Dendritic spine

A dendritic spine (or spine) is a small membranous protrusion from a neuron's

Dendritic spine
dendrite that typically receives input from a single axon at the synapse.
Dendritic spines serve as a storage site for synaptic strength and help transmit
electrical signals to the neuron's cell body. Most spines have a bulbous head (the
spine head), and a thin neck that connects the head of the spine to the shaft of
the dendrite. The dendrites of a single neuron can contain hundreds to thousands
of spines. In addition to spines providing an anatomical substrate for memory
storage and synaptic transmission, they may also serve to increase the number of
possible contacts between neurons.

Contents
Structure Spiny dendrite of a striatal medium
Distribution spiny neuron.
Cytoskeleton and organelles
Physiology
Receptor activity
Plasticity
Importance to learning and memory
Evidence of importance
Importance contested

Modeling
Baer and Rinzel's continuum model
Spike-diffuse-spike model
Modeling spine calcium transients
Development
Clinical significance
History
Imaging
References
Further reading
Common types of dendritic spines.
External links
Details
Identifiers
Structure Latin gemmula dendritica

Dendritic spines are small with spine head volumes ranging 0.01 µm3 to TH H2.00.06.1.00036
0.8 µm3. Spines with strong synaptic contacts typically have a large spine head, Anatomical terms of microanatomy
which connects to the dendrite via a membranous neck. The most notable
classes of spine shape are "thin", "stubby", "mushroom", and "branched". Electron microscopy studies have shown that there is a
continuum of shapes between these categories. The variable spine shape and volume is thought to be correlated with the strength and
maturity of each spine-synapse.
Distribution
Dendritic spines usually receive excitatory input from axons although sometimes both inhibitory and excitatory connections are made
onto the same spine head. Spines are found on the dendrites of most principal neurons in the brain, including the pyramidal neurons
of the neocortex, the medium spiny neuronsof the striatum, and the Purkinje cells of the cerebellum.

Dendritic spines occur at a density of up to 5 spines/1 µm stretch of dendrite. 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 lar
ger.

Cytoskeleton and organelles

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. These changes in shape might affect the electrical
properties of the spine. The cytoskeleton of dendritic spines is primarily made of filamentous actin (F-actin). tubulin Monomers and
microtubule-associated proteins(MAPs) are present, and organized microtubules are present.[1] 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, RhoA, 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. Stacked discs of the smooth endoplasmic reticulum (SERs) have been identified in dendritic spines.
Formation of this "spine apparatus" depends on the protein synaptopodin and is believed to play an important role in calcium
handling. "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 in the dendrite.

Physiology

Receptor activity
Dendritic spines express glutamate receptors (e.g. AMPA receptor and NMDA receptor) on their surface. 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 contains an electron-
dense region referred to as the "postsynaptic density" (PSD). The PSD directly apposes the active zone of its synapsing axon and
comprises ~10% of the spine's membrane surface area; neurotransmitters released from the active zone bind receptors in the
postsynaptic density of the spine. Half of the synapsing axons and dendritic spines are physically tethered by calcium-dependent
cadherin, which forms cell-to-cell adherent junctions between two neurons.

Glutamate receptors (GluRs) are localized to the postsynaptic density, and are anchored by cytoskeletal elements to the membrane.
They are positioned directly above their signalling 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 signalling elements to activate
signal transduction cascades. The localization of signalling elements to their GluRs is particularly important in ensuring signal
cascade activation, as GluRs would be unable to af
fect particular downstream effects without nearby signallers.

Signalling from GluRs is mediated by the presence of an abundance 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 signallers, such as CaMKII, are
upregulated in response to activity.

Spines are particularly advantageous to neurons by compartmentalizing biochemical signals. This can help to encode changes in the
state of an individual synapse without necessarily affecting the state of other synapses of the same neuron. The length and width of
the spine neck has a large effect on the degree of compartmentalization, with thin spines being the most biochemically isolated
spines.

Plasticity
Dendritic spines are very "plastic", that is, spines change significantly in shape, volume, and number in small time courses. Because
spines have a primarilyactin cytoskeleton, they are dynamic, and the majority of spines change their shape within seconds to minutes
because of the dynamicity of actin remodeling. Furthermore, spine number is very variable and spines come and go; in a matter of
hours, 10-20% of spines can 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[2] and activity-independent. BDNF partially determines spine levels,[3] 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 depending on the types of stimuli that are presented to a synapse.

Importance to learning and memory

Evidence of importance

Experience-dependent spine formation and elimination

Spine plasticity is implicated in motivation, learning, and memory.[4][5][6] 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. Because dendritic
spines are plastic structures whose lifespan is influenced by input activity,[7] spine dynamics may play an important role in the
maintenance of memory over a lifetime.

Age-dependent changes in the rate of spine turnover suggest that spine stability impacts developmental learning. In youth, dendritic
spine turnover is relatively high and produces a net loss of spines.[8][9][10] This high rate of spine turnover may characterize critical
periods of development and reflect learning capacity in adolescence—different cortical areas exhibit differing levels of synaptic
turnover during development, possibly reflecting varying critical periods for specific brain regions.[5][9] In adulthood, however, most
spines remain persistent, and the half-life of spines increases.[8] This stabilization occurs due to a developmentally regulated slow-
.[8][9]
down of spine elimination, a process which may underlie the stabilization of memories in maturity

Experience-induced changes in dendritic spine stability also point to spine turnover as a mechanism involved in the maintenance of
long-term memories, though it is unclear how sensory experience affects neural circuitry. Two general models might describe the
impact of experience on structural plasticity. On the one hand, experience and activity may drive the discrete formation of relevant
synaptic connections that store meaningful information in order to allow for learning. On the other hand, synaptic connections may
[8]
be formed in excess, and experience and activity may lead to the pruning of extraneous synaptic connections.

In lab animals of all ages, environmental enrichment has been related to dendritic branching, spine density, and overall number of
synapses.[8] In addition, skill training has been shown to lead to the formation and stabilization of new spines while destabilizing old
spines,[4][11] suggesting that the learning of a new skill involves a rewiring process of neural circuits. Since the extent of spine
remodeling correlates with success of learning, this suggests a crucial role of synaptic structural plasticity in memory formation.[11]
[4][5]
In addition, changes in spine stability and strengthening occur rapidly and have been observed within hours after training.

Conversely, while enrichment and training are related to increases in spine formation and stability, long-term sensory deprivation
leads to an increase in the rate of spine elimination[8][9] and therefore impacts long-term neural circuitry. Upon restoring sensory
experience after deprivation in adolescence, spine elimination is accelerated, suggesting that experience plays an important role in the
net loss of spines during development.[9] In addition, other sensory deprivation paradigms—such as whisker trimming—have been
shown to increase the stability of new spines.[12]

Research in neurological diseases and injuries shed further light on the nature and importance of spine turnover. After stroke, a
marked increase in structural plasticity occurs near the trauma site, and a five- to eightfold increase from control rates in spine
turnover has been observed.[13] Dendrites disintegrate and reassemble rapidly during ischemia—as with stroke, survivors showed an
increase in dendritic spine turnover.[14] While a net loss of spines is observed in Alzheimer's disease and cases of intellectual
disability, cocaine and amphetamine use have been linked to increases in dendritic branching and spine density in the prefrontal
cortex and the nucleus accumbens.[15] Because significant changes in spine density occur in various brain diseases, this suggests a
balanced state of spine dynamics in normal circumstances, which may be susceptible to disequilibrium under varying pathological
conditions.[15]

There is also some evidence for loss of dendritic spines as a consequence of aging. One study using mice has noted a correlation
between age-related reductions in spine densities in the hippocampus that and age-dependent declines in hippocampal learning and
memory.[16]

Importance contested
Despite experimental findings that suggest a role for dendritic spine dynamics in mediating learning and memory, the degree of
structural plasticity’s importance remains debatable. For instance, studies estimate that only a small portion of spines formed during
training actually contribute to lifelong learning.[11] In addition, the formation of new spines may not significantly contribute to the
connectivity of the brain, and spine formation may not bear as much of an influence on memory retention as other properties of
structural plasticity, such as the increase in size of spine heads.[17]

Modeling
Theoreticians have for decades hypothesized about the potential electrical function of spines, yet our inability to examine their
electrical properties has until recently stopped theoretical work from progressing too far. Recent advances in imaging techniques
along with increased use of two-photon glutamate uncaging have led to a wealth of new discoveries; we now suspect that there are
voltage-dependent sodium,[18] potassium,[19] and calcium[20] channels in the spine heads.[21]

Cable theory provides the theoretical framework behind the most "simple" method for modelling the flow of electrical currents along
passive neural fibres. Each spine can be treated as two compartments, one representing the neck, the other representing the spine
head. The compartment representing the spine head alone should carry the active properties.

Baer and Rinzel's continuum model

To facilitate the analysis of interactions between many spines, Baer & Rinzel formulated a new cable theory for which the
distribution of spines is treated as a continuum.[22] In this representation, spine head voltage is the local spatial average of membrane
potential in adjacent spines. The formulation maintains the feature that there is no direct electrical coupling between neighboring
spines; voltage spread along dendrites is the only way for spines to interact.

Spike-diffuse-spike model
The SDS model was intended as a computationally simple version of the full Baer and Rinzel model.[23] It was designed to be
analytically tractable and have as few free parameters as possible while retaining those of greatest significance, such as spine neck
resistance. The model drops the continuum approximation and instead uses a passive dendrite coupled to excitable spines at discrete
points. Membrane dynamics in the spines are modelled using integrate and fire processes. The spike events are modelled in a discrete
fashion with the wave form conventionally represented as a rectangular function.

Modeling spine calcium transients

Calcium transients in spines are a key trigger for synaptic plasticity.[24] NMDA receptors, which have a high permeability for
calcium, only conduct ions if the membrane potential is suffiently depolarized. The amount of calcium entering a spine during
synaptic activity therefore depends on the depolarization of the spine head. Evidence from calcium imaging experiments (two-photon
microscopy) and from compartmental modellingindicates that spines with high resistance necks experience larger calcium transients
during synaptic activity.[21][25]

Development
Dendritic spines can develop directly from dendritic shafts or from dendritic filopodia.[26] During synaptogenesis, dendrites rapidly
sprout and retract filopodia, small membrane organelle-lacking membranous protrusions. Recently, I-BAR protein MIM was found to
contribute to the initiation process.[27] 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 spiny dendrites but also small, stubby spines that protrude
from spiny dendrites. In the development of certain filopodia into spines, filopodia 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.

Clinical significance
Cognitive disorders such as ADHD, autism, intellectual disability, and fragile X syndrome, may be resultant from abnormalities in
dendritic spines, especially the number of spines and their maturity.[28] The ratio of matured to immature spines is important in their
signaling, as immature spines have impaired synaptic signaling. Fragile X syndrome is characterized by an overabundance of
immature spines that have multiple filopodia in cortical dendrites.

History
Dendritic spines were first described at the end of the 19th century by Santiago Ramón y Cajal on cerebellar neurons.[29] Ramón y
Cajal then proposed that dendritic spines could serve as contacting sites between neurons. This was demonstrated more than 50 years
later thanks to the emergence of electron microscopy.[30] Until the development of confocal microscopy on living tissues, it was
commonly admitted that spines were formed during embryonic development and then would remain stable after birth. In this
paradigm, variations of synaptic weight were considered as sufficient to explain memory processes at the cellular level. But since
about a decade ago, new techniques of confocal microscopy demonstrated that dendritic spines are indeed motile and dynamic
structures that undergo a constant turnover, even after birth.[31][32][26]

Imaging
In 2015 study published in Cell [33] by Jeff Lichtman lab at Harvard researchers describe automated technologies to probe the
structure of neural tissue at nanometer resolution and use them to generate a saturated reconstruction of a sub-volume of mouse
neocortex in which all cellular objects (axons, dendrites, and glia) and many sub-cellular components (synapses, synaptic vesicles,
spines, spine apparati, postsynaptic densities, and mitochondria) are rendered and itemized in a database. By tracing the trajectories
of all excitatory axons and noting their juxtapositions, both synaptic and non-synaptic, with every dendritic spine the study refutes the
idea that physical proximity is sufficient to predict synaptic connectivity (the so-called Peters’ rule).

References
1. Kapitein, 2010
2. De Roo, M.; Klauser, P.; Mendez, P.; Poglia, L.; Muller, D. (2007). "Activity-Dependent PSD Formation and
Stabilization of Newly Formed Spines in Hippocampal Slice Cultures".Cerebral Cortex. 18 (1): 151–161.
doi:10.1093/cercor/bhm041(https://doi.org/10.1093%2Fcercor%2Fbhm041) . ISSN 1047-3211 (https://www.worldcat.
org/issn/1047-3211).
3. Kaneko M.; Xie Y.; An JJ.; Stryker MP.; Xu B. (2012). "Dendritic BDNF synthesis is required for late-phase spine
maturation and recovery of cortical responses following sensory deprivation"
(https://www.ncbi.nlm.nih.gov/pmc/articl
es/PMC3356781). J. Neurosci. 32 (14): 4790–4802. doi:10.1523/JNEUROSCI.4462-11.2012(https://doi.org/10.152
3%2FJNEUROSCI.4462-11.2012). PMC 3356781 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356781) .
PMID 22492034 (https://www.ncbi.nlm.nih.gov/pubmed/22492034).
4. Xu, T.; Yu, X.; Perlik, A. J.; Tobin, W. F.; Zweig, J. A.; Tennant, K.; Jones, T.; Zuo, Y. (2009). "Rapid formation and
selective stabilization of synapses for enduring motor memories"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC284
4762). Nature. 462: 915–919. doi:10.1038/nature08389 (https://doi.org/10.1038%2Fnature08389). PMC 2844762 (ht
tps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844762) . PMID 19946267 (https://www.ncbi.nlm.nih.gov/pubmed/19
946267).
5. Roberts, T.; Tschida, K.; Klein, M.; Mooney, R. (2010). "Rapid spine stabilization and synaptic enhancement at the
onset of behavioural learning"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2918377). Nature. 463 (7283): 948–
952. doi:10.1038/nature08759 (https://doi.org/10.1038%2Fnature08759). PMC 2918377 (https://www.ncbi.nlm.nih.go
v/pmc/articles/PMC2918377) . PMID 20164928 (https://www.ncbi.nlm.nih.gov/pubmed/20164928).
6. Tschida, K. A.; Mooney, R. (2012). "Deafening drives cell-type-specific changes to dendritic spines in a sensorimotor
nucleus important to learned vocalizations"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299981). Neuron. 73:
1028–1039. doi:10.1016/j.neuron.2011.12.038(https://doi.org/10.1016%2Fj.neuron.2011.12.038) . PMC 3299981 (htt
ps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3299981) . PMID 22405211 (https://www.ncbi.nlm.nih.gov/pubmed/224
05211).
7. De Roo, M.; Klauser, P.; Muller, D. (2008). "LTP promotes a selective long-term stabilization and clustering of
dendritic spines". PLoS Biol. 6: e219. doi:10.1371/journal.pbio.0060219(https://doi.org/10.1371%2Fjournal.pbio.006
0219).
8. Alvarez, V.; Sabatini, B. (2007). "Anatomicaland Physiological Plasticity of Dendritic Spines".Annual Review of
Neuroscience. 30: 79–97. doi:10.1146/annurev.neuro.30.051606.094222(https://doi.org/10.1146%2Fannurev.neuro.
30.051606.094222). PMID 17280523 (https://www.ncbi.nlm.nih.gov/pubmed/17280523).
9. Zuo, Y.; Lin, A.; Chang, P.; Gan, W. B. (2005). "Development of long-term dendritic spine stability in diverse regions
of cerebral cortex". Neuron. 46 (2): 181–189. doi:10.1016/j.neuron.2005.04.001(https://doi.org/10.1016%2Fj.neuron.
2005.04.001). PMID 15848798 (https://www.ncbi.nlm.nih.gov/pubmed/15848798).
10. Holtmaat, A. J.; Trachtenberg, J. T.; Wilbrecht, L.; Shepherd, G. M.; Zhang, X.; et al. (2005). "T
ransient and
persistent dendritic spines in the neocortex in vivo".Neuron. 45 (2): 279–291. doi:10.1016/j.neuron.2005.01.003(htt
ps://doi.org/10.1016%2Fj.neuron.2005.01.003) . PMID 15664179 (https://www.ncbi.nlm.nih.gov/pubmed/15664179).
11. Yang, G.; Pan, F.; Gan, W. B. (2009). "Stably maintained dendritic spines are associated with lifelong memories".
Nature. 462 (7275): 920–924. doi:10.1038/nature08577 (https://doi.org/10.1038%2Fnature08577). PMID 19946265
(https://www.ncbi.nlm.nih.gov/pubmed/19946265).
12. Holtmaat, A.; Wilbrecht, L.; Knott, G. W.; Welker, E.; Svoboda, K. (2006). "Experience-dependent and cell-type-
specific spine growth in the neocortex".Nature. 441 (7096): 979–983. doi:10.1038/nature04783 (https://doi.org/10.10
38%2Fnature04783). PMID 16791195 (https://www.ncbi.nlm.nih.gov/pubmed/16791195).
13. Brown, C.; Li, P.; Boyd, J.; Delaney, K.; Murphy, T. (2007). "Extensive Turnover of Dendritic Spines and Vascular
Remodeling in Cortical Tissues Recovering from Stroke". Journal of Neuroscience. 27 (15): 4101–4109.
doi:10.1523/JNEUROSCI.4295-06.2007(https://doi.org/10.1523%2FJNEUROSCI.4295-06.2007) . PMID 17428988
(https://www.ncbi.nlm.nih.gov/pubmed/17428988).
14. Brown, C.; Murphy, T. H. (2008). "Livin' on the edge: imaging dendritic spine turnover in th
e peri-infarct zone during
ischemic stroke and recovery".Neuroscientist. 14 (2): 139–146. doi:10.1177/1073858407309854(https://doi.org/10.
1177%2F1073858407309854). PMID 18039977 (https://www.ncbi.nlm.nih.gov/pubmed/18039977).
15. Bhatt, D.; Zhang, S.; Gan, W. B. (2009). Dendritic Spine Dynamics. Annual Review of Physiology. 71. pp. 261–282.
doi:10.1146/annurev.physiol.010908.163140(https://doi.org/10.1146%2Fannurev.physiol.010908.163140).
PMID 19575680 (https://www.ncbi.nlm.nih.gov/pubmed/19575680).
16. von Bohlen und Halbach O, Zacher C, Gass P , Unsicker K (2006). "Age-related alterations in hippocampal spines
and deficiencies in spatial memory in mice".J Neurosci Res. 83: 525–531. doi:10.1002/jnr.20759 (https://doi.org/10.1
002%2Fjnr.20759). PMID 16447268 (https://www.ncbi.nlm.nih.gov/pubmed/16447268).
17. Harris, K.; Fiala, J.; Ostroff, L. (2003). "Structural Changes at Dendritic Spine Synapses during Long-T
erm
Potentiation" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1693146). Philosophical Transactions: Biological
Sciences. 358 (1432): 745–748. doi:10.1098/rstb.2002.1254(https://doi.org/10.1098%2Frstb.2002.1254).
PMC 1693146 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1693146) . PMID 12740121 (https://www.ncbi.nlm.ni
h.gov/pubmed/12740121).
18. Araya, R.; Nikolenko, V.; Eisenthal, K. B.; Yuste, R. (2007). "Sodium channels amplify spine potentials"(https://www.
ncbi.nlm.nih.gov/pmc/articles/PMC1924793). PNAS. 104 (30): 12347–12352. doi:10.1073/pnas.0705282104(https://
doi.org/10.1073%2Fpnas.0705282104). PMC 1924793 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1924793) .
PMID 17640908 (https://www.ncbi.nlm.nih.gov/pubmed/17640908).
19. Ngo-Anh, T. J.; Bloodgood, B. L.; Lin, M.; Sabatini, B. L.; Maylie, J.; Adelman, J. P
. (2005). "SK channels and NMDA
receptors form a Ca2+-mediated feedback loop in dendritic spines".Nature Neuroscience. 8 (5): 642–649.
doi:10.1038/nn1449 (https://doi.org/10.1038%2Fnn1449). PMID 15852011 (https://www.ncbi.nlm.nih.gov/pubmed/15
852011).
20. Yuste, R.; Denk, W. (1995). "Dendritic spines as basic functional units of neuronal integrat
ion". Nature. 375 (6533):
682–684. doi:10.1038/375682a0 (https://doi.org/10.1038%2F375682a0). PMID 7791901 (https://www.ncbi.nlm.nih.g
ov/pubmed/7791901).
21. Bywalez, W. G.; Patirniche, D.; Rupprecht, V.; Stemmler, M.; Herz, A. V.; Pálfi, D.; Balázs, R.; Egger, V. (2015).
"Local postsynaptic voltage-gated sodium channel activation in dendritic spines of olfactory bulb granule cells".
Neuron. 85 (3): 590–601. doi:10.1016/j.neuron.2014.12.051(https://doi.org/10.1016%2Fj.neuron.2014.12.051) .
22. Baer, S. M.; Rinzel, J. (1991). "Propagation of dendritic spikes mediated by excitable spines: a continuum theory".
Journal of Neurophysiology. 65 (4): 874–890. PMID 2051208 (https://www.ncbi.nlm.nih.gov/pubmed/2051208).
23. Coombes, S.; Bressloff, P. C. (2000). "Solitary Waves in a Model of Dendritic Cable with Active Spines".SIAM
Journal on Applied Mathematics. 61 (2): 432–453. doi:10.1137/s0036139999356600(https://doi.org/10.1137%2Fs00
36139999356600). JSTOR 3061734 (https://www.jstor.org/stable/3061734).
24. Nevian, T.; Sakmann, B. (2006). "Spine Ca2+signaling in spike-timing-dependent plasticity".Journal of
Neuroscience. 26 (43): 11001–11013. doi:10.1523/JNEUROSCI.1749-06.2006(https://doi.org/10.1523%2FJNEURO
SCI.1749-06.2006). PMID 17065442 (https://www.ncbi.nlm.nih.gov/pubmed/17065442).
25. Grunditz, A.; Holbro, N.; Tian, L.; Zuo, Y.; Oertner, T. G. (2008). "Spine neck plasticity controls postsynaptic calcium
signals through electrical compartmentalization".Journal of Neuroscience. 28 (50): 13457–13466.
doi:10.1523/JNEUROSCI.2702-08.2008(https://doi.org/10.1523%2FJNEUROSCI.2702-08.2008) . PMID 19074019
(https://www.ncbi.nlm.nih.gov/pubmed/19074019).
26. Yoshihara, Y., De Roo, M. & Muller, D. "Dendritic spine formation and stabilization. Curr O
pin Neurobiol (2009).
27. Saarikangas, Juha, et al. "MIM-induced membrane bending promotes dendritic spine initiation." Developmental cell
33.6 (2015): 644-659.
28. Penzes, P.; Cahill, M. E.; Jones, K. A.; Vanleeuwen, J. E.; Woolfrey, K. M. (2011). "Dendritic spine pathology in
neuropsychiatric disorders".Nat Neurosci. 14: 285–293. doi:10.1038/nn.2741 (https://doi.org/10.1038%2Fnn.2741).
29. Ramón y Cajal, S. Estructura de los centros nerviosos de las aves. Rev
. Trim. Histol. Norm. Pat. 1, 1-10 (1888).
30. Gray, E. G. (1959). "Electron microscopy of synaptic contacts on dendrite spines of the cerebral cortex".Nature. 183:
1592–1593. doi:10.1038/1831592a0 (https://doi.org/10.1038%2F1831592a0). PMID 13666826 (https://www.ncbi.nl
m.nih.gov/pubmed/13666826).
31. Dailey, M. E.; Smith, S. J. (1996). "The dynamics of dendritic structure in developing hippocampal slices".J
Neurosci. 16: 2983–2994.
32. Bonhoeffer, T.; Yuste, R. (2002). "Spine motility. Phenomenology, mechanisms, and function".Neuron. 35: 1019–
1027. doi:10.1016/s0896-6273(02)00906-6(https://doi.org/10.1016%2Fs0896-6273%2802%2900906-6) .
PMID 12354393 (https://www.ncbi.nlm.nih.gov/pubmed/12354393).
33. Kasthuri, Narayanan; et al. (2015). "Saturated Reconstruction of a olume
V of Neocortex". Cell. 162 (3): 648–661.
doi:10.1016/j.cell.2015.06.054(https://doi.org/10.1016%2Fj.cell.2015.06.054). ISSN 0092-8674 (https://www.worldca
t.org/issn/0092-8674).

Further reading
Sudhof, T. C.; Stevens, C. F.; Cowan, W. M. (2001). Synapses. Baltimore: The Johns Hopkins University Press.
ISBN 0-8018-6498-4.
Levitan, I. B.; Kaczmarek, L. K. (2002).The Neuron: Cell and Molecular Biology(Third ed.). New York: Oxford
University Press. ISBN 0-19-514522-4.
Nimchinsky E, Sabatini B, Svoboda K (2002). "Structure and function of dendritic spines".
Annu Rev Physiol. 64:
313–53. doi:10.1146/annurev.physiol.64.081501.160008. PMID 11826272.
Matsuzaki M, Honkura N, Ellis-Davies G, Kasai H (2004). "Structural basis of long-term potentiation in single
dendritic spines". Nature. 429 (6993): 761–6. doi:10.1038/nature02617. PMID 15190253.
Yuste R, Majewska A, Holthoff K (2000). "From form to function: calcium compartmentalization in dendritic spines".
Nat Neurosci. 3 (7): 653–9. doi:10.1038/76609. PMID 10862697.
Lieshoff C, Bischof H (2003). "The dynamicsof spine density changes".Behav Brain Res. 140 (1–2): 87–95.
doi:10.1016/S0166-4328(02)00271-1. PMID 12644282.
Kasai H, Matsuzaki M, Noguchi J, Yasumatsu N (2002). "Dendritic spine structures and functions".Nihon Shinkei
Seishin Yakurigaku Zasshi. 22 (5): 159–64. PMID 12451686.
Lynch G, Rex CS, Gall CM (2007). "LTP consolidation: substrates, explanatory power , and functional significance".
Neuropharmacology. 52 (1): 12–23. doi:10.1016/j.neuropharm.2006.07.027. PMID 16949110.

External links
Spiny Dendrite - Cell Centered Database

Retrieved from "https://en.wikipedia.org/w/index.php?title=Dendritic_spine&oldid=828496395

"

This page was last edited on 2 March 2018, at 22:27.

Text is available under theCreative Commons Attribution-ShareAlike License ; additional terms may apply. By using this
site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of theWikimedia
Foundation, Inc., a non-profit organization.