biological Process |
| SynGO term: | modulation of chemical synaptic transmission (GO:0050804) |
| Synapse type(s): | Schaffer collateral synapse (CA3->CA1) |
| Annotated paper: | Sudarov A, et al. "Mature Hippocampal Neurons Require LIS1 for Synaptic Integrity: Implications for Cognition" Biol Psychiatry. 2018 Mar 15;83(6):518-529 PMID:29150182 |
| Figure(s): | Fig.2 |
| Annotation description: | Figure 2. "Electrophysiological characterization of hippocampal CA1 pyramidal neurons 30 to 40 days after Lis1 inactivation." - "Whole-cell and patch-clamp recordings of Lis1fl/+ and Lis1cko hippocampal slices (including CaMKIICre;Lis1fl/+ slices in Supplemental Figure S6) compared basic membrane properties, spontaneous synaptic events, and evoked responses and LTP in Schaffer collateral input to CA1. At postnatal day 16, before expression of CaMKII-driven Cre, all physiological properties were comparable in control and Lis1cko mice (Supplemental Figure S5). At postnatal day 60, CA1 pyramidal neurons from Lis1cko mice showed decreases in the frequencies of miniature (spike-independent) EPSCs and IPSCs, with miniature postsynaptic current amplitudes unchanged (Figure 2A-D). On the other hand, spontaneous-EPSCs and -IPSCs, which depend more on exocytotic neurotransmitter release, were decreased in both frequency and amplitude, with most of these deficits observed as early as postnatal day 30 (Supplemental Figure S6D-I). Taken together, these results are consistent with deficits in synaptic release from at least a subset of glutamatergic and GABAergic inputs to CA1 pyramidal neurons, but may also reflect abnormalities in the postsynaptic compartments of these synapses. " - "We examined synaptic responses evoked by stimulation of Schaffer collateral inputs to CA1 (Figure 2E), as well as LTP (Figure 2F, G) in this pathway. The paired pulse amplitude ratio for evoked EPSCs was not different between Lis1cko and control hippocampal slices (interstimulus interval range 20-200 ms) (Figure 2E), suggesting intact spike-dependent glutamate release in the CA3 inputs to CA1 pyramidal neurons in the Lis1cko hippocampus. Induction of long-term potentiation, using a classical pairing protocol 11, 12 (Figure 2F, G), revealed markedly diminished LTP in the Schaeffer collateral-CA1 circuit of Lis1cko mice, while input resistances of recorded neurons remained constant over time (Figure 2G, bottom). Taken together, the electrophysiological data indicate that a postjuvenile loss of LIS1 in CA1 projection neurons produces marked deficits in the fundamental components of synaptic transmission at these neurons, and a loss of plasticity in synaptic activity driven by the Schaffer collaterals." |
| Evidence tracking, Biological System: | Intact tissue |
| Evidence tracking, Protein Targeting: | Genetic transformation (eg; knockout, knockin, mutations) |
| Evidence tracking, Experiment Assay: | Whole-cell patch clamp |
| Annotator(s): | Pim van Nierop (ORCID:0000-0003-0593-3443) Guus Smit (ORCID:0000-0002-2286-1587) Matthijs Verhage (ORCID:0000-0002-2514-0216) |
| Lab: | Department of Functional Genomics, Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Vrije Universiteit Amsterdam, 1081 HV Amsterdam, The Netherlands |
| SynGO annotation ID: | 3808 |
| Dataset release (version): | 20231201 |
| View annotation as GO-CAM model: |  |