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Axon terminal

The axon terminal, also known as the synaptic bouton or terminal bouton, is the distal end of a neuron's axon where synaptic vesicles containing neurotransmitters are stored and released to transmit signals to adjacent neurons, muscle cells, or gland cells.^[1] These specialized structures form the presynaptic component of chemical synapses, facilitating communication across the synaptic cleft—a narrow gap of 20–40 nm^[2]—through the exocytosis of neurotransmitters triggered by calcium influx upon arrival of an action potential.^[3] Structurally, axon terminals are bulbous swellings or varicosities at the end of axonal branches, lacking ribosomes and rough endoplasmic reticulum but rich in mitochondria, microtubules, neurofilaments, and synaptic vesicles clustered near the active zone for rapid release.^[4] Functionally, they convert electrical impulses into chemical signals, enabling excitatory or inhibitory neurotransmission essential for neural circuit integration, learning, memory, and motor control, with axonal transport systems delivering vesicles and proteins at rates up to 400 mm/day.^[1] In histology, axon terminals appear as tapered telodendrons under light microscopy with stains like Golgi, and electron microscopy reveals their synaptic knobs in direct apposition to postsynaptic densities.^[4] Disruptions in axon terminal function, such as impaired neurotransmitter release, underlie various neurodegenerative diseases.^[3]

Anatomy and Structure

Location and Types

The axon terminal, also known as the synaptic bouton or end-foot, represents the distal extremity of a neuron's axon, where it interfaces with target cells to convert electrical impulses into chemical signals via neurotransmitter release at synapses.^[3] This specialized structure is primarily situated at the far end of the axon, often branching into fine extensions termed telodendria that facilitate multiple synaptic connections.^[5] In some cases, axon terminals form en passant along the axon's length rather than solely at its terminus, allowing for interspersed synaptic contacts without dedicated end structures.^[6] Axon terminals exhibit morphological diversity depending on their neural context, categorized into several types based on size, shape, and target tissue. Terminal boutons are enlarged, bulbous swellings typically found at the axon's endpoint, serving as presynaptic sites for synaptic transmission.^[6] Varicosities, or bead-like enlargements, occur along unmyelinated axons and are common in autonomic fibers, forming diffuse release sites rather than discrete synapses.^[7] Neuromuscular junctions constitute a distinct type in the peripheral nervous system, featuring expanded axon terminals that form specialized end plates on skeletal muscle fibers for robust motor signaling.^[8] In the central nervous system (CNS), axon terminals often manifest as multiple small boutons, either as terminal ends or en passant swellings, enabling widespread connectivity among neurons, as observed in hippocampal circuits.^[6] Conversely, in the peripheral nervous system (PNS), terminals tend to be larger and more specialized; for instance, motor neurons form expansive neuromuscular end plates on skeletal muscle, while autonomic terminals in smooth muscle display varicosities for broader effector influence.^[7]^[8] These variations reflect adaptations to the functional demands of neural circuits, with CNS terminals prioritizing precision and PNS terminals emphasizing force or modulation.

Ultrastructure and Components

The axon terminal, or presynaptic bouton, exhibits a highly organized ultrastructure adapted for efficient synaptic function, featuring a dense array of organelles and protein complexes within a compact space typically measuring 0.4–1 μm in diameter.^[9] Electron microscopy reveals a cytoplasmic matrix filled with synaptic vesicles clustered near the presynaptic membrane, interspersed with mitochondria and segments of endoplasmic reticulum (ER), all anchored by a filamentous cytomatrix that provides structural support and spatial organization.^[10] This architecture ensures precise positioning of components at the active zone, the specialized site of neurotransmitter release. Synaptic vesicles represent the primary vesicular components, existing in two main forms: clear synaptic vesicles, approximately 40–50 nm in diameter, which store small-molecule neurotransmitters, and dense-core vesicles, larger at 80–120 nm, containing neuropeptides or larger signaling molecules.^[11] These vesicles, numbering 100–500 per terminal, are clustered and tethered via filamentous connectors less than 40 nm long, forming organized pools within the cytomatrix.^[9] Mitochondria, often small and elongated with volumes ranging from 0.04 to 0.38 μm³ depending on the brain region, are embedded throughout the terminal, maintaining a compact morphology confined within presynaptic boundaries.^[10] The ER manifests as a network of anastomosed tubules or small cisternae with narrow lumens, branching within the terminal to envelop mitochondria and vesicles, forming close structural contacts that integrate organelle positioning. The active zone forms a protein-dense disc-like region, 0.2–0.5 μm wide and 50–100 nm thick, embedded in the presynaptic membrane and serving as the primary docking platform for vesicles. This zone comprises a cytomatrix of interconnected filaments and tethers, including short projections (5–20 nm) that link vesicles to the membrane, organized in a hexagonal grid-like array.^[12] Key scaffold proteins such as RIM and Munc13 concentrate here, forming a core complex that mediates vesicle docking sites and stabilizes the presynaptic density.^[13] The presynaptic cytomatrix extends beyond the active zone as a filamentous meshwork, interconnecting over 80% of vesicles into clusters and anchoring organelles to prevent diffusion.^[9] Ultrastructural variations occur across synapse types, notably in ribbon synapses of sensory neurons, where a prominent electron-dense ribbon structure tethers hundreds of vesicles in a stacked, perpendicular array to the active zone, facilitating sustained release.^[14] In contrast, conventional central nervous system terminals display more compact vesicle pools without such ribbons, emphasizing the adaptability of the axon terminal's internal architecture to specialized signaling demands.^[12]

Function in Neural Communication

Role in Synaptic Transmission

The axon terminal functions primarily as the presynaptic site in chemical synapses, where it receives action potentials propagating along the axon and initiates the release of neurotransmitters across the synaptic cleft to convey signals to adjacent neurons or target cells.^[15] This process transforms electrical impulses into chemical messengers, enabling targeted intercellular communication essential for neural signaling.^[15] As the endpoint of the axon, the terminal ensures that signals terminate appropriately, preventing indiscriminate propagation and allowing for localized influence on postsynaptic elements.^[16] Within neural circuits, axon terminals serve as the presynaptic components that enforce unidirectional transmission in most chemical synapses, directing information flow from one neuron to another or to effectors like muscle cells.^[15] They integrate into diverse synaptic configurations, such as axodendritic connections on dendrites for excitatory input or axosomatic synapses on cell bodies for inhibitory modulation, thereby contributing to the computational complexity of neural networks.^[15] This presynaptic positioning allows terminals to regulate the timing and strength of signals, facilitating coordinated activity across brain regions and spinal circuits.^[16] Axon terminals participate in both excitatory and inhibitory signaling pathways; for instance, glutamatergic terminals in the hippocampus release glutamate to depolarize postsynaptic neurons, promoting excitation, while GABAergic terminals release GABA to hyperpolarize targets, suppressing activity.^[17] In the peripheral nervous system, terminals at neuromuscular junctions release acetylcholine onto skeletal muscle fibers, generating endplate potentials that initiate contraction and support motor function.^[8] These roles highlight the terminal's versatility in modulating neural output and effector responses.^[8] The axon terminal's involvement in synaptic transmission exhibits evolutionary conservation, with similar presynaptic structures and neurotransmitter release functions present in nervous systems from invertebrates, such as nematodes and insects, to vertebrates including mammals.^[18] This preservation across metazoans underscores the terminal's ancient origin and critical role in the development of complex neural communication.^[18]

Signal Arrival and Processing

The arrival of an electrical signal at the axon terminal occurs through the propagation of an action potential along the axon, which is initiated at the axon hillock and travels toward the terminal via sequential activation of voltage-gated sodium channels. These channels open in response to local depolarization, allowing a rapid influx of Na⁺ ions that further depolarizes the membrane and propagates the signal in a self-regenerating manner. Upon reaching the axon terminal, the action potential causes a localized depolarization of the presynaptic membrane, setting the stage for chemical transmission.^[19] In the axon terminal, which often features branched structures, the invading action potential can actively propagate into these fine branches, though propagation may fail in narrower or more distal segments due to increased axial resistance and reduced safety factors for conduction. This local processing includes potential backpropagation from the terminal toward the soma in some cases, but failures at branch points can lead to variable signal fidelity across terminals of the same axon. Such dynamics ensure that not all branches necessarily receive the full amplitude of the action potential, influencing the reliability of synaptic output.^[20]^[21] Myelination along the axon plays a crucial role in efficient signal delivery to the unmyelinated terminal regions by enabling saltatory conduction, where the action potential jumps between nodes of Ranvier—gaps in the myelin sheath enriched with voltage-gated sodium channels. The final node of Ranvier, typically located just proximal to the terminal, regenerates the action potential with high fidelity, preventing decrement as the signal transitions into the unmyelinated terminal zone. This mechanism minimizes conduction delays and energy expenditure, ensuring timely depolarization at the synapse.^[22] At the axon terminal, the depolarizing signal interacts with discrete release sites on the presynaptic membrane, where neurotransmitter release follows quantal principles: each site has an associated probability (p) of releasing a quantum of transmitter in response to the action potential, with the number of sites (n) determining the potential scale of release. This probabilistic framework, established through quantal analysis, underscores the stochastic nature of signal processing at the terminal without implying deterministic fusion events. Representative studies at the neuromuscular junction have quantified these parameters, showing mean quantal content (np) values around 100-200 under physiological conditions, highlighting the terminal's capacity for reliable yet variable transmission.

Neurotransmitter Release Mechanisms

Vesicular Exocytosis Process

The vesicular exocytosis process at the axon terminal involves a series of tightly regulated stages that enable synaptic vesicles to release neurotransmitters into the synaptic cleft. Synaptic vesicles, filled with neurotransmitters, initially undergo docking at the presynaptic plasma membrane near the active zone. This docking is mediated by the formation of trans-SNARE complexes, where v-SNARE (VAMP, or synaptobrevin) on the vesicle membrane interacts with t-SNAREs (syntaxin and SNAP-25) on the plasma membrane, bridging the two bilayers and positioning the vesicle for subsequent steps.^[23] Following docking, the vesicles enter a priming phase, where the SNARE proteins zipper into a four-helix bundle, stabilizing the complex and preparing the vesicle for fusion by dehydrating the intervening space between membranes.^[24] Fusion then occurs as the SNARE complex drives the merging of vesicle and plasma membranes, releasing the vesicle contents into the cleft through a transient fusion pore.^[23] Exocytosis can proceed via two primary modes: synchronous and asynchronous. Synchronous exocytosis is rapid and tightly coupled to action potential arrival, involving coordinated fusion of multiple vesicles to ensure precise temporal signaling in neural communication. In contrast, asynchronous exocytosis features delayed and more variable release events, often manifesting as spontaneous miniature synaptic currents independent of immediate stimulation, which contributes to baseline synaptic tone and plasticity. Both modes rely on the core SNARE-mediated fusion machinery but differ in their kinetics and spatial organization within the terminal. After fusion, synaptic vesicles are recycled to sustain repeated release, primarily through two exocytosis subtypes: full fusion and kiss-and-run. In full fusion, the vesicle completely collapses into the plasma membrane, dispersing its lipids and proteins, which necessitates retrieval via clathrin-mediated endocytosis to reform vesicles.^[25] Clathrin-mediated endocytosis involves the assembly of clathrin coats on the membrane, invagination, and pinching off to generate new vesicles that are refilled with neurotransmitters.^[25] Alternatively, kiss-and-run fusion allows partial membrane merging via a narrow fusion pore, enabling neurotransmitter release without full collapse, followed by rapid vesicle retrieval and reuse, which supports high-frequency transmission.^[25] The timing of exocytosis is highly precise, with neurotransmitter release occurring within a 1-2 ms window following terminal depolarization, ensuring minimal delay in synaptic transmission.^[26] This rapidity is governed by the dynamics of vesicle pools, particularly the readily releasable pool (RRP), which comprises approximately 5-10 docked and primed vesicles per active zone site, available for immediate fusion upon stimulation.^[27] The RRP size limits the initial burst of release, after which recycling replenishes the pool to maintain synaptic efficacy.^[27]

Calcium-Dependent Regulation

Upon arrival of an action potential at the axon terminal, depolarization activates voltage-gated calcium channels, primarily P/Q-type (Ca_V2.1) and N-type (Ca_V2.2), which are clustered at the presynaptic active zones.^[28] These channels open rapidly, permitting a brief influx of Ca²⁺ ions that directly triggers synaptic vesicle fusion and neurotransmitter release.^[28] The influx is tightly coupled to exocytosis, occurring within microseconds to ensure precise temporal control of transmission.^[29] The Ca²⁺ signal is confined to localized microdomains near the channels, where concentrations transiently rise to 10–100 μM at the active zones, far exceeding bulk cytosolic levels of ~100 nM.^[30] These nanometer-scale gradients bind to synaptotagmin-1 (or isoforms like synaptotagmin-2), the primary Ca²⁺ sensor on the vesicle surface, which undergoes a conformational change to promote SNARE-mediated membrane fusion.^[31] Synaptotagmin's C2 domains exhibit high-affinity Ca²⁺ binding, enabling synchronous release with cooperativity.^[29] Release probability (P_r) is finely tuned by factors such as channel density at active zones and endogenous Ca²⁺ buffers, which shape the microdomain profile and coupling distance to vesicles.^[28] Higher channel density increases P_r by enhancing local Ca²⁺ elevation, while buffers like calbindin limit diffusion to sustain domain specificity.^[30] Quantitatively, P_r follows a steep sigmoidal dependence on [Ca²⁺], approximated by a Hill-like function with cooperativity n = 3–5:

P_r \approx 1 - e^{-\frac{[\mathrm{Ca}^{2+}]^n}{K_d}}

where K_d is the half-activation constant (~10–50 μM), reflecting the nonlinear amplification of release.^[32] This steepness ensures all-or-none responses to action potentials.^[33] Negative feedback via presynaptic autoreceptors, such as GABA_B or muscarinic types, inhibits Ca²⁺ channels through G-protein βγ subunits, reducing influx and P_r to prevent excessive release.^[34] Conversely, second messengers like cAMP, activated by adenylyl cyclase, enhance transmission by phosphorylating channels via PKA to increase conductance or by promoting vesicle priming and tighter channel-vesicle coupling.^[35] These modulations adjust synaptic strength dynamically without altering basal Ca²⁺ dynamics.^[36]

Imaging and Visualization

Optical and Functional Imaging

Optical and functional imaging techniques enable the visualization of dynamic processes in living axon terminals, such as calcium influx and neurotransmitter release, providing insights into synaptic activity without disrupting neural function. These methods rely on fluorescent indicators that report changes in ion concentrations or molecular events associated with vesicle fusion. Calcium imaging, for instance, uses synthetic dyes like Fluo-4, which exhibit increased fluorescence upon binding intracellular calcium, allowing real-time monitoring of action potential-evoked calcium transients in presynaptic terminals.^[37] Genetically encoded calcium indicators (GECIs), such as variants of GCaMP, offer targeted expression in axons and superior signal-to-noise ratios for long-term imaging in vivo.^[38] To observe exocytosis directly, Synapto-pHluorin—a pH-sensitive GFP fused to the luminal domain of synaptophysin—serves as a key reporter, as synaptic vesicles acidify during endocytosis and neutralize upon fusion with the plasma membrane, causing a rapid fluorescence increase.^[39] This probe has been widely applied to track vesicle recycling dynamics at individual presynaptic sites, revealing the spatial and temporal patterns of release events.^[40] Advanced genetically encoded sensors further refine these measurements; GCaMP6 variants, for example, provide high sensitivity to calcium dynamics in synaptic terminals, enabling detection of single action potentials with millisecond precision during high-frequency stimulation.^[38] For neurotransmitter release, iGluSnFR sensors monitor glutamate kinetics by binding extracellular glutamate and fluorescing proportionally, capturing quantal release profiles from presynaptic terminals at frequencies up to 100 Hz.^[41] These tools facilitate in vivo applications, such as quantifying release probability at single synapses using two-photon microscopy, which achieves sub-micron resolution to isolate terminal-specific calcium signals and correlate them with postsynaptic responses in hippocampal circuits.^[42] Recent advances incorporate super-resolution techniques like stimulated emission depletion (STED) microscopy to track vesicle movements on the nanoscale, resolving fusion pore dynamics and endocytosis in live axon terminals with ~50 nm precision.^[43] Post-2020 developments in optogenetics have enabled terminal-specific stimulation, such as projection-targeted Channelrhodopsin variants that activate presynaptic sites without somatic interference, allowing precise control of release probability and integration with functional imaging for studying circuit-level plasticity.^[44] These combined approaches have illuminated activity-dependent modulation of axon terminal function in behaving animals.^[45]

Structural Imaging Techniques

Structural imaging techniques for axon terminals have evolved from early histological methods to advanced electron and light microscopy approaches, enabling detailed visualization of their static architecture. In the late 1890s, Santiago Ramón y Cajal utilized the Golgi staining technique to observe and illustrate axon terminals, revealing their branching patterns and synaptic contacts in neural tissue for the first time.^[46] This method impregnated neurons with silver chromate, selectively staining entire cells including terminals, which laid the foundation for understanding presynaptic structures.^[47] Electron microscopy (EM) remains the gold standard for resolving the ultrastructure of axon terminals at nanometer scales. Transmission electron microscopy (TEM) provides high-contrast images of synaptic vesicles, active zones, and mitochondrial distributions within fixed terminals by passing electrons through ultrathin tissue sections.^[48] For three-dimensional (3D) analysis, serial section EM involves cutting consecutive thin sections of tissue, imaging each with TEM, and computationally reconstructing synaptic boutons to map their volume and connectivity.^[49] This approach has quantified bouton morphologies, such as en passant versus varicosity types, in regions like the hippocampus.^[49] Immuno-EM enhances specificity by labeling proteins in axon terminals using gold particle conjugates. In pre-embedding or post-embedding protocols, antibodies against markers like synaptophysin are visualized as electron-dense gold particles (typically 10-20 nm in diameter) clustered amid synaptic vesicles in presynaptic terminals.^[50] For instance, large gold particles (15-20 nm) have been used to tag synaptophysin in hippocampal cultures, confirming its localization to vesicle pools.^[50] This technique distinguishes terminal subtypes based on protein expression, such as in dopaminergic axons.^[51] Extensions of light microscopy, such as expansion microscopy (ExM), achieve nanoscale resolution of axon terminal components without electron beams. ExM physically expands fixed tissue via hydrogel embedding, enabling ~20 nm lateral resolution of active zones in presynaptic terminals using conventional fluorescence microscopes.^[52] At the Drosophila neuromuscular junction, ExM has resolved active zone scaffolds and associated proteins in boutons at ~70 nm effective resolution post-expansion.^[53] Modern correlative light and electron microscopy (CLEM) integrates these modalities for multimodal imaging of axon terminals. CLEM aligns fluorescence-labeled terminals viewed by light microscopy with their EM ultrastructure, allowing precise correlation of molecular markers with fine anatomy, such as vesicle docking sites.^[54] This hybrid method has traced PHA-L-stained axon terminals from light to EM levels, revealing synaptic densities in brain slices.^[54]

Development and Pathology

Embryonic Formation

During embryogenesis, the initial outgrowth of axons toward their target regions is guided by extracellular cues such as netrins and semaphorins, which direct pathfinding and branching decisions. Netrin-1, acting through its receptor DCC/UNC-40, promotes axon attraction and outgrowth by activating downstream signaling pathways that reorganize the cytoskeleton, as demonstrated in studies of commissural axons in the developing spinal cord.^[55] Conversely, semaphorins, including semaphorin 3A, often exert repulsive effects to refine trajectories and prevent aberrant branching, with signaling through plexin receptors inhibiting collateral formation via Rho GTPases.^[56] These guidance molecules ensure that growing axons navigate complex environments to reach appropriate targets during early neural circuit assembly. As axons contact their synaptic partners, terminal arborization occurs, elaborating branched structures that increase contact surface area; this process is promoted by target-derived cues like brain-derived neurotrophic factor (BDNF). BDNF, secreted from target cells such as retinal ganglion cell targets in the visual system, binds TrkB receptors on axon terminals to enhance branching complexity through microtubule dynamics and actin remodeling, coinciding with the period of arbor patterning in Xenopus and mammalian models.^[57] In mammals, initial axon projections begin around embryonic day 10-12 (E10-E12) in mice, with thalamocortical and corticostriatal axons extending toward their destinations shortly after neuronal birth.^[58] By E16, basic presynaptic differentiation emerges, including early vesicle clustering.^[59] Maturation of axon terminals follows synapse contact, involving the assembly of active zones and clustering of synaptic vesicles, orchestrated by adhesion molecules such as neurexins and neuroligins. Presynaptic neurexins interact trans-synaptically with postsynaptic neuroligins to recruit active zone proteins like Bassoon and Piccolo, stabilizing release sites and promoting vesicle docking; disruptions in these interactions impair terminal maturation and synapse function in cultured neurons and in vivo models.^[60] This refinement continues perinatally, with widespread synapse elimination shaping connectivity; activity-dependent pruning mechanisms, driven by competitive neural activity, reduce the initial overabundance of terminals by approximately 50%, as observed in retinogeniculate and cortical circuits where weaker connections are retracted to strengthen functional wiring.^[61] By birth, these processes yield more precise terminal arbors essential for mature neural communication.

Associated Disorders and Dysfunctions

In Alzheimer's disease, axon terminals exhibit dystrophic changes characterized by swellings and abnormal accumulations of amyloid-beta (Aβ) peptides, which precede neuronal loss and contribute to synaptic dysfunction.^[62] These dystrophies often surround Aβ plaques, impairing axonal transport and leading to microtubule disruption in presynaptic terminals.^[63] In Parkinson's disease, there is progressive loss of dopamine axon terminals in the striatum, with estimates indicating 50-80% depletion by symptom onset, driving motor impairments through reduced neurotransmitter release.^[64] This terminal degeneration occurs early, often before substantial neuronal cell body loss in the substantia nigra.^[65] Synaptic vesicle defects, such as those caused by mutations in the Munc18-1 gene (STXBP1), impair exocytosis at axon terminals and are linked to early infantile epileptic encephalopathies.^[66] These mutations reduce Munc18-1 levels, disrupting syntaxin-1 interactions essential for vesicle priming and neurotransmitter release, resulting in severe seizures and developmental delays.^[67] In autism spectrum disorder, disruptions in neuroligin proteins, particularly neuroligin-3 and -4 mutations, alter postsynaptic organization at glutamatergic synapses, indirectly affecting presynaptic axon terminal function and leading to imbalances in excitatory-inhibitory signaling.^[68] These changes manifest as impaired striatal synapse function and repetitive behaviors in model systems.^[69] Therapeutically, botulinum toxin (Botox) targets neuromuscular axon terminals to treat dystonia by cleaving SNAP-25, thereby inhibiting acetylcholine exocytosis and inducing reversible muscle paralysis.^[70] This approach effectively reduces involuntary contractions in focal dystonias, with effects lasting 3-6 months post-injection.^[71] In schizophrenia, positron emission tomography (PET) imaging using synaptic vesicle protein 2A (SV2A) markers reveals reduced axon terminal density, correlating with glutamate dysregulation and supporting hypotheses of presynaptic hypofunction in prefrontal circuits.^[72] Post-2020 studies have identified inflammation-induced degeneration and swelling of axon terminals in retinal cone photoreceptors of COVID-19 patients, where structural alterations occur without overt cell death, potentially contributing to sensory dysfunctions.^[73] These changes are driven by SARS-CoV-2-associated immune responses, exacerbating nerve vulnerabilities in long COVID syndromes.^[74]

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Axonal Degeneration in AD: The Contribution of Aβ and Tau - PMC
In this context, progressive axonal degeneration has been associated with early stages of AD and linked to Aβ and tau accumulation. As the axonal degeneration ...
[57]
Presynaptic dystrophic neurites surrounding amyloid plaques are ...
Our study supports the hypothesis that Aβ induces microtubule disruption in presynaptic dystrophic neurites that surround plaques, thus impairing axonal ...Murine Tissue... · Results · Aβ42 Causes Neuritic...
[58]
Striatal Dopamine Loss in Early Parkinson's Disease - NIH
Neuropathological studies, based on small samples, suggest that symptoms of Parkinson's disease (PD) emerge when dopamine/nigrostriatal loss is around 50–80%.
[59]
Axon Degeneration in Parkinson's Disease - PMC - PubMed Central
Estimates of dopamine terminal loss at time of disease onset are less for those obtained with [18F] dopa (20–50% in putamen) than for those obtained with ...
[60]
Functional analysis of epilepsy‐associated variants in STXBP1 ... - NIH
Genetic variants in STXBP1, which encodes the conserved exocytosis protein Munc18‐1, are associated with a variety of infantile epilepsy syndromes.
[61]
Reduced MUNC18-1 Levels, Synaptic Proteome Changes, and ...
Its gene product MUNC18-1 organizes synaptic vesicle exocytosis and is essential for synaptic transmission. Patients present with developmental delay ...Archival Report · Munc18-1 Protein And Rna... · Stxbp1-Rd Neurons Maintain...
[62]
Synaptopathology Involved in Autism Spectrum Disorder - PMC
Disorder-associated mutations lead to functional inactivation of neuroligins ... Autism-related neuroligin-3 mutation alters social behavior and spatial learning.
[63]
Autism-Associated Neuroligin-3 Mutations Commonly Impair Striatal ...
Jul 3, 2014 · Different autism-associated neuroligin-3 mutations cause a common increase in acquired repetitive behaviors by impairing a specific striatal synapse.Missing: axon | Show results with:axon
[64]
BOTULINUM TOXIN - PMC - NIH
Intramuscular administration of botulinum toxin acts at the neuromuscular junction to cause muscle paralysis by inhibiting the release of acetylcholine from ...
[65]
Use of botulinum toxin for movement disorders - PubMed Central
BoNT is the standard treatment for focal and segmental dystonias. The recommended levels for the treatment of dystonia and other movement disorders with BoNTs ...
[66]
The relationship between synaptic density marker SV2A, glutamate ...
Glutamatergic excitotoxicity is hypothesised to underlie synaptic loss in schizophrenia pathogenesis, but it is unknown whether synaptic markers are related ...
[67]
Microglia activation and neuronal alterations in retinas from COVID ...
Mar 1, 2023 · COVID-19 retinas showed swelling at the axon terminal of cone photoreceptors but cell death was not detectable. Cone photoreceptors of retinas ...
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Peripheral nervous system involvement associated with COVID-19 ...
Apr 6, 2023 · PNS involvement in COVID-19 may be an important cause of hospitalization and post COVID-19 sequelae, increasing the burden on the healthcare systems.