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Related Concept Videos

Overview of Secretory Vesicles01:33

Overview of Secretory Vesicles

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Secretory vesicles, also known as dense core vesicles (DCVs), are membrane-bound vesicles that transport secretory proteins, such as hormones or neurotransmitters. Regulated secretory vesicles transport proteins from the trans-Golgi network to the exterior of the cell. Proteins present in regulated secretory vesicles are required to be rapidly exocytosed in large amounts upon a specific stimulus.
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Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
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Synaptic Signaling01:09

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Neurons communicate at synapses, or junctions, to excite or inhibit the activity of other neurons or target cells, such as muscles. Synapses may be chemical or electrical.
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Assembly of Signaling Complexes01:30

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Multiprotein signaling complexes are formed in a dynamic process involving protein-protein interactions at the cytoplasmic domain of transmembrane receptors or enzymatic and non-enzymatic proteins associated with the receptor. These complexes ensure the activation and propagation of intracellular signals that regulate cell functions.
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SNAREs and Membrane Fusion01:43

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Once a transport vesicle has recognized its target organelle, the vesicular membrane needs to fuse with the target membrane to unload the cargo. Transmembrane proteins called SNAREs present on organelle membranes and their vesicles, mediate vesicle fusion.
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Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and...
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Updated: Mar 25, 2026

Preparation of Synaptic Plasma Membrane and Postsynaptic Density Proteins Using a Discontinuous Sucrose Gradient
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SYNGAP1: Mind the Gap.

Nallathambi Jeyabalan1, James P Clement2

  • 1Narayana Nethralaya Post-Graduate Institute of Ophthalmology, Narayana Nethralaya Foundation, Narayana Health City Bangalore, India.

Frontiers in Cellular Neuroscience
|February 26, 2016
PubMed
Summary
This summary is machine-generated.

Mutations in the SYNGAP1 gene disrupt synaptic function, leading to neurodevelopmental disorders like intellectual disability and autism. Understanding SYNGAP1

Keywords:
SYNGAPautism spectrum disordersintellectual disabilitylearning and memoryneurodevelopmental disorderssynaptic plasticity

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Area of Science:

  • Neuroscience
  • Genetics
  • Developmental Biology

Background:

  • Early brain development relies on sensory, cognitive, and emotional experiences shaping neuronal circuits.
  • Alterations in these processes are linked to neurodevelopmental and psychiatric disorders, affecting 3-4% of the global population.
  • Mutations in synaptic function genes are common causes of these disorders, often leading to synaptopathies.

Purpose of the Study:

  • To investigate the role of SYNGAP1 (Synaptic Ras-GTPase-activating protein) in neurodevelopmental disorders.
  • To understand how SYNGAP1 regulates synaptic plasticity and neuronal homeostasis.
  • To explore SYNGAP1 as a potential therapeutic target during critical developmental periods.

Main Methods:

  • Utilizing gain or loss of function approaches to study gene mutations.
  • Employing Syngap1 mouse models for neurophysiological investigations.
  • Analyzing alterations in dendritic spine structure, function, and plasticity.

Main Results:

  • SYNGAP1 mutations are associated with Intellectual Disability (ID), Autism Spectrum Disorder (ASD), and epilepsy in children.
  • SYNGAP1 acts as a negative regulator of Ras, Rap, and AMPA receptor trafficking.
  • Studies reveal SYNGAP1's role in regulating downstream signaling proteins and synaptic plasticity.

Conclusions:

  • SYNGAP1 is crucial for regulating synaptic plasticity and neuronal homeostasis.
  • Dysfunction of SYNGAP1 contributes to neurodevelopmental disorders.
  • Targeting SYNGAP1 during critical developmental periods may offer therapeutic potential.