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PreprintCited by 19

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Compartment-Specific Neurexin Nanodomains Orchestrate Tripartite Synapse Assembly

Trotter, Justin H., Dargaei, Zahra, Sclip, Alessandra, Essayan-Perez, Sofia, Liakath-Ali, Kif, Raju, Karthik, Nabet, Amber, Liu, Xinran, Wöhr, Markus, Südhof, Thomas C.·2020
DOI 10.1101/2020.08.21.262097
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Abstract

At tripartite synapses, astrocytes enmesh synaptic contacts, but how astrocytes contribute to the formation, maturation and plasticity of synapses remains elusive. Here we show that both astrocytes and neurons abundantly express neurexin-1, a presynaptic adhesion molecule that controls synaptic properties. Using super-resolution imaging, we demonstrate that presynaptic neuronal and astrocytic neurexin-1 form discrete nanoclusters at excitatory synapses. We find that distinct patterns of heparan sulfate modification and alternative splicing confer onto astrocytic and neuronal neurexin-1 different ligand specificities, thereby enabling compartment-specific signaling by neurexin-1. At hippocampal Schaffer-collateral synapses, deletion of neurexin-1 from either astrocytes or neurons did not alter synapse numbers, but differentially impaired synapse function. Neuronal neurexin-1 was essential for NMDA-receptor-mediated synaptic responses, whereas astrocytic neurexin-1 was required for maturation of silent synapses, AMPA-receptor recruitment, and long-term potentiation. Thus, astrocytes and neurons surprisingly use the same synaptic adhesion molecule to control distinct synapse properties.

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Figures

Figure 1 Astrocytes express and target the major synapse organizer Nrxn1 to vascular endfeet and synapses. a, Profile of synapse adhesion molecule enrichment in ribosome-bound
Figure 1 Astrocytes express and target the major synapse organizer Nrxn1 to vascular endfeet and synapses. a, Profile of synapse adhesion molecule enrichment in ribosome-boundCC-BY-NC-ND · From the PDF
Figure 2 Astrocytes and neurons employ distinct molecular programs that involve Nrxn1. a, Cartoon of major Nrxn1 isoforms (i.e.,  ,  , and  ). The location of splice sites 1-6 (SS1-SS6) are indicated to the left. Bottom right, key of major structural features. b, Quantifications of major neurexin isoform transcripts via quantitative RT-PCR using either astrocyte- or neuron-specific ribosome-bound mRNAs (targeted using 'RiboTag') and compared to total RNA (input). c, Representative immunoblots of Nrxn1  or Nrxn1/2/3  using antibodies with different degrees of specificity. Total brain lysates from neuron- and astrocyte-specific Nrxn1 cKO mice and littermate controls were examined. d-e , Summary graphs of Nrxn1  ( d ) or pan-Nrxn1/2/3  ( e ) levels
Figure 2 Astrocytes and neurons employ distinct molecular programs that involve Nrxn1. a, Cartoon of major Nrxn1 isoforms (i.e.,  ,  , and  ). The location of splice sites 1-6 (SS1-SS6) are indicated to the left. Bottom right, key of major structural features. b, Quantifications of major neurexin isoform transcripts via quantitative RT-PCR using either astrocyte- or neuron-specific ribosome-bound mRNAs (targeted using 'RiboTag') and compared to total RNA (input). c, Representative immunoblots of Nrxn1  or Nrxn1/2/3  using antibodies with different degrees of specificity. Total brain lysates from neuron- and astrocyte-specific Nrxn1 cKO mice and littermate controls were examined. d-e , Summary graphs of Nrxn1  ( d ) or pan-Nrxn1/2/3  ( e ) levelsCC-BY-NC-ND · From the PDF
Figure 3 Deletion of Nrxn1 from astrocytes suppresses spontaneous excitatory synaptic transmission without altering synapse numbers. a-b, Astrocyte- but not neuron-specific deletion of Nrxn1 in cKO mice reduces the mEPSC frequency without changing the mEPSC amplitude. mEPSCs were recorded at P22-P26 in acute slices from CA1 pyramidal neurons
Figure 3 Deletion of Nrxn1 from astrocytes suppresses spontaneous excitatory synaptic transmission without altering synapse numbers. a-b, Astrocyte- but not neuron-specific deletion of Nrxn1 in cKO mice reduces the mEPSC frequency without changing the mEPSC amplitude. mEPSCs were recorded at P22-P26 in acute slices from CA1 pyramidal neuronsCC-BY-NC-ND · From the PDF
Figure 4 Neuronal and astrocytic Nrxn1 regulate distinct postsynaptic functions. a-f, EPSCs were evoked by electrical stimulation of the Schaffer collaterals, and recorded from hippocampal CA1 pyramidal neurons in acute slices from P22-P26 mice of the indicated genotypes. Sample
Figure 4 Neuronal and astrocytic Nrxn1 regulate distinct postsynaptic functions. a-f, EPSCs were evoked by electrical stimulation of the Schaffer collaterals, and recorded from hippocampal CA1 pyramidal neurons in acute slices from P22-P26 mice of the indicated genotypes. SampleCC-BY-NC-ND · From the PDF
Figure 5 Astrocytes promote synapse unsilencing and long-term potentiation in a Nrxn1-
Figure 5 Astrocytes promote synapse unsilencing and long-term potentiation in a Nrxn1-CC-BY-NC-ND · From the PDF
Extended Data Figure 1 | Confirmation of RiboTag pulldown purity by quantitative RTPCR (a), In situ hybridization for Nrxn1 in the hippocampus, and validation of neuron- and
Extended Data Figure 1 | Confirmation of RiboTag pulldown purity by quantitative RTPCR (a), In situ hybridization for Nrxn1 in the hippocampus, and validation of neuron- andCC-BY-NC-ND · From the PDF
Extended Data Figure 2 | Astrocytes Contribute Significantly to Nrxn1 Levels in Hippocampal Neuropil (data complement those shown in Figure 1). a , Nrxn1 (green) was visualized using a dye-conjugated HA antibody in lightly fixed hippocampal slices (i.e. 15 minute post-fixation). Nuclei (blue) were stained using DAPI. Ctrl mice (top) have abundant and layerspecific labeling in the hippocampus, which is entirely absent in sections from non-transgenic mice (bottom). b-c , Representative images (left) and summary graphs (right) of HA-Nrxn1 levels detected in sections from Nrxn1 neuron cKO-T ( b ) and astrocyte cKO-T mice ( c ). Background was subtracted based on fluorescence levels detected in labelled non-transgenic sections. Nrxn1 levels were then quantified in major synaptic subfields of CA1 ( Stratum oriens or s.o ., Stratum pyramidale or s.p. , Stratum radiatum or s.r. , and Stratum lacunosum moleculare or s.l.m. ), CA3 ( s.o. , s.p. , Stratum lucidum or s.l. , and s.r. ), and the dentate gyrus (DG; molecular layer or m.l. , granule cell layer or g.c.l., and the hilus). Remaining Nrxn1 levels in neuron cKO-T ( b ) and astrocyte cKO-T mice ( c ) are considered to be putative astrocyte and neuron Nrxn1 signal, respectively. The loss of signal corresponding to the cKO-T mice is calculated by subtracting cKOT levels from WT levels. Data are means ± SEM. n = 8 sections / 3 WT mice, 11 sections / 4 neuron cKO mice ( b ); 9 sections / 3 WT mice, 18 sections / 6 astrocyte cKO mice ( c ).
Extended Data Figure 2 | Astrocytes Contribute Significantly to Nrxn1 Levels in Hippocampal Neuropil (data complement those shown in Figure 1). a , Nrxn1 (green) was visualized using a dye-conjugated HA antibody in lightly fixed hippocampal slices (i.e. 15 minute post-fixation). Nuclei (blue) were stained using DAPI. Ctrl mice (top) have abundant and layerspecific labeling in the hippocampus, which is entirely absent in sections from non-transgenic mice (bottom). b-c , Representative images (left) and summary graphs (right) of HA-Nrxn1 levels detected in sections from Nrxn1 neuron cKO-T ( b ) and astrocyte cKO-T mice ( c ). Background was subtracted based on fluorescence levels detected in labelled non-transgenic sections. Nrxn1 levels were then quantified in major synaptic subfields of CA1 ( Stratum oriens or s.o ., Stratum pyramidale or s.p. , Stratum radiatum or s.r. , and Stratum lacunosum moleculare or s.l.m. ), CA3 ( s.o. , s.p. , Stratum lucidum or s.l. , and s.r. ), and the dentate gyrus (DG; molecular layer or m.l. , granule cell layer or g.c.l., and the hilus). Remaining Nrxn1 levels in neuron cKO-T ( b ) and astrocyte cKO-T mice ( c ) are considered to be putative astrocyte and neuron Nrxn1 signal, respectively. The loss of signal corresponding to the cKO-T mice is calculated by subtracting cKOT levels from WT levels. Data are means ± SEM. n = 8 sections / 3 WT mice, 11 sections / 4 neuron cKO mice ( b ); 9 sections / 3 WT mice, 18 sections / 6 astrocyte cKO mice ( c ).CC-BY-NC-ND · From the PDF
Extended Data Figure 3 | Control stains for Nrxn1 labeling of blood vessels (BVs) (a) and comparison of Nrnx1 nanocluster properties in Nrxn1 neuron and astrocyte cKO-T mice (be; data complement those shown in figure 1). a , Representative images of Nrxn1 labeling in sections from HA-Nrxn1 cKI (i.e. Ctrl) and non-transgenic mice. Brains were lightly fixed (i.e. 15 minutes post-fixation) and stained for HA-Nrxn1 (green) with dye-conjugated primary antibody, GFAP (astrocytes, magenta), and laminin-alpha2 (blood vessels, blue). Yellow box, enlarged on right. b-e , Summary graphs comparing the properties of putative astrocytic Nrxn1 nanoclusters (found in neuron cKO-T mice) and presynaptic Nrxn1 nanoclusters (found in astrocyte cKO-T mice). Properties measured include the average number of localizations per Nrxn1 nanocluster ( b ), the density of localizations per Nrxn1 nanocluster ( c ), the minimum intercluster distance between Nrxn1 and Homer1 clusters ( d ), and Nrxn1 nanocluster size measured as the radius of gyration ( e ). Numerical data are means ± SEM. n = 190 synapses / 3 neuron cKO-T mice, 227 synapses / 3 astrocyte cKO-T mice ( b-c, e ) and 130 synapses / 3 neuron cKO-T mice, 190 synapses / 3 astrocyte
Extended Data Figure 3 | Control stains for Nrxn1 labeling of blood vessels (BVs) (a) and comparison of Nrnx1 nanocluster properties in Nrxn1 neuron and astrocyte cKO-T mice (be; data complement those shown in figure 1). a , Representative images of Nrxn1 labeling in sections from HA-Nrxn1 cKI (i.e. Ctrl) and non-transgenic mice. Brains were lightly fixed (i.e. 15 minutes post-fixation) and stained for HA-Nrxn1 (green) with dye-conjugated primary antibody, GFAP (astrocytes, magenta), and laminin-alpha2 (blood vessels, blue). Yellow box, enlarged on right. b-e , Summary graphs comparing the properties of putative astrocytic Nrxn1 nanoclusters (found in neuron cKO-T mice) and presynaptic Nrxn1 nanoclusters (found in astrocyte cKO-T mice). Properties measured include the average number of localizations per Nrxn1 nanocluster ( b ), the density of localizations per Nrxn1 nanocluster ( c ), the minimum intercluster distance between Nrxn1 and Homer1 clusters ( d ), and Nrxn1 nanocluster size measured as the radius of gyration ( e ). Numerical data are means ± SEM. n = 190 synapses / 3 neuron cKO-T mice, 227 synapses / 3 astrocyte cKO-T mice ( b-c, e ) and 130 synapses / 3 neuron cKO-T mice, 190 synapses / 3 astrocyteCC-BY-NC-ND · From the PDF
Extended Data Figure 4 | Generation of Cell-Specific Nrxn1 cKO Mice and Quantification of Neurexin Protein Levels (data complement those shown in figures 1-2). a-b, Breeding
Extended Data Figure 4 | Generation of Cell-Specific Nrxn1 cKO Mice and Quantification of Neurexin Protein Levels (data complement those shown in figures 1-2). a-b, BreedingCC-BY-NC-ND · From the PDF
Extended Data Figure 5 | Astrocytic Nrxn1 is Preferentially Modified by Heparan Sulfate ( data complement those shown in figure 2). a-c, Nrxn1α is expressed primarily as a heparansulfate proteoglycan in cultured astrocytes, whereas Nrxn1α is present in cultured neurons mostly without the heparan-sulfate modification. Nrxn1 was immunoprecipitated at DIV14-16 from cultures of glia and neurons, or of glia alone, that were obtained from Nrxn1 HA-knockin mice. Immunoprecipitates were analyzed by immunoblotting without or with treatment with heparinases that cleave heparan-sulfate modifications, exposing a heparan-sulfate stub that can be visualized by an antibody (left, representative immunoblots; right, relative levels of heparan-sulfate stubs normalized for total Nrxn1α levels). Quantification of the amounts of Nrxn1α that are highly modified based on their apparent molecular weight as analyzed by immunoblotting of Nrxn1α
Extended Data Figure 5 | Astrocytic Nrxn1 is Preferentially Modified by Heparan Sulfate ( data complement those shown in figure 2). a-c, Nrxn1α is expressed primarily as a heparansulfate proteoglycan in cultured astrocytes, whereas Nrxn1α is present in cultured neurons mostly without the heparan-sulfate modification. Nrxn1 was immunoprecipitated at DIV14-16 from cultures of glia and neurons, or of glia alone, that were obtained from Nrxn1 HA-knockin mice. Immunoprecipitates were analyzed by immunoblotting without or with treatment with heparinases that cleave heparan-sulfate modifications, exposing a heparan-sulfate stub that can be visualized by an antibody (left, representative immunoblots; right, relative levels of heparan-sulfate stubs normalized for total Nrxn1α levels). Quantification of the amounts of Nrxn1α that are highly modified based on their apparent molecular weight as analyzed by immunoblotting of Nrxn1αCC-BY-NC-ND · From the PDF
Extended Data Figure 6 | Nrxn1 alternative splicing differs between astrocytes and neurons ( data complement those shown in figure 2). a-f, Comparison of Nrxn1 alternative splicing at SS1 to SS6 in neurons vs. astrocytes reveals profound differences. Translating mRNAs were immunoprecipitated from neurons or astrocytes using Cre-dependent RiboTag mice crossed with neuron- or astrocyte-specific Cre-driver mice. Alternative splicing was quantified using junctionflanking PCR. Each panel depicts a single site of alternative splicing (left, representative gel
Extended Data Figure 6 | Nrxn1 alternative splicing differs between astrocytes and neurons ( data complement those shown in figure 2). a-f, Comparison of Nrxn1 alternative splicing at SS1 to SS6 in neurons vs. astrocytes reveals profound differences. Translating mRNAs were immunoprecipitated from neurons or astrocytes using Cre-dependent RiboTag mice crossed with neuron- or astrocyte-specific Cre-driver mice. Alternative splicing was quantified using junctionflanking PCR. Each panel depicts a single site of alternative splicing (left, representative gelCC-BY-NC-ND · From the PDF
Extended Data Figure 7 | Ultrastructural parameters of excitatory synapses in the CA1 region analyzed in mice with an astrocyte-specific Nrxn1 deletion (a-f) and immunoblotting analyses of the hippocampus of mice with neuron- or astrocyte-specific Nrxn1 deletions (g-l; data complement those shown in figure 3). Ultrastructural data on excitatory synapses after astrocyte-specific deletion of Nrxn1, extending the data shown in Fig. 3g & 3h ( a , postsynaptic spine area; b , PSD thickness; c , PSD length; d , number of docked synaptic vesicles/synapse; e , number of synaptic vesicles per terminal; f , width of synaptic cleft). g-l, Immunoblotting analyses show that the neuron- ( g, i, k ) or astrocyte-specific ( h, j, l ) Nrxn1 deletions do not produce
Extended Data Figure 7 | Ultrastructural parameters of excitatory synapses in the CA1 region analyzed in mice with an astrocyte-specific Nrxn1 deletion (a-f) and immunoblotting analyses of the hippocampus of mice with neuron- or astrocyte-specific Nrxn1 deletions (g-l; data complement those shown in figure 3). Ultrastructural data on excitatory synapses after astrocyte-specific deletion of Nrxn1, extending the data shown in Fig. 3g & 3h ( a , postsynaptic spine area; b , PSD thickness; c , PSD length; d , number of docked synaptic vesicles/synapse; e , number of synaptic vesicles per terminal; f , width of synaptic cleft). g-l, Immunoblotting analyses show that the neuron- ( g, i, k ) or astrocyte-specific ( h, j, l ) Nrxn1 deletions do not produceCC-BY-NC-ND · From the PDF
Extended Data Figure 8 | RNAseq reveals that neuronal and astrocytic Nrxn1 control distinct hippocampal transcriptional programs. a, Volcano plots of batch-normalized differential gene expression in the hippocampus of neuron- (left) and astrocyte-specific Nrxn1 cKOs (right). Bulk RNAseq analysis was performed at P26 in two batches with 2 control and cKO mice each (2 males and 2 females). b, qPCR validation of top differentially expressed genes emerging from RNAseq experiments (left, neuron-specific cKO; right, astrocyte-specific cKO; n = 4 per genotype). c, Plot of Nrxn1 mRNA levels as determined by RNAseq validating the quantitative RT-PCR data of Fig. 2 . Data in B and C are means ± SEM. Statistical significance was assessed with a two-tailed unpaired t-test to controls (B and C; for statistical analysis of RNAseq data, see Experimental Procedures), with * = p < 0.05; ** = p < 0.01; *** = p < 0.001; **** = p < 0.0001.
Extended Data Figure 8 | RNAseq reveals that neuronal and astrocytic Nrxn1 control distinct hippocampal transcriptional programs. a, Volcano plots of batch-normalized differential gene expression in the hippocampus of neuron- (left) and astrocyte-specific Nrxn1 cKOs (right). Bulk RNAseq analysis was performed at P26 in two batches with 2 control and cKO mice each (2 males and 2 females). b, qPCR validation of top differentially expressed genes emerging from RNAseq experiments (left, neuron-specific cKO; right, astrocyte-specific cKO; n = 4 per genotype). c, Plot of Nrxn1 mRNA levels as determined by RNAseq validating the quantitative RT-PCR data of Fig. 2 . Data in B and C are means ± SEM. Statistical significance was assessed with a two-tailed unpaired t-test to controls (B and C; for statistical analysis of RNAseq data, see Experimental Procedures), with * = p < 0.05; ** = p < 0.01; *** = p < 0.001; **** = p < 0.0001.CC-BY-NC-ND · From the PDF
Extended Data Figure 9 | Neuron- or astrocyte-specific deletion of Nrxn1 has no effect on the kinetics of mEPSCs (a-d), and do not alter the paired-pulse ratio of evoked AMPARmediated EPSCs (e, f). a-b , mEPSC rise ( a ) and decay times ( b ) were not significantly altered by the neuron-specific deletion of Nrxn1. (c-d) Same as a-b , but for the astrocyte-specific deletion of Nrxn1. e-f, Neuron- and astrocyte-specific deletions of Nrxn1 do not change the paired-pulse ratios of Schaffer-collateral AMPAR-mediated EPSCs, suggesting that deletion of Nrxn1 in neurons has no effect on release probability (top, sample traces; left bottom, summary plot; right bottom, summary graph of the paired-pulse ratio at a 100 ms interstimulus interval). Numerical data are means ± SEM. n = 15 cells / 4 mice ctrl., 11 cells / 4 mice neuron cKO ( a-b ); 14 cells / 4 mice ctrl., 13 cells / 3 mice astrocyte cKO ( c-d ); 12 cells / 3 mice ctrl., 15 cells / 4 mice neuron cKO ( e ); 19 cells / 4 mice ctrl., 18 cells / 4 mice astrocyte cKO ( f ). Statistical significance was assessed with the two-tailed unpaired Student's t-test.
Extended Data Figure 9 | Neuron- or astrocyte-specific deletion of Nrxn1 has no effect on the kinetics of mEPSCs (a-d), and do not alter the paired-pulse ratio of evoked AMPARmediated EPSCs (e, f). a-b , mEPSC rise ( a ) and decay times ( b ) were not significantly altered by the neuron-specific deletion of Nrxn1. (c-d) Same as a-b , but for the astrocyte-specific deletion of Nrxn1. e-f, Neuron- and astrocyte-specific deletions of Nrxn1 do not change the paired-pulse ratios of Schaffer-collateral AMPAR-mediated EPSCs, suggesting that deletion of Nrxn1 in neurons has no effect on release probability (top, sample traces; left bottom, summary plot; right bottom, summary graph of the paired-pulse ratio at a 100 ms interstimulus interval). Numerical data are means ± SEM. n = 15 cells / 4 mice ctrl., 11 cells / 4 mice neuron cKO ( a-b ); 14 cells / 4 mice ctrl., 13 cells / 3 mice astrocyte cKO ( c-d ); 12 cells / 3 mice ctrl., 15 cells / 4 mice neuron cKO ( e ); 19 cells / 4 mice ctrl., 18 cells / 4 mice astrocyte cKO ( f ). Statistical significance was assessed with the two-tailed unpaired Student's t-test.CC-BY-NC-ND · From the PDF

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Metadata

Authors
Trotter, J. H., Dargaei, Z., Sclip, A., Essayan-Perez, S., Liakath-Ali, K., Raju, K., Nabet, A., Liu, X., Wöhr, M., & Südhof, T. C.
Publisher
openRxiv
Published
2020-08-21
DOI
10.1101/2020.08.21.262097
Cited by
19
References
17
Type
Preprint
Licence
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)

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