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Dendritic spine


A dendritic spine is a small membranous protrusion from the central stalk of a dendrite that is typically electrophysiologically active and synapses with a single axon. Typically, spines have a bulbous head (the spine head), and a thin neck that connects the head of the spine to the stalk of the dendrite. Spiny dendritic stalks host tens of thousands of spines, so because each individual spine typically synapses with a reciprocal axon, a spiny dendrite could receive a multitude of signals whereas a traditional dendrite would receive very few.



Dendritic spines typically are in excitatory synapses, and thus typically receive the neurotransmitter glutamate from their partner axon. Spines are found on the dendrites of most principal neurons in the brain, and are notably found in the pyramidal neurons of the cerebral cortex, the medium spiny neurons of the striatum, and the Purkinje cells of the cerebellum.

Dendritic spines occur at high density on spiny dendrites, and up to 200 spines can project from 100 micrometers of a mature neuron's dendritic stalk. Hippocampal and cortical pyramidal neurons may receive tens of thousands of mostly excitatory inputs from other neurons onto their equally numerous spines, whereas the number of spines on Purkinje neuron dendrites is an order of magnitude larger.


Dendritic spines are small, typically of sub-micrometer length, but can be of varying volumes, between 0.01 mm3 and 0.8mm3 in volume. However, most mature spines typically have a developed "head" that is connected by a membranous neck to the dendritic stalk. Spines are also of different shapes and morphologies, and their most notable classes by shape are "thin", "stubby", "mushroom", and "branched". Electron microscopy studies have shown that there is a continuum of shapes between these categories. However, spine volume and shape is extremely variable, and are believed to change rapidly during spine development and spine functioning.


Receptor activity

Dendritic spines are typically excitatory, and thus receive glutamate, and express glutamate receptors (the AMPA receptor and the NMDA receptor) on their surfaces. The TrkB receptor for BDNF is also expressed on the spine surface, and is believed to play a role in spine survival. The tip of the spine is the "postsynaptic density" (PSD), an unusually dense area of the dendritic spine. The PSD is directly parallel to the active zone of its synapsing axon; neurotransmitters released from the active zone are received by the postsynaptic density of the spine, which comprises 10% of the spine's membrane surface area. One-half of synapsing axons and dendritic spines are physically tethered by calcium-dependent cadherin, which forms a cell-to-cell adherens junction between the synapsing neurites.

Glutamate receptors (GluRs) are localized to the postsynaptic density, and are anchored by cytoskeletal elements to the membrane. They are positioned directly above their signaling machinery, which is typically tethered to the underside of the plasma membrane, allowing signals transmitted by the GluRs into the cytosol to be further propagated by their nearby signaling elements to activate signal transduction cascades. The localization of signaling elements to their GluRs is particularly important in ensuring signal cascade activation, as GluRs would be unable to effect particular downstream effects without nearby signalers.

Signaling from GluRs is mediated by the presence of an abdundance of proteins, especially kinases, that are localized to the postsynaptic density. These include calcium-dependent calmodulin, CaMKII (calmodulin-dependent protein kinase II), PKC (Protein Kinase C), PKA (Protein Kinase A), Protein Phosphatase-1 (PP-1), and Fyn tyrosine kinase. Certain signalers, such as CaMKII, are upregulated in response to activity.

Smooth endoplasmic reticulae present in the dendritic spine are responsible for the release of calcium, which is important in signaling transduction cascades in response to receptor activity.

Spines are particularly advantageous to neurons by compartmentalizing signals; a signal delivered to one spine effects only the recipient spine and not the entire neuron. They thus localize synaptic signaling by forming biochemical compartments that can encode changes in the state of an individual synapse without necessarily affecting the state of other synapses of the same neuron. This compartmentalization arises from the restriction of diffusion of ions and second messengers from the spine to the dendritic stalk.


The cytoskeleton of dendritic spines is particularly important in their synaptic plasticity; without a dynamic cytoskeleton, spines would be unable to rapidly change their volumes or shapes in responses to stimuli. The cytoskeleton of dendritic spines is primarily made of filamentous actin (F-actin). While tubulin monomers and microtubule-associated proteins (MAPs) are present, organized microtubules are not present. Because spines have a cytoskeleton of primarily actin, this allows them to be highly dynamic in shape and size. The actin cytoskeleton directly determines the morphology of the spine, and actin regulators, small GTPases such as Rac, Rho, and CDC42, rapidly modify this cytoskeleton. Overactive Rac1 results in consistently smaller dendritic spines.

In addition to their electrophysiological activity and their receptor-mediated activity, spines appear to be vesicularly active and may even translate proteins. Stacks of smooth endoplasmic reticulae (SERs) bound by an unknown amorphous material, named the "spine apparatus", have been identified in dendritic spines, and are believed to be implicated in vesicular trafficking in spines. "Smooth" vesicles have also been identified in spines, supporting the vesicular activity in dendritic spines. The presence of polyribosomes in spines also suggests protein translational activity in the spine itself, not just the dendrite's stalk.


See also: Synaptic plasticity

As aforementioned, dendritic spines are very "plastic", that is, spines change significantly in shape, volume, and number in small time courses. Because spines have a primarily actin cytoskeleton, they are dynamic, and the majority of spines change their shape within seconds to minutes because of the dynamicity of actin remodelling. Furthermore, spine number is very variable and spines come and ago; in matter of hours, 10-20% of spines spontaneously appear or disappear on the pyramidal cells of the cerebral cortex, although the larger "mushroom"-shaped spines are the most stable.

Spine maintenance and plasticity is activity-dependent and activity-independent. BDNF partially determines spine levels, and low levels of AMPA receptor activity is necessary to maintain spine survival, and synaptic activity involving NMDA receptors encourages spine growth. Furthermore, two-photon laser scanning microscopy and confocal microscopy have shown that spine volume changes according depending on the types of stimuli that are presented to a synapse.

Spine plasticity is implicated in motivation, learning, and memory. In particular, long-term memory is mediated in part by the growth of new dendritic spines (or the enlargement of pre-existing spines) to reinforce a particular neural pathway. By strengthening the connection between two neurons, the ability of the presynaptic cell to activate the postsynaptic cell is enhanced. This type of synaptic regulation forms the basis of synaptic plasticity.


Dendritic spines are believed to develop from filopodia. During synaptogenesis, dendrites rapidly sprout and retract filopodia, small membrane organelle-lacking membranous protrusions. During the first week of birth, the brain is predominated by filopodia, which eventually develop synapses. However, after this first week, filopodia are replaced by aspiny dendrites but also small, stubby spines that protrude from spiny dendrites. In the development of certain filopodia into spines, filopedia recruit presynaptic contact to the dendrite, which encourages the production of spines to handle specialized postsynaptic contact with the presynaptic protrusions.

Spines, however, require maturation after formation. Immature spines have impaired signaling capabilities, and typically lack "heads" (or have very small heads), only necks, while matured spines maintain both heads and necks.


Cognitive disorders such as autism, mental retardation, and Fragile X Syndrome, may be resultant from abnormalities in dendritic spines, especially the number of spines and their maturity. The ratio of matured to immature spines is important in their signaling, as immature spines have impared synaptic signaling. Fragile X Syndrome is characterized by an overabundance of immature spines that have multiple filopodia in cortical dendrites.


General Sources

  • Sudhof TC, Stevens CF, Cowan WM. Synapses. The Johns Hopkins University Press, Baltimore (2001). ISBN 0-8018-6498-4
  • Levitan IB, Kaczmarek LK. The Neuron: Cell and Molecular Biology, Third Edition. Oxford University Press, New York (2002). ISBN 0-19-514522-4
  • Plummer M, Page C, Hsu SC, Firestein B, Davis R. Advanced Neurobiology I/Neuroscience Lecture Notes (unpublished).
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Dendritic_spine". A list of authors is available in Wikipedia.
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