Publications by authors named "Sandra Jurado"

17 Publications

  • Page 1 of 1

A retention-release mechanism based on RAB11FIP2 for AMPA receptor synaptic delivery during long-term potentiation.

J Cell Sci 2019 12 16;132(24). Epub 2019 Dec 16.

Department of Neurobiology, Centro de Biología Molecular 'Severo Ochoa' (CSIC-UAM), 28049 Madrid, Spain

It is well--established that Rab11-dependent recycling endosomes drive the activity-dependent delivery of AMPA receptors (AMPARs) into synapses during long-term potentiation (LTP). Nevertheless, the molecular basis for this specialized function of recycling endosomes is still unknown. Here, we have investigated RAB11FIP2 (FIP2 hereafter) as a potential effector of Rab11-dependent trafficking during LTP in rat hippocampal slices. Surprisingly, we found that FIP2 operates independently from Rab11 proteins, and acts as a negative regulator of AMPAR synaptic trafficking. Under basal conditions, FIP2 associates with AMPARs at immobile compartments, separately from recycling endosomes. Using shRNA-mediated knockdown, we found that FIP2 prevents GluA1 (encoded by the gene) AMPARs from reaching the surface of dendritic spines in the absence of neuronal stimulation. Upon induction of LTP, FIP2 is rapidly mobilized, dissociates from AMPARs and undergoes dephosphorylation. Interestingly, this dissociation of the FIP2-AMPAR complex, together with FIP2 dephosphorylation, is required for LTP, but the interaction between FIP2 and Rab11 proteins is not. Based on these results, we propose a retention-release mechanism, where FIP2 acts as a gate that restricts the trafficking of AMPARs, until LTP induction triggers their release and allows synaptic delivery.
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http://dx.doi.org/10.1242/jcs.234237DOI Listing
December 2019

Postsynaptic SNARE Proteins: Role in Synaptic Transmission and Plasticity.

Neuroscience 2019 11 17;420:12-21. Epub 2018 Nov 17.

Instituto de Neurociencias CSIC-UMH, 03550 San Juan de Alicante, Spain. Electronic address:

Soluble N-ethylmaleimide sensitive factor attachment protein receptor (SNARE) proteins mediate membrane fusion events in eukaryotic cells. Traditionally recognized as major players in regulating presynaptic neurotransmitter release, accumulative evidence over recent years has identified several SNARE proteins implicated in important postsynaptic processes such as neurotransmitter receptor trafficking and synaptic plasticity. Here we analyze the emerging data revealing this novel functional dimension for SNAREs with a focus on the molecular specialization of vesicular recycling and fusion in dendrites compared to those at axon terminals and its impact in synaptic transmission and plasticity.
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http://dx.doi.org/10.1016/j.neuroscience.2018.11.012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6525081PMC
November 2019

AMPA Receptor Trafficking in Natural and Pathological Aging.

Authors:
Sandra Jurado

Front Mol Neurosci 2017 9;10:446. Epub 2018 Jan 9.

Instituto de Neurociencias CSIC-UMH, San Juan de Alicante, Spain.

α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) enable most excitatory transmission in the brain and are crucial for mediating basal synaptic strength and plasticity. Because of the importance of their function, AMPAR dynamics, activity and subunit composition undergo a tight regulation which begins as early as prenatal development and continues through adulthood. Accumulating evidence suggests that the precise regulatory mechanisms involved in orchestrating AMPAR trafficking are challenged in the aging brain. In turn dysregulation of AMPARs can be linked to most neurological and neurodegenerative disorders. Understanding the mechanisms that govern AMPAR signaling during natural and pathological cognitive decline will guide the efforts to develop most effective ways to tackle neurodegenerative diseases which are one of the primary burdens afflicting an increasingly aging population. In this review, I provide a brief overview of the molecular mechanisms involved in AMPAR trafficking highlighting what is currently known about how these processes change with age and disease. As a particularly well-studied example of AMPAR dysfunction in pathological aging I focus in Alzheimer's disease (AD) with special emphasis in how the production of neurofibrillary tangles (NFTs) and amyloid-β plaques may contribute to disruption in AMPAR function.
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http://dx.doi.org/10.3389/fnmol.2017.00446DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5767248PMC
January 2018

Excitatory and Inhibitory Neurons in the Hippocampus Exhibit Molecularly Distinct Large Dense Core Vesicles.

Front Cell Neurosci 2016 31;10:202. Epub 2016 Aug 31.

Department of Pharmacology, University of Maryland School of Medicine Baltimore, MD, USA.

Hippocampal interneurons comprise a diverse family of inhibitory neurons that are critical for detailed information processing. Along with gamma-aminobutyric acid (GABA), interneurons secrete a myriad of neuroactive substances via secretory vesicles but the molecular composition and regulatory mechanisms remain largely unknown. In this study, we have carried out an immunohistofluorescence analysis to describe the molecular content of vesicles in distinct populations of hippocampal neurons. Our results indicate that phogrin, an integral protein of secretory vesicles in neuroendocrine cells, is highly enriched in parvalbumin-positive interneurons. Consistently, immunoelectron microscopy revealed phogrin staining in axon terminals of symmetrical synapses establishing inhibitory contacts with cell bodies of CA1 pyramidal neurons. Furthermore, phogrin is highly expressed in CA3 and dentate gyrus (DG) interneurons which are both positive for PV and neuropeptide Y. Surprisingly, chromogranin B a canonical large dense core vesicle marker, is excluded from inhibitory cells in the hippocampus but highly expressed in excitatory CA3 pyramidal neurons and DG granule cells. Our results provide the first evidence of phogrin expression in hippocampal interneurons and suggest the existence of molecularly distinct populations of secretory vesicles in different types of inhibitory neurons.
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http://dx.doi.org/10.3389/fncel.2016.00202DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5005380PMC
September 2016

Synaptic Function of Rab11Fip5: Selective Requirement for Hippocampal Long-Term Depression.

J Neurosci 2015 May;35(19):7460-74

Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University Medical School, Stanford, California 94305,

Postsynaptic AMPA-type glutamate receptors (AMPARs) are among the major determinants of synaptic strength and can be trafficked into and out of synapses. Neuronal activity regulates AMPAR trafficking during synaptic plasticity to induce long-term changes in synaptic strength, including long-term potentiation (LTP) and long-term depression (LTD). Rab family GTPases regulate most membrane trafficking in eukaryotic cells; particularly, Rab11 and its effectors are implicated in mediating postsynaptic AMPAR insertion during LTP. To explore the synaptic function of Rab11Fip5, a neuronal Rab11 effector and a candidate autism-spectrum disorder gene, we performed shRNA-mediated knock-down and genetic knock-out (KO) studies. Surprisingly, we observed robust shRNA-induced synaptic phenotypes that were rescued by a Rab11Fip5 cDNA but that were nevertheless not observed in conditional KO neurons. Both in cultured neurons and acute slices, KO of Rab11Fip5 had no significant effect on basic parameters of synaptic transmission, indicating that Rab11Fip5 is not required for fundamental synaptic operations, such as neurotransmitter release or postsynaptic AMPAR insertion. KO of Rab11Fip5 did, however, abolish hippocampal LTD as measured both in acute slices or using a chemical LTD protocol in cultured neurons but did not affect hippocampal LTP. The Rab11Fip5 KO mice performed normally in several behavioral tasks, including fear conditioning, but showed enhanced contextual fear extinction. These are the first findings to suggest a requirement for Rab11Fip5, and presumably Rab11, during LTD.
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http://dx.doi.org/10.1523/JNEUROSCI.1581-14.2015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429152PMC
May 2015

Retinoic Acid and LTP Recruit Postsynaptic AMPA Receptors Using Distinct SNARE-Dependent Mechanisms.

Neuron 2015 Apr 2;86(2):442-56. Epub 2015 Apr 2.

Department of Neurosurgery, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305-5453, USA. Electronic address:

Retinoic acid (RA)-dependent homeostatic plasticity and NMDA receptor-dependent long-term potentiation (LTP), a form of Hebbian plasticity, both enhance synaptic strength by increasing the abundance of postsynaptic AMPA receptors (AMPARs). However, it is unclear whether the molecular mechanisms mediating AMPAR trafficking during homeostatic and Hebbian plasticity differ, and it is unknown how RA signaling impacts Hebbian plasticity. Here, we show that RA increases postsynaptic AMPAR abundance using an activity-dependent mechanism that requires a unique SNARE (soluble NSF-attachment protein receptor)-dependent fusion machinery different from that mediating LTP. Specifically, RA-induced AMPAR trafficking did not involve complexin, which activates SNARE complexes containing syntaxin-1 or -3, but not complexes containing syntaxin-4, whereas LTP required complexin. Moreover, RA-induced AMPAR trafficking utilized the Q-SNARE syntaxin-4, whereas LTP utilized syntaxin-3; both additionally required the Q-SNARE SNAP-47 and the R-SNARE synatobrevin-2. Finally, acute RA treatment blocked subsequent LTP expression, probably by increasing AMPAR trafficking. Thus, RA-induced homeostatic plasticity involves a novel, activity-dependent postsynaptic AMPAR-trafficking pathway mediated by a unique SNARE-dependent fusion machinery.
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http://dx.doi.org/10.1016/j.neuron.2015.03.009DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4578641PMC
April 2015

B-lymphocyte-mediated delayed cognitive impairment following stroke.

J Neurosci 2015 Feb;35(5):2133-45

Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California 94305, Department of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305

Each year, 10 million people worldwide survive the neurologic injury associated with a stroke. Importantly, stroke survivors have more than twice the risk of subsequently developing dementia compared with people who have never had a stroke. The link between stroke and the later development of dementia is not understood. There are reports of oligoclonal bands in the CSF of stroke patients, suggesting that in some people a B-lymphocyte response to stroke may occur in the CNS. Therefore, we tested the hypothesis that a B-lymphocyte response to stroke could contribute to the onset of dementia. We discovered that, in mouse models, activated B-lymphocytes infiltrate infarcted tissue in the weeks after stroke. B-lymphocytes undergo isotype switching, and IgM, IgG, and IgA antibodies are found in the neuropil adjacent to the lesion. Concurrently, mice develop delayed deficits in LTP and cognition. Genetic deficiency, and the pharmacologic ablation of B-lymphocytes using an anti-CD20 antibody, prevents the appearance of delayed cognitive deficits. Furthermore, immunostaining of human postmortem tissue revealed that a B-lymphocyte response to stroke also occurs in the brain of some people with stroke and dementia. These data suggest that some stroke patients may develop a B-lymphocyte response to stroke that contributes to dementia, and is potentially treatable with FDA-approved drugs that target B cells.
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http://dx.doi.org/10.1523/JNEUROSCI.4098-14.2015DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4315838PMC
February 2015

The dendritic SNARE fusion machinery involved in AMPARs insertion during long-term potentiation.

Authors:
Sandra Jurado

Front Cell Neurosci 2014 22;8:407. Epub 2014 Dec 22.

Department of Pharmacology, University of Maryland School of Medicine Baltimore, MD, USA.

Sorting endosomes carry α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPARs) from their maturation sites to their final destination at the dendritic plasma membrane through both constitutive and regulated exocytosis. Insertion of functional AMPARs into the postsynaptic membrane is essential for maintaining fast excitatory synaptic transmission and plasticity. Despite this crucial role in neuronal function, the machinery mediating the fusion of AMPAR-containing endosomes in dendrites has been largely understudied in comparison to presynaptic vesicle exocytosis. Increasing evidence suggests that similarly to neurotransmitter release, AMPARs insertion relies on the formation of a SNARE complex (soluble NSF-attachment protein receptor), whose composition in dendrites has just begun to be elucidated. This review analyzes recent findings of the fusion machinery involved in regulated AMPARs insertion and discusses how dendritic exocytosis and AMPARs lateral diffusion may work together to support synaptic plasticity.
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http://dx.doi.org/10.3389/fncel.2014.00407DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4273633PMC
January 2015

Chronic pain. Decreased motivation during chronic pain requires long-term depression in the nucleus accumbens.

Science 2014 Aug;345(6196):535-42

Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA.

Several symptoms associated with chronic pain, including fatigue and depression, are characterized by reduced motivation to initiate or complete goal-directed tasks. However, it is unknown whether maladaptive modifications in neural circuits that regulate motivation occur during chronic pain. Here, we demonstrate that the decreased motivation elicited in mice by two different models of chronic pain requires a galanin receptor 1-triggered depression of excitatory synaptic transmission in indirect pathway nucleus accumbens medium spiny neurons. These results demonstrate a previously unknown pathological adaption in a key node of motivational neural circuitry that is required for one of the major sequela of chronic pain states and syndromes.
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http://dx.doi.org/10.1126/science.1253994DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4219555PMC
August 2014

LTP requires a unique postsynaptic SNARE fusion machinery.

Neuron 2013 Feb;77(3):542-58

Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, 265 Campus Drive, Stanford, CA 94305, USA.

Membrane fusion during exocytosis is mediated by assemblies of SNARE (soluble NSF-attachment protein receptor) and SM (Sec1/Munc18-like) proteins. The SNARE/SM proteins involved in vesicle fusion during neurotransmitter release are well understood, whereas little is known about the protein machinery that mediates activity-dependent AMPA receptor (AMPAR) exocytosis during long-term potentiation (LTP). Using direct measurements of LTP in acute hippocampal slices and an in vitro LTP model of stimulated AMPAR exocytosis, we demonstrate that the Q-SNARE proteins syntaxin-3 and SNAP-47 are required for regulated AMPAR exocytosis during LTP but not for constitutive basal AMPAR exocytosis. In contrast, the R-SNARE protein synaptobrevin-2/VAMP2 contributes to both regulated and constitutive AMPAR exocytosis. Both the central complexin-binding and the N-terminal Munc18-binding sites of syntaxin-3 are essential for its postsynaptic role in LTP. Thus, postsynaptic exocytosis of AMPARs during LTP is mediated by a unique fusion machinery that is distinct from that used during presynaptic neurotransmitter release.
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http://dx.doi.org/10.1016/j.neuron.2012.11.029DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3569727PMC
February 2013

Microscale AMPAR reorganization and dynamics of the postsynaptic density.

J Neurosci 2012 May;32(21):7103-5

Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, California 94304, USA.

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http://dx.doi.org/10.1523/JNEUROSCI.1048-12.2012DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6622299PMC
May 2012

A calcineurin/AKAP complex is required for NMDA receptor-dependent long-term depression.

Nat Neurosci 2010 Sep 8;13(9):1053-5. Epub 2010 Aug 8.

Nancy Pritzker Laboratory, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Palo Alto, California, USA.

AKAP79/150 is a protein scaffold that is thought to position specific kinases (protein kinase A and C) and phosphatases (calcineurin) in appropriate synaptic domains so that their activities can regulate excitatory synaptic strength. Using a viral-mediated molecular replacement strategy in rat hippocampal slices, we found that AKAP is required for NMDA receptor-dependent long-term depression solely because of its interaction with calcineurin.
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http://dx.doi.org/10.1038/nn.2613DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943866PMC
September 2010

PTEN is recruited to the postsynaptic terminal for NMDA receptor-dependent long-term depression.

EMBO J 2010 Aug 13;29(16):2827-40. Epub 2010 Jul 13.

Department of Pharmacology, University of Michigan Medical School, Ann Arbor, MI, USA.

Phosphatase and tensin homolog deleted on chromosome ten (PTEN) is an important regulator of phosphatidylinositol-(3,4,5,)-trisphosphate signalling, which controls cell growth and differentiation. However, PTEN is also highly expressed in the adult brain, in which it can be found in dendritic spines in hippocampus and other brain regions. Here, we have investigated specific functions of PTEN in the regulation of synaptic function in excitatory hippocampal synapses. We found that NMDA receptor activation triggers a PDZ-dependent association between PTEN and the synaptic scaffolding molecule PSD-95. This association is accompanied by PTEN localization at the postsynaptic density and anchoring within the spine. On the other hand, enhancement of PTEN lipid phosphatase activity is able to drive depression of AMPA receptor-mediated synaptic responses. This activity is specifically required for NMDA receptor-dependent long-term depression (LTD), but not for LTP or metabotropic glutamate receptor-dependent LTD. Therefore, these results reveal PTEN as a regulated signalling molecule at the synapse, which is recruited to the postsynaptic membrane upon NMDA receptor activation, and is required for the modulation of synaptic activity during plasticity.
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http://dx.doi.org/10.1038/emboj.2010.160DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2924645PMC
August 2010

NMDA induces post-transcriptional regulation of alpha2-guanylyl-cyclase-subunit expression in cerebellar granule cells.

J Cell Sci 2006 Apr 28;119(Pt 8):1622-31. Epub 2006 Mar 28.

Departamento de Bioquímica, Facultad de Veterinaria, Universidad Complutense, Madrid, E-28040 Spain.

Activation of N-methyl-D-aspartate (NMDA) glutamate receptors commonly affects gene expression in different neurons. We reported previously that chronic treatment of rat cerebellar granule cells with NMDA (24 hours) upregulates the expression of mRNA encoding the alpha2 subunit of the nitric-oxide-sensitive guanylyl cyclase. However, the molecular mechanisms involved in this process remained to be elucidated. Here, we have performed mRNA-decay experiments using the transcriptional inhibitor actinomycin D, providing evidence that the half-life of alpha2 mRNA is significantly prolonged in cells exposed to NMDA. The role of the 3' untranslated region of the alpha2 transcripts in NMDA-induced mRNA stabilisation was examined and an association between the RNA-binding proteins AUF1 and ELAV-like protein 1 (HuR/HuA), and endogenous alpha2 mRNA was demonstrated in vivo, as revealed by coimmunoprecipitation experiments with specific antibodies against AUF1 and HuR. Further studies indicated that stimulation of the NMDA receptor induces a downregulation in AUF1 levels stabilising the alpha2 mRNA transcripts. These events are triggered through a mechanism that depends on formation of nitric oxide, and on the subsequent activation of guanylyl cyclase and cGMP dependent protein kinases.
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http://dx.doi.org/10.1242/jcs.02867DOI Listing
April 2006

Expression of cGMP-dependent protein kinases (I and II) and neuronal nitric oxide synthase in the developing rat cerebellum.

Brain Res Bull 2005 Mar 8;65(2):111-5. Epub 2005 Jan 8.

Department de Bioquímica, Facultad de Veterinaria, Universidad Complutense, Avda. Puerta de Hierro s/n, 28040 Madrid, Spain.

The expression of neuronal nitric oxide synthase (nNOS) and the cGMP-dependent protein kinases cGKI and cGKII in rat cerebellum was evaluated at different developmental stages by quantitative RT-PCR and Western blotting. mRNAs coding for these proteins were detected in the cerebella of rats aged 7, 14 and 21 days. Expression levels, nevertheless, varied significantly at each of these developmental stages. While nNOS and cGKI mRNA levels steadily increased during development, cGKII mRNA showed a different behaviour pattern, with similar levels observed on postnatal days 7 and 14 and increased levels noted on postnatal day 21. Moreover, protein expression profiles for nNOS and cGKI showed similar patterns to the mRNAs encoding these proteins. Our results reveal the developmental regulation of the expression of these proteins in the cerebellum, giving rise to higher levels as the cerebellum matures.
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http://dx.doi.org/10.1016/j.brainresbull.2004.12.001DOI Listing
March 2005

Elements of the nitric oxide/cGMP pathway expressed in cerebellar granule cells: biochemical and functional characterisation.

Neurochem Int 2004 Nov;45(6):833-43

Departamento de Bioquímica, Facultad de Veterinaria, Universidad Complutense, 28040-Madrid, Spain.

It is known that the nitric oxide (NO)/cGMP pathway affects neuronal development and the expression of the different proteins is developmentally dependent in several brain areas. However, so far there are no data on the expression of the proteins involved in this signalling system during the development of the cerebellar granule cell, one of the most widely used models of neuronal development. This study was accordingly designed to analyse the developmental regulation of neuronal nitric oxide synthase (nNOS), soluble guanylyl cyclase subunits (alpha1, alpha2 and beta1) and cGMP-dependent protein kinases (cGK I and cGK II) in cerebellar granule cells through real time-polymerase chain reaction (RT-PCR) and Western blotting. We were able to detect guanylyl cyclase subunits and cGK I and cGK II in cerebellar granule cells at every stage of development examined (cells freshly isolated from 7-day-old rat pups, and cells cultured for 7 days or 14 days). Expression levels, nevertheless, varied significantly at each stage. nNOS, alpha2 and beta1 and cGK II levels increased during granule cell development, while alpha1 and cGK I showed an opposite behaviour pattern; the levels of these latter proteins diminished as the cells matured. The functionality of this pathway was assessed by stimulating cells kept in culture for 7 days with DEA/NO or with N-methyl-D-aspartate (NMDA). Cells responded by increasing intracellular cGMP and activating cGMP-dependent protein kinase activity, which effectively phosphorylated two well-known substrates of this activity, the vasodilator stimulated phosphoprotein (VASP) and the cAMP response element binding protein (CREB). In summary, through both functional and biochemical tests, this is the first demonstration of a complete NO/cGMP signalling transduction pathway in cerebellar granule cells. Our results also indicate the developmental regulation of the proteins in this system.
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http://dx.doi.org/10.1016/j.neuint.2004.03.013DOI Listing
November 2004

Differential expression of NO-sensitive guanylyl cyclase subunits during the development of rat cerebellar granule cells: regulation via N-methyl-D-aspartate receptors.

J Cell Sci 2003 Aug 10;116(Pt 15):3165-75. Epub 2003 Jun 10.

Departamento de Bioquímica, Facultad de Veterinaria, Universidad Complutense, 28040 Madrid, Spain.

In primary cultures of rat cerebellar granule cells with a functional network of glutamatergic neurons, the expression pattern of the different subunits of nitric-oxide (NO)-sensitive guanylyl cyclase changes during cell differentiation. These cells express the alpha1, alpha2 and beta1 subunits of NO-sensitive guanylyl cyclase and synthesize cyclic guanosine monophosphate (cGMP) in response to exogenous or endogenous nitric oxide. In this study, we determined the protein content of the alpha1 and beta1 subunits and quantified alpha1, alpha2 and beta1 mRNA by reverse transcription coupled to a polymerase chain reaction (RT-PCR). Expression of the beta1 subunit increased with the degree of cell differentiation, although most marked changes occurred at the alpha subunit level. In cells freshly isolated from rat pups on postnatal day 7 (P7) the most abundant alpha subunit was alpha1, while alpha2 appeared as the predominant subunit of this type in cultured cells. N-methyl-D-aspartate (NMDA) receptor stimulation in 7- or 14-day-cultured cells led to the upregulation of guanylyl cyclase subunit mRNAs; alpha2 mRNA levels undergoing most significant change. This enhanced subunit expression was accompanied by an increase in the amount of cGMP synthesized in response to NO. Thus, it seems that alpha2 subunits are increasingly expressed as granule cells mature. The presence of this subunit in the guanylyl cyclase heterodimer facilitates its localization at synaptic membranes, where the enzyme acts as a sensor for NO formed by the postsynaptic protein 95 (PSD-95)-associated neuronal NO synthase.
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http://dx.doi.org/10.1242/jcs.00620DOI Listing
August 2003