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Artículos de revistas sobre el tema "Inhibitory synapse"

Autor: Grafiati

Publicado: 14 de diciembre de 2024

Última modificación: 31 de julio de 2025

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1

Pettem, Katherine L., Daisaku Yokomaku, Hideto Takahashi, Yuan Ge, and Ann Marie Craig. "Interaction between autism-linked MDGAs and neuroligins suppresses inhibitory synapse development." Journal of Cell Biology 200, no. 3 (2013): 321–36. http://dx.doi.org/10.1083/jcb.201206028.

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Rare variants in MDGAs (MAM domain–containing glycosylphosphatidylinositol anchors), including multiple protein-truncating deletions, are linked to autism and schizophrenia, but the function of these genes is poorly understood. Here, we show that MDGA1 and MDGA2 bound to neuroligin-2 inhibitory synapse–organizing protein, also implicated in neurodevelopmental disorders. MDGA1 inhibited the synapse-promoting activity of neuroligin-2, without altering neuroligin-2 surface trafficking, by inhibiting interaction of neuroligin-2 with neurexin. MDGA binding and suppression of synaptogenic activity w

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2

Dejanovic, Borislav, Tiffany Wu, Ming-Chi Tsai, et al. "Complement C1q-dependent excitatory and inhibitory synapse elimination by astrocytes and microglia in Alzheimer’s disease mouse models." Nature Aging 2, no. 9 (2022): 837–50. http://dx.doi.org/10.1038/s43587-022-00281-1.

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AbstractMicroglia and complement can mediate neurodegeneration in Alzheimer’s disease (AD). By integrative multi-omics analysis, here we show that astrocytic and microglial proteins are increased in TauP301S synapse fractions with age and in a C1q-dependent manner. In addition to microglia, we identified that astrocytes contribute substantially to synapse elimination in TauP301S hippocampi. Notably, we found relatively more excitatory synapse marker proteins in astrocytic lysosomes, whereas microglial lysosomes contained more inhibitory synapse material. C1q deletion reduced astrocyte–synapse

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3

Hu, Xiaoge, Jian-hong Luo, and Junyu Xu. "The Interplay between Synaptic Activity and Neuroligin Function in the CNS." BioMed Research International 2015 (2015): 1–13. http://dx.doi.org/10.1155/2015/498957.

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Neuroligins (NLs) are postsynaptic transmembrane cell-adhesion proteins that play a key role in the regulation of excitatory and inhibitory synapses. Previousin vitroandin vivostudies have suggested that NLs contribute to synapse formation and synaptic transmission. Consistent with their localization, NL1 and NL3 selectively affect excitatory synapses, whereas NL2 specifically affects inhibitory synapses. Deletions or mutations in NL genes have been found in patients with autism spectrum disorders or mental retardations, and mice harboring the reported NL deletions or mutations exhibit autism-

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4

Suckow, Arthur T., Davide Comoletti, Megan A. Waldrop та ін. "Expression of Neurexin, Neuroligin, and Their Cytoplasmic Binding Partners in the Pancreatic β-Cells and the Involvement of Neuroligin in Insulin Secretion". Endocrinology 149, № 12 (2008): 6006–17. http://dx.doi.org/10.1210/en.2008-0274.

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The composition of the β-cell exocytic machinery is very similar to that of neuronal synapses, and the developmental pathway of β-cells and neurons substantially overlap. β-Cells secrete γ-aminobutyric acid and express proteins that, in the brain, are specific markers of inhibitory synapses. Recently, neuronal coculture experiments have identified three families of synaptic cell-surface molecules (neurexins, neuroligins, and SynCAM) that drive synapse formation in vitro and that control the differentiation of nascent synapses into either excitatory or inhibitory fully mature nerve terminals. T

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5

Jasinska, Malgorzata, Ewa Siucinska, Ewa Jasek, Jan A. Litwin, Elzbieta Pyza, and Malgorzata Kossut. "Effect of Associative Learning on Memory Spine Formation in Mouse Barrel Cortex." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/9828517.

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Associative fear learning, in which stimulation of whiskers is paired with mild electric shock to the tail, modifies the barrel cortex, the functional representation of sensory receptors involved in the conditioning, by inducing formation of new inhibitory synapses on single-synapse spines of the cognate barrel hollows and thus producing double-synapse spines. In the barrel cortex of conditioned, pseudoconditioned, and untreated mice, we analyzed the number and morphological features of dendritic spines at various maturation and stability levels: sER-free spines, spines containing smooth endop

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6

Overstreet, Linda S., and Gary L. Westbrook. "Synapse Density Regulates Independence at Unitary Inhibitory Synapses." Journal of Neuroscience 23, no. 7 (2003): 2618–26. http://dx.doi.org/10.1523/jneurosci.23-07-02618.2003.

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7

Hines, Pamela J. "Inhibitory synapse specificity." Science 363, no. 6425 (2019): 360.6–361. http://dx.doi.org/10.1126/science.363.6425.360-f.

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8

Jasinska, Malgorzata, Ewa Siucinska, Stansislaw Glazewski, Elzbieta Pyza, and And Kossut. "Characterization and plasticity of the double synapse spines in the barrel cortex of the mouse." Acta Neurobiologiae Experimentalis 66, no. 2 (2006): 99–104. http://dx.doi.org/10.55782/ane-2006-1595.

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The somatosensory barrel cortex of rodents and its afferent pathway from the facial vibrissae is a very useful model for studying neuronal plasticity. Dendritic spines are the most labile elements of synaptic circuitry and the most likely substrate of experience-dependent alterations in neuronal circuits in cerebral cortex. We characterized morphologically and numerically a specific population of spines, i.e. double synapse spines, which have two different inputs &#150; one excitatory and the other inhibitory, in the B2 barrel of mouse somatosensory cortex. We also described changes in mor

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9

Wilson, Emily S., and Karen Newell-Litwa. "Stem cell models of human synapse development and degeneration." Molecular Biology of the Cell 29, no. 24 (2018): 2913–21. http://dx.doi.org/10.1091/mbc.e18-04-0222.

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Many brain disorders exhibit altered synapse formation in development or synapse loss with age. To understand the complexities of human synapse development and degeneration, scientists now engineer neurons and brain organoids from human-induced pluripotent stem cells (hIPSC). These hIPSC-derived brain models develop both excitatory and inhibitory synapses and functional synaptic activity. In this review, we address the ability of hIPSC-derived brain models to recapitulate synapse development and insights gained into the molecular mechanisms underlying synaptic alterations in neuronal disorders

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10

Barreira da Silva, Rosa, Claudine Graf, and Christian Münz. "Cytoskeletal stabilization of inhibitory interactions in immunologic synapses of mature human dendritic cells with natural killer cells." Blood 118, no. 25 (2011): 6487–98. http://dx.doi.org/10.1182/blood-2011-07-366328.

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Abstract Human mature dendritic cells (DCs) can efficiently stimulate natural killer (NK)–cell responses without being targeted by their cytotoxicity. To understand this important regulatory crosstalk, we characterized the development of the immunologic synapse between mature DCs and resting NK cells. Conjugates between these 2 innate leukocyte populations formed rapidly, persisted for prolonged time periods and matured with DC-derived f-actin polymerization at the synapse. Polarization of IL-12 and IL-12R to the synapse coincided with f-actin polymerization, while other activating and inhibit

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11

Treanor, Bebhinn, Peter M. P. Lanigan, Sunil Kumar, et al. "Microclusters of inhibitory killer immunoglobulin–like receptor signaling at natural killer cell immunological synapses." Journal of Cell Biology 174, no. 1 (2006): 153–61. http://dx.doi.org/10.1083/jcb.200601108.

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We report the supramolecular organization of killer Ig–like receptor (KIR) phosphorylation using a technique applicable to imaging phosphorylation of any green fluorescent protein–tagged receptor at an intercellular contact or immune synapse. Specifically, we use fluorescence lifetime imaging (FLIM) to report Förster resonance energy transfer (FRET) between GFP-tagged KIR2DL1 and a Cy3-tagged generic anti-phosphotyrosine monoclonal antibody. Visualization of KIR phosphorylation in natural killer (NK) cells contacting target cells expressing cognate major histocompatibility complex class I pro

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12

Takesian, Anne E., Vibhakar C. Kotak, and Dan H. Sanes. "Age-dependent effect of hearing loss on cortical inhibitory synapse function." Journal of Neurophysiology 107, no. 3 (2012): 937–47. http://dx.doi.org/10.1152/jn.00515.2011.

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The developmental plasticity of excitatory synapses is well established, particularly as a function of age. If similar principles apply to inhibitory synapses, then we would expect manipulations during juvenile development to produce a greater effect and experience-dependent changes to persist into adulthood. In this study, we first characterized the maturation of cortical inhibitory synapse function from just before the onset of hearing through adulthood. We then examined the long-term effects of developmental conductive hearing loss (CHL). Whole cell recordings from gerbil thalamocortical br

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13

Flores, Carmen E., Irina Nikonenko, Pablo Mendez, Jean-Marc Fritschy, Shiva K. Tyagarajan, and Dominique Muller. "Activity-dependent inhibitory synapse remodeling through gephyrin phosphorylation." Proceedings of the National Academy of Sciences 112, no. 1 (2014): E65—E72. http://dx.doi.org/10.1073/pnas.1411170112.

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Maintaining a proper balance between excitation and inhibition is essential for the functioning of neuronal networks. However, little is known about the mechanisms through which excitatory activity can affect inhibitory synapse plasticity. Here we used tagged gephyrin, one of the main scaffolding proteins of the postsynaptic density at GABAergic synapses, to monitor the activity-dependent adaptation of perisomatic inhibitory synapses over prolonged periods of time in hippocampal slice cultures. We find that learning-related activity patterns known to induce N-methyl-d-aspartate (NMDA) receptor

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14

Ramaglia, Valeria, Mohit Dubey, M. Alfonso Malpede, et al. "Complement-associated loss of CA2 inhibitory synapses in the demyelinated hippocampus impairs memory." Acta Neuropathologica 142, no. 4 (2021): 643–67. http://dx.doi.org/10.1007/s00401-021-02338-8.

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AbstractThe complement system is implicated in synapse loss in the MS hippocampus, but the functional consequences of synapse loss remain poorly understood. Here, in post-mortem MS hippocampi with demyelination we find that deposits of the complement component C1q are enriched in the CA2 subfield, are linked to loss of inhibitory synapses and are significantly higher in MS patients with cognitive impairments compared to those with preserved cognitive functions. Using the cuprizone mouse model of demyelination, we corroborated that C1q deposits are highest within the demyelinated dorsal hippoca

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15

Su, Jianmin, Jiang Chen, Kumiko Lippold, et al. "Collagen-derived matricryptins promote inhibitory nerve terminal formation in the developing neocortex." Journal of Cell Biology 212, no. 6 (2016): 721–36. http://dx.doi.org/10.1083/jcb.201509085.

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Inhibitory synapses comprise only ∼20% of the total synapses in the mammalian brain but play essential roles in controlling neuronal activity. In fact, perturbing inhibitory synapses is associated with complex brain disorders, such as schizophrenia and epilepsy. Although many types of inhibitory synapses exist, these disorders have been strongly linked to defects in inhibitory synapses formed by Parvalbumin-expressing interneurons. Here, we discovered a novel role for an unconventional collagen—collagen XIX—in the formation of Parvalbumin+ inhibitory synapses. Loss of this collagen results not

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16

Legendre, P. "The glycinergic inhibitory synapse." Cellular and Molecular Life Sciences 58, no. 5 (2001): 760–93. http://dx.doi.org/10.1007/pl00000899.

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17

Holmes, William R., and William B. Levy. "Quantifying the Role of Inhibition in Associative Long-Term Potentiation in Dentate Granule Cells With Computational Models." Journal of Neurophysiology 78, no. 1 (1997): 103–16. http://dx.doi.org/10.1152/jn.1997.78.1.103.

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Holmes, William R. and William B. Levy. Quantifying the role of inhibition in associative long-term potentiation in dentate granule cells with computational models. J. Neurophysiol. 78: 103–116, 1997. In the dentate gyrus, coactivation of a mildly strong ipsilateral perforant path (pp) input with a weak contralateral pp input will not induce associative long-term potentiation in the weak input path unless both inputs project to the same part of the molecular layer. This “spatial convergence requirement” is thought to arise from either voltage attenuation between input locations or inhibition.

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18

Woodin, Melanie A., Toshiro Hamakawa, Mayumi Takasaki, Ken Lukowiak, and Naweed I. Syed. "Trophic Factor-Induced Plasticity of Synaptic Connections Between Identified Lymnaea Neurons." Learning & Memory 6, no. 3 (1999): 307–16. http://dx.doi.org/10.1101/lm.6.3.307.

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Neurotrophic factors participate in both developmental and adult synaptic plasticity; however, the underlying mechanisms remain unknown. Using soma–soma synapses between the identified Lymnaea neurons, we demonstrate that the brain conditioned medium (CM)-derived trophic factors are required for the formation of excitatory but not the inhibitory synapse. Specifically, identified presynaptic [right pedal dorsal 1 (RPeD1) and visceral dorsal 4 (VD4)] and postsynaptic [visceral dorsal 2/3 (VD2/3) and left pedal dorsal 1 (LPeD1)] neurons were soma–soma paired either in the absence or presence of C

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19

Hoon, Mrinalini, Raunak Sinha, Haruhisa Okawa, et al. "Neurotransmission plays contrasting roles in the maturation of inhibitory synapses on axons and dendrites of retinal bipolar cells." Proceedings of the National Academy of Sciences 112, no. 41 (2015): 12840–45. http://dx.doi.org/10.1073/pnas.1510483112.

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Neuronal output is modulated by inhibition onto both dendrites and axons. It is unknown whether inhibitory synapses at these two cellular compartments of an individual neuron are regulated coordinately or separately during in vivo development. Because neurotransmission influences synapse maturation and circuit development, we determined how loss of inhibition affects the expression of diverse types of inhibitory receptors on the axon and dendrites of mouse retinal bipolar cells. We found that axonal GABA but not glycine receptor expression depends on neurotransmission. Importantly, axonal and

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20

ELMARIAH, SARINA B., ETHAN G. HUGHES, EUN JOO OH, and RITA J. BALICE-GORDON. "Neurotrophin signaling among neurons and glia during formation of tripartite synapses." Neuron Glia Biology 1, no. 4 (2004): 339–49. http://dx.doi.org/10.1017/s1740925x05000189.

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Synapse formation in the CNS is a complex process that involves the dynamic interplay of numerous signals exchanged between pre- and postsynaptic neurons as well as perisynaptic glia. Members of the neurotrophin family, which are widely expressed in the developing and mature CNS and are well-known for their roles in promoting neuronal survival and differentiation, have emerged as key synaptic modulators. However, the mechanisms by which neurotrophins modulate synapse formation and function are poorly understood. Here, we summarize our work on the role of neurotrophins in synaptogenesis in the

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21

Ko, Jaewon, Gilberto J. Soler-Llavina, Marc V. Fuccillo, Robert C. Malenka, and Thomas C. Südhof. "Neuroligins/LRRTMs prevent activity- and Ca2+/calmodulin-dependent synapse elimination in cultured neurons." Journal of Cell Biology 194, no. 2 (2011): 323–34. http://dx.doi.org/10.1083/jcb.201101072.

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Neuroligins (NLs) and leucine-rich repeat transmembrane proteins (LRRTMs) are postsynaptic cell adhesion molecules that bind to presynaptic neurexins. In this paper, we show that short hairpin ribonucleic acid–mediated knockdowns (KDs) of LRRTM1, LRRTM2, and/or NL-3, alone or together as double or triple KDs (TKDs) in cultured hippocampal neurons, did not decrease synapse numbers. In neurons cultured from NL-1 knockout mice, however, TKD of LRRTMs and NL-3 induced an ∼40% loss of excitatory but not inhibitory synapses. Strikingly, synapse loss triggered by the LRRTM/NL deficiency was abrogated

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22

Jasinska, Malgorzata, Anna Grzegorczyk, Ewa Jasek, et al. "Daily rhythm of synapse turnover in mouse somatosensory cortex." Acta Neurobiologiae Experimentalis 74, no. 1 (2014): 104–10. http://dx.doi.org/10.55782/ane-2014-1977.

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The whisker representations in the somatosensory barrel cortex of mice are modulated by sensory inputs associated with animal motor behavior which shows circadian rhythmicity. In a C57/BL mouse strain kept under a light/dark (LD 12:12) regime, we observed daily structural changes in the barrel cortex, correlated with the locomotor activity level. Stereological analysis of serial electron microscopic sections of the barrel cortex of mice sacrificed during their active or rest period, revealed an increase in the total numerical density of synapses and in the density of excitatory synapses locate

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23

Woo, Jooyeon, Seok-Kyu Kwon, Jungyong Nam, et al. "The adhesion protein IgSF9b is coupled to neuroligin 2 via S-SCAM to promote inhibitory synapse development." Journal of Cell Biology 201, no. 6 (2013): 929–44. http://dx.doi.org/10.1083/jcb.201209132.

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Synaptic adhesion molecules regulate diverse aspects of synapse formation and maintenance. Many known synaptic adhesion molecules localize at excitatory synapses, whereas relatively little is known about inhibitory synaptic adhesion molecules. Here we report that IgSF9b is a novel, brain-specific, homophilic adhesion molecule that is strongly expressed in GABAergic interneurons. IgSF9b was preferentially localized at inhibitory synapses in cultured rat hippocampal and cortical interneurons and was required for the development of inhibitory synapses onto interneurons. IgSF9b formed a subsynapti

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24

Levinson, Joshua N., and Alaa El-Husseini. "New Players Tip the Scales in the Balance between Excitatory and Inhibitory Synapses." Molecular Pain 1 (January 1, 2005): 1744–8069. http://dx.doi.org/10.1186/1744-8069-1-12.

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Synaptogenesis is a highly controlled process, involving a vast array of players which include cell adhesion molecules, scaffolding and signaling proteins, neurotransmitter receptors and proteins associated with the synaptic vesicle machinery. These molecules cooperate in an intricate manner on both the pre- and postsynaptic sides to orchestrate the precise assembly of neuronal contacts. This is an amazing feat considering that a single neuron receives tens of thousands of synaptic inputs but virtually no mismatch between pre- and postsynaptic components occur in vivo. One crucial aspect of sy

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25

Lee, Sang-Eun, Yoonju Kim, Jeong-Kyu Han, et al. "nArgBP2 regulates excitatory synapse formation by controlling dendritic spine morphology." Proceedings of the National Academy of Sciences 113, no. 24 (2016): 6749–54. http://dx.doi.org/10.1073/pnas.1600944113.

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Neural Abelson-related gene-binding protein 2 (nArgBP2) was originally identified as a protein that directly interacts with synapse-associated protein 90/postsynaptic density protein 95-associated protein 3 (SAPAP3), a postsynaptic scaffolding protein critical for the assembly of glutamatergic synapses. Although genetic deletion of nArgBP2 in mice leads to manic/bipolar-like behaviors resembling many aspects of symptoms in patients with bipolar disorder, the actual function of nArgBP2 at the synapse is completely unknown. Here, we found that the knockdown (KD) of nArgBP2 by specific small hair

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26

Thakar, Sonal, Liqing Wang, Ting Yu, et al. "Evidence for opposing roles of Celsr3 and Vangl2 in glutamatergic synapse formation." Proceedings of the National Academy of Sciences 114, no. 4 (2017): E610—E618. http://dx.doi.org/10.1073/pnas.1612062114.

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The signaling mechanisms that choreograph the assembly of the highly asymmetric pre- and postsynaptic structures are still poorly defined. Using synaptosome fractionation, immunostaining, and coimmunoprecipitation, we found that Celsr3 and Vangl2, core components of the planar cell polarity (PCP) pathway, are localized at developing glutamatergic synapses and interact with key synaptic proteins. Pyramidal neurons from the hippocampus of Celsr3 knockout mice exhibit loss of ∼50% of glutamatergic synapses, but not inhibitory synapses, in culture. Wnts are known regulators of synapse formation, a

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27

Ojima, Daiki, Yoko Tominaga, Takashi Kubota, et al. "Impaired Hippocampal Long-Term Potentiation and Memory Deficits upon Haploinsufficiency of MDGA1 Can Be Rescued by Acute Administration of d-Cycloserine." International Journal of Molecular Sciences 25, no. 17 (2024): 9674. http://dx.doi.org/10.3390/ijms25179674.

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The maintenance of proper brain function relies heavily on the balance of excitatory and inhibitory neural circuits, governed in part by synaptic adhesion molecules. Among these, MDGA1 (MAM domain-containing glycosylphosphatidylinositol anchor 1) acts as a suppressor of synapse formation by interfering with Neuroligin-mediated interactions, crucial for maintaining the excitatory–inhibitory (E/I) balance. Mdga1−/− mice exhibit selectively enhanced inhibitory synapse formation in their hippocampal pyramidal neurons, leading to impaired hippocampal long-term potentiation (LTP) and hippocampus-dep

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28

Apollonio, Benedetta, Mariam Fanous, Mohamed-Reda Benmebarek, et al. "CC-122 Repairs T Cell Activation in Chronic Lymphocytic Leukemia That Results in a Concomitant Increase in PD-1:PD-L1 and CTLA-4 Immune Checkpoint Expression at the Immunological Synapse." Blood 126, no. 23 (2015): 1738. http://dx.doi.org/10.1182/blood.v126.23.1738.1738.

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Abstract Immunomodulatory drugs (IMiDs®) such as lenalidomide and immune checkpoint blockade (ICB) antibodies can enhance autologous anti-tumor T cell immunity and have the potential to elicit durable control of disease in B cell malignancies. These immunotherapies are likely to be most effective when employed in treatment combinations. Thus, the goal of pre-clinical research should be to reveal mechanisms of action (MOA) in the tumor microenvironment (TME) and identify biomarkers to guide development of combination therapy for patients. CC-122 is a novel first-in-class pleiotropic pathway mod

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Ishibashi, Masaru, Kiyoshi Egawa, and Atsuo Fukuda. "Diverse Actions of Astrocytes in GABAergic Signaling." International Journal of Molecular Sciences 20, no. 12 (2019): 2964. http://dx.doi.org/10.3390/ijms20122964.

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An imbalance of excitatory and inhibitory neurotransmission leading to over excitation plays a crucial role in generating seizures, while enhancing GABAergic mechanisms are critical in terminating seizures. In recent years, it has been reported in many studies that astrocytes are deeply involved in synaptic transmission. Astrocytes form a critical component of the “tripartite” synapses by wrapping around the pre- and post-synaptic elements. From this location, astrocytes are known to greatly influence the dynamics of ions and transmitters in the synaptic cleft. Despite recent extensive researc

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30

Zhang, Lulu, Yongzhi Zhang, Furong Liu, Qingyuan Chen, Yangbo Lian, and Quanlong Ma. "On-Chip Photonic Synapses with All-Optical Memory and Neural Network Computation." Micromachines 14, no. 1 (2022): 74. http://dx.doi.org/10.3390/mi14010074.

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Inspired by the human brain, neural network computing was expected to break the bottleneck of traditional computing, but the integrated design still faces great challenges. Here, a readily integrated membrane-system photonic synapse was demonstrated. By pre-pulse training at 1064 nm (cutoff wavelength), the photonic synapse can be regulated both excitatory and inhibitory at tunable wavelengths (1200–2000 nm). Furthermore, more weights and memory functions were shown through the photonic synapse integrated network. Additionally, the digital recognition function of the single-layer perceptron ne

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Kuljis, Dika A., Kristina D. Micheva, Ajit Ray, et al. "Gephyrin-Lacking PV Synapses on Neocortical Pyramidal Neurons." International Journal of Molecular Sciences 22, no. 18 (2021): 10032. http://dx.doi.org/10.3390/ijms221810032.

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Gephyrin has long been thought of as a master regulator for inhibitory synapses, acting as a scaffold to organize γ-aminobutyric acid type A receptors (GABAARs) at the post-synaptic density. Accordingly, gephyrin immunostaining has been used as an indicator of inhibitory synapses; despite this, the pan-synaptic localization of gephyrin to specific classes of inhibitory synapses has not been demonstrated. Genetically encoded fibronectin intrabodies generated with mRNA display (FingRs) against gephyrin (Gephyrin.FingR) reliably label endogenous gephyrin, and can be tagged with fluorophores for c

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Wichmann, Carolin, and Thomas Kuner. "Heterogeneity of glutamatergic synapses: cellular mechanisms and network consequences." Physiological Reviews 102, no. 1 (2022): 269–318. http://dx.doi.org/10.1152/physrev.00039.2020.

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Chemical synapses are commonly known as a structurally and functionally highly diverse class of cell-cell contacts specialized to mediate communication between neurons. They represent the smallest “computational” unit of the brain and are typically divided into excitatory and inhibitory as well as modulatory categories. These categories are subdivided into diverse types, each representing a different structure-function repertoire that in turn are thought to endow neuronal networks with distinct computational properties. The diversity of structure and function found among a given category of sy

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33

Gonzalez-Burgos, Guillermo, Diana C. Rotaru, Aleksey V. Zaitsev, Nadezhda V. Povysheva, and David A. Lewis. "GABA Transporter GAT1 Prevents Spillover at Proximal and Distal GABA Synapses Onto Primate Prefrontal Cortex Neurons." Journal of Neurophysiology 101, no. 2 (2009): 533–47. http://dx.doi.org/10.1152/jn.91161.2008.

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The plasma membrane GABA transporter GAT1 is thought to mediate uptake of synaptically released GABA. In the primate dorsolateral prefrontal cortex (DLPFC), GAT1 expression changes significantly during development and in schizophrenia. The consequences of such changes, however, are not well understood because GAT1's role has not been investigated in primate neocortical circuits. We thus studied the effects of the GAT1 blocker 1,2,5,6-tetrahydro-1-[2-[[(diphenylmethylene)amino]oxy] ethyl]- 3-pyridinecarboxylic acid hydrochloride (NO711) on GABA transmission onto pyramidal neurons of monkey DLPF

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Harrison, John M., Richard G. Allen, Michael J. Pellegrino, John T. Williams, and Olivier J. Manzoni. "Chronic Morphine Treatment Alters Endogenous Opioid Control of Hippocampal Mossy Fiber Synaptic Transmission." Journal of Neurophysiology 87, no. 5 (2002): 2464–70. http://dx.doi.org/10.1152/jn.2002.87.5.2464.

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Synaptic adaptations are thought to be an important component of the consequences of drug abuse. One such adaptation is an up-regulation of adenylyl cyclase that has been shown to increase transmitter release at several inhibitory synapses. In this study the effects of chronic morphine treatment were studied on mossy fiber synapses in the guinea pig hippocampus using extracellular field potential recordings. This opioid-sensitive synapse was chosen because of the known role of the adenylyl cyclase cascade in the regulation of glutamate release. Long-term potentiation (LTP) at the mossy fiber s

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35

PEREIRA, T., M. S. BAPTISTA, J. KURTHS, and M. B. REYES. "ONSET OF PHASE SYNCHRONIZATION IN NEURONS WITH CHEMICAL SYNAPSE." International Journal of Bifurcation and Chaos 17, no. 10 (2007): 3545–49. http://dx.doi.org/10.1142/s0218127407019342.

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We study the onset of synchronous states in realistic chaotic neurons coupled by mutually inhibitory chemical synapses. For the realistic parameters, namely the synaptic strength and the intrinsic current, this synapse introduces noncoherences in the neuronal dynamics, yet allowing for chaotic phase synchronization in a large range of parameters. As we increase the synaptic strength, the neurons reach a periodic state, and no chaotic complete synchronization is found.

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Qian, N., and T. J. Sejnowski. "When is an inhibitory synapse effective?" Proceedings of the National Academy of Sciences 87, no. 20 (1990): 8145–49. http://dx.doi.org/10.1073/pnas.87.20.8145.

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37

Zhao, Qing-Tai, Fengben Xi, Yi Han, Andreas Grenmyr, Jin Hee Bae, and Detlev Gruetzmacher. "Ferroelectric Devices for Neuromorphic Computing." ECS Meeting Abstracts MA2022-02, no. 32 (2022): 1183. http://dx.doi.org/10.1149/ma2022-02321183mtgabs.

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Neuromorphic computing inspired by the neural network systems of the human brain enables energy efficient computing for big-data processing. A neural network is formed by thousands or even millions of neurons which are connected by even a higher number of synapses. Neurons communicate with each other through the connected synapses. The main responsibility of synapses is to transfer information from the pre-synaptic to the postsynaptic neurons. Synapses can memorize and process the information simultaneously. The plasticity of a synapse to strengthen or weaken their activity over time make it c

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38

Fenyves, Bánk G., Gábor S. Szilágyi, Zsolt Vassy, Csaba Sőti, and Peter Csermely. "Synaptic polarity and sign-balance prediction using gene expression data in the Caenorhabditis elegans chemical synapse neuronal connectome network." PLOS Computational Biology 16, no. 12 (2020): e1007974. http://dx.doi.org/10.1371/journal.pcbi.1007974.

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Graph theoretical analyses of nervous systems usually omit the aspect of connection polarity, due to data insufficiency. The chemical synapse network of Caenorhabditis elegans is a well-reconstructed directed network, but the signs of its connections are yet to be elucidated. Here, we present the gene expression-based sign prediction of the ionotropic chemical synapse connectome of C. elegans (3,638 connections and 20,589 synapses total), incorporating available presynaptic neurotransmitter and postsynaptic receptor gene expression data for three major neurotransmitter systems. We made predict

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39

Grimes, William N., Jun Zhang, Hua Tian, et al. "Complex inhibitory microcircuitry regulates retinal signaling near visual threshold." Journal of Neurophysiology 114, no. 1 (2015): 341–53. http://dx.doi.org/10.1152/jn.00017.2015.

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Neuronal microcircuits, small, localized signaling motifs involving two or more neurons, underlie signal processing and computation in the brain. Compartmentalized signaling within a neuron may enable it to participate in multiple, independent microcircuits. Each A17 amacrine cell in the mammalian retina contains within its dendrites hundreds of synaptic feedback microcircuits that operate independently to modulate feedforward signaling in the inner retina. Each of these microcircuits comprises a small (<1 μm) synaptic varicosity that typically receives one excitatory synapse from a presyna

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40

Lee, Seong-Eun, and Gum Hwa Lee. "Reelin Affects Signaling Pathways of a Group of Inhibitory Neurons and the Development of Inhibitory Synapses in Primary Neurons." International Journal of Molecular Sciences 22, no. 14 (2021): 7510. http://dx.doi.org/10.3390/ijms22147510.

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Reelin is a secretory protein involved in a variety of processes in forebrain development and function, including neuronal migration, dendrite growth, spine formation, and synaptic plasticity. Most of the function of Reelin is focused on excitatory neurons; however, little is known about its effects on inhibitory neurons and inhibitory synapses. In this study, we investigated the phosphatidylinositol 3-kinase/Akt pathway of Reelin in primary cortical and hippocampal neurons. Individual neurons were visualized using immunofluorescence to distinguish inhibitory neurons from excitatory neurons. R

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41

Nerlich, Jana, Thomas Kuenzel, Christian Keine, Andrej Korenic, Rudolf Rübsamen, and Ivan Milenkovic. "Dynamic fidelity control to the central auditory system: synergistic glycine/GABAergic inhibition in the cochlear nucleus." Journal of Neuroscience 34, no. 35 (2014): 11604–20. https://doi.org/10.1523/JNEUROSCI.0719-14.2014.

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GABA and glycine are the major inhibitory transmitters that attune neuronal activity in the CNS of mammals. The respective transmitters are mostly spatially separated, that is, synaptic inhibition in the forebrain areas is mediated by GABA, whereas glycine is predominantly used in the brainstem. Accordingly, inhibition in auditory brainstem circuits is largely mediated by glycine, but there are few auditory synapses using both transmitters in maturity. Little is known about physiological advantages of such a two-transmitter inhibitory mechanism. We explored the benefit of engaging both glycine

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42

Gardner, D. "Sets of synaptic currents paired by common presynaptic or postsynaptic neurons." Journal of Neurophysiology 61, no. 4 (1989): 845–53. http://dx.doi.org/10.1152/jn.1989.61.4.845.

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1. In the buccal ganglia of Aplysia, presynaptic neurons B4 and B5 produce similar inhibitory postsynaptic currents (PSCs) in several postsynaptic follower cells. Previous work has shown that both duration and amplitude of these PSCs vary, that each parameter may be altered transiently by manipulating presynaptic activity, and that these variations affect synaptic efficacy. 2. To permit synapse-to-synapse comparisons, the mean and coefficient of variation (CV) of both peak conductance (gpeak) and time constant of decay (tau) were determined for sets of synaptic currents evoked by direct intrac

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43

Ali, Heba, Lena Marth, and Dilja Krueger-Burg. "Neuroligin-2 as a central organizer of inhibitory synapses in health and disease." Science Signaling 13, no. 663 (2020): eabd8379. http://dx.doi.org/10.1126/scisignal.abd8379.

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Postsynaptic organizational protein complexes play central roles both in orchestrating synapse formation and in defining the functional properties of synaptic transmission that together shape the flow of information through neuronal networks. A key component of these organizational protein complexes is the family of synaptic adhesion proteins called neuroligins. Neuroligins form transsynaptic bridges with presynaptic neurexins to regulate various aspects of excitatory and inhibitory synaptic transmission. Neuroligin-2 (NLGN2) is the only member that acts exclusively at GABAergic inhibitory syn

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44

Unda, Brianna K., Vickie Kwan, and Karun K. Singh. "Neuregulin-1 Regulates Cortical Inhibitory Neuron Dendrite and Synapse Growth through DISC1." Neural Plasticity 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/7694385.

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Cortical inhibitory neurons play crucial roles in regulating excitatory synaptic networks and cognitive function and aberrant development of these cells have been linked to neurodevelopmental disorders. The secreted neurotrophic factor Neuregulin-1 (NRG1) and its receptor ErbB4 are established regulators of inhibitory neuron connectivity, but the developmental signalling mechanisms regulating this process remain poorly understood. Here, we provide evidence that NRG1-ErbB4 signalling functions through the multifunctional scaffold protein, Disrupted in Schizophrenia 1 (DISC1), to regulate the de

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45

Niraula, Suraj, Shirley ShiDu Yan, and Jaichandar Subramanian. "Amyloid pathology impairs experience-dependent inhibitory synaptic plasticity." Journal of Neuroscience, November 27, 2023, JN—RM—0702–23. http://dx.doi.org/10.1523/jneurosci.0702-23.2023.

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Alzheimer's disease patients and mouse models exhibit aberrant neuronal activity and altered excitatory-to-inhibitory synaptic ratio. Using multicolor two-photon microscopy, we test how amyloid pathology alters the structural dynamics of excitatory and inhibitory synapses and their adaptation to altered visual experiencein vivoin the visual cortex. We show that the baseline dynamics of mature excitatory synapses and their adaptation to visual deprivation are not altered in amyloidosis. Likewise, the baseline dynamics of inhibitory synapses are not affected. In contrast, visual deprivation fail

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Dzyubenko, Egor, Michael Fleischer, Daniel Manrique-Castano, et al. "Inhibitory control in neuronal networks relies on the extracellular matrix integrity." Cellular and Molecular Life Sciences, June 15, 2021. http://dx.doi.org/10.1007/s00018-021-03861-3.

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AbstractInhibitory control is essential for the regulation of neuronal network activity, where excitatory and inhibitory synapses can act synergistically, reciprocally, and antagonistically. Sustained excitation-inhibition (E-I) balance, therefore, relies on the orchestrated adjustment of excitatory and inhibitory synaptic strength. While growing evidence indicates that the brain’s extracellular matrix (ECM) is a crucial regulator of excitatory synapse plasticity, it remains unclear whether and how the ECM contributes to inhibitory control in neuronal networks. Here we studied the simultaneous

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47

Boxer, Emma E., and Jason Aoto. "Neurexins and their ligands at inhibitory synapses." Frontiers in Synaptic Neuroscience 14 (December 21, 2022). http://dx.doi.org/10.3389/fnsyn.2022.1087238.

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Since the discovery of neurexins (Nrxns) as essential and evolutionarily conserved synaptic adhesion molecules, focus has largely centered on their functional contributions to glutamatergic synapses. Recently, significant advances to our understanding of neurexin function at GABAergic synapses have revealed that neurexins can play pleiotropic roles in regulating inhibitory synapse maintenance and function in a brain-region and synapse-specific manner. GABAergic neurons are incredibly diverse, exhibiting distinct synaptic properties, sites of innervation, neuromodulation, and plasticity. Differ

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48

Hernández-Vivanco, Alicia, Esther Jiménez-Redondo, Nuria Cano-Adamuz, and Pablo Méndez. "Protein kinase A-dependent plasticity of local inhibitory synapses from hilar somatostatin-expressing neurons." eneuro, September 21, 2023, ENEURO.0089–23.2023. http://dx.doi.org/10.1523/eneuro.0089-23.2023.

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Hippocampal Inhibitory Neurons (INs) contact local targets and project to different brain areas to form synapses on distal neurons. Despite the importance of INs for hippocampal function and interregional brain communication, the impact of activity-dependent plasticity mechanisms on local and long-range GABAergic synapses formed by hippocampal INs remains to be fully elucidated. Here, we use optogenetic-coupled electrophysiology in mice to show that protein kinase A (PKA), a master regulator of GABAergic synapse plasticity, causes a form of long-term potentiation of inhibitory synapses (iLTP)

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49

Wilson, Emily, Warren Knudson, and Karen Newell-Litwa. "Hyaluronan regulates synapse formation and function in developing neural networks." Scientific Reports 10, no. 1 (2020). http://dx.doi.org/10.1038/s41598-020-73177-y.

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Abstract Neurodevelopmental disorders present with synaptic alterations that disrupt the balance between excitatory and inhibitory signaling. For example, hyperexcitability of cortical neurons is associated with both epilepsy and autism spectrum disorders. However, the mechanisms that initially establish the balance between excitatory and inhibitory signaling in brain development are not well understood. Here, we sought to determine how the extracellular matrix directs synapse formation and regulates synaptic function in a model of human cortical brain development. The extracellular matrix, ma

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50

Luo, Bin, Ziyang Liu, Dong Lin, et al. "ErbB4 promotes inhibitory synapse formation by cell adhesion, independent of its kinase activity." Translational Psychiatry 11, no. 1 (2021). http://dx.doi.org/10.1038/s41398-021-01485-6.

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AbstractThe precise control of the nervous system function under the vitality of synapses is extremely critical. Efforts have been taken to explore the underlying cellular and molecular mechanisms for synapse formation. Cell adhesion molecules have been found important for synapse assembly in the brain. Many trans-adhesion complexes have been identified to modulate excitatory synapse formation. However, little is known about the synaptogenic mechanisms for inhibitory synapses. ErbB4 is a receptor tyrosine kinase enriched in interneurons. Here, we showed that overexpressing ErbB4 in HEK293T cel

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