Key Points
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Dendritic spines are morphological specializations that protrude from the main shaft of dendrites. Most excitatory synapses in the mature mammalian brain occur on spines. So, spines represent the main unitary postsynaptic compartment for excitatory input.
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Spines have been classified by shape as thin, stubby, mushroom- and cup-shaped. However, spine morphology is not static; spines change size and shape over variable timescales. In addition, most spines exhibit a single, continuous postsynaptic density (PSD), but some PSDs are discontinuous or perforated.
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What is the significance of dendritic spines? There is no definitive answer to this question, but the prevailing view is that their primary function is to provide a microcompartment for segregating postsynaptic chemical responses, such as elevated calcium.
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Dendritic filopodia are widely believed to be the precursors of dendritic spines. However, a simple developmental relationship between filopodia and spines does not seem to exist. So, the filopodium–spine transition is unlikely to be a predestined process, but instead one that is reversible and regulated by factors such as synaptic activity.
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Regulated changes in spine number might reflect mechanisms for converting transient changes in synaptic activity into long-lasting alterations. Indeed, changes in spine density have been observed in response to changes in the efficacy of neurotransmission. In general terms, spines seem to be maintained by an 'optimal' level of synaptic activity: spine density increases when there is insufficient activity, and decreases when stimulation is excessive. Moreover, spine morphology is markedly influenced by the activity of glutamate receptors.
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Dendritic spines exhibit rapid motility. Most spines can change shape in seconds. The shape change involves a remodelling of the cytoskeleton in the spine, and actin-based protrusive activity from the spine head. The underlying molecular mechanisms of this motile behaviour, and its functional significance, are unknown.
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Considerable progress has been made in identifying the molecules that control spine growth and maturation. The cytoskeleton is crucial for their development and stability, and an expanding set of actin-binding and actin-regulatory molecules has also been implicated in these processes. They include GTPases of the Rho/Rac/Cdc42 family, the small GTPase Ras, and a series of receptors and scaffold proteins.
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Several questions remain to be answered in this nascent field. For example, what is the actual function of spines in brain plasticity and behaviour? What are the intrinsic and extrinsic factors that determine the formation of spines? What is the relationship between the structural plasticity of spines, and the movements of molecules and membranes into and out of this postsynaptic compartment?
Abstract
Dendritic spines are tiny protrusions that receive excitatory synaptic input and compartmentalize postsynaptic responses. Heterogeneous in size and shape, and modifiable by activity and experience, dendritic spines have long been thought to provide a morphological basis for synaptic plasticity. Although advanced imaging techniques have highlighted the rapid and regulated motility of spines in living neurons, the functional significance of spine plasticity remains elusive. Recent insights into the molecular mechanisms that regulate spine morphogenesis offer potential ways to manipulate dendritic spines in vivo and to explore their physiological roles in the brain.
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References
Harris, K. M. & Kater, S. B. Dendritic spines: cellular specializations imparting both stability and flexibility to synaptic function. Annu. Rev. Neurosci. 17, 341–371 (1994).
Chicurel, M. E. & Harris, K. M. Three-dimensional analysis of the structure and composition of CA3 branched dendritic spines and their synaptic relationships with mossy fiber boutons in the rat hippocampus. J. Comp. Neurol. 325, 169–182 (1992).
Sorra, K. E. & Harris, K. M. Overview on the structure, composition, function, development, and plasticity of hippocampal dendritic spines. Hippocampus 10, 501–511 (2000).
Harris, K. M. Structure, development, and plasticity of dendritic spines. Curr. Opin. Neurobiol. 9, 343–348 (1999).
Chang, F. L. & Greenough, W. T. Transient and enduring morphological correlates of synaptic activity and efficacy change in the rat hippocampal slice. Brain Res. 309, 35–46 (1984).
Peters, A. & Kaiserman-Abramof, I. R. The small pyramidal neuron of the rat cerebral cortex. The perikaryon, dendrites and spines. Am. J. Anat. 127, 321–355 (1970).
Harris, K. M., Jensen, F. E. & Tsao, B. Three-dimensional structure of dendritic spines and synapses in rat hippocampus (CA1) at postnatal day 15 and adult ages: implications for the maturation of synaptic physiology and long-term potentiation. J. Neurosci. 12, 2685–2705 (1992).
Fiala, J. C., Feinberg, M., Popov, V. & Harris, K. M. Synaptogenesis via dendritic filopodia in developing hippocampal area CA1. J. Neurosci. 18, 8900–8911 (1998).
Spacek, J. & Harris, K. Three-dimensional organization of smooth endoplasmic reticulum in hippocampal CA1 dendrites and dendritic spines of the immature and mature rat. J. Neurosci. 17, 190–203 (1997).
Parnass, Z., Tashiro, A. & Yuste, R. Analysis of spine morphological plasticity in developing hippocampal pyramidal neurons. Hippocampus 10, 561–568 (2000).
Dunaevsky, A., Tashiro, A., Majewska, A., Mason, C. & Yuste, R. Developmental regulation of spine motility in the mammalian central nervous system. Proc. Natl Acad. Sci. USA 96, 13438–13443 (1999).Using time-lapse imaging, the authors observed high motility of spines and filopodia in slices from different brain areas. Spine motility declined with the maturation of neurons, but was not changed by the blockade or stimulation of neuronal activity.
Nusser, Z. et al. Cell type and pathway dependence of synaptic AMPA receptor number and variability in the hippocampus. Neuron 21, 545–559 (1998).
Schikorski, T. & Stevens, C. F. Quantitative ultrastructural analysis of hippocampal excitatory synapses. J. Neurosci. 17, 5858–5867 (1997).
Calverley, R. K. & Jones, D. G. Contributions of dendritic spines and perforated synapses to synaptic plasticity. Brain Res. Brain Res. Rev. 15, 215–249 (1990).
Toni, N., Buchs, P. A., Nikonenko, I., Bron, C. R. & Muller, D. LTP promotes formation of multiple spine synapses between a single axon terminal and a dendrite. Nature 402, 421–425 (1999).Using a calcium-precipitate protocol to reveal stimulated synapses in hippocampal slices, the authors examined structural changes in synapses after the induction of LTP. This resulted in a transient increase in the proportion of perforated synapses, followed by an increase in the number of spines on a dendrite contacting the same axon terminal. These findings indicate that LTP is associated with a duplication of spines, and the formation of new, possibly functional synapses with an activated axon terminal.
Toni, N. et al. Remodeling of synaptic membranes after induction of long-term potentiation. J. Neurosci. 21, 6245–6251 (2001).This paper gives a detailed description of structural changes in the postsynaptic membrane after synaptic potentiation. Three-dimensional reconstruction showed that perforated synapses have larger PSD areas and contain more coated vesicles, indicating enhanced recycling of synaptic membrane, which has been proposed to occur after LTP.
Sorra, K. E., Fiala, J. C. & Harris, K. M. Critical assessment of the involvement of perforations, spinules, and spine branching in hippocampal synapse formation. J. Comp. Neurol. 398, 225–240 (1998).
Desmond, N. L. & Weinberg, R. J. Enhanced expression of AMPA receptor protein at perforated axospinous synapses. Neuroreport 9, 857–860 (1998).
Hayashi, Y. et al. Driving AMPA receptors into synapses by LTP and CaMKII: requirement for GluR1 and PDZ domain interaction. Science 287, 2262–2267 (2000).
Passafaro, M., Piech, V. & Sheng, M. Subunit-specific temporal and spatial patterns of AMPA receptor exocytosis in hippocampal neurons. Nature Neurosci. 4, 917–926 (2001).
Shi, S., Hayashi, Y., Esteban, J. A. & Malinow, R. Subunit-specific rules governing AMPA receptor trafficking to synapses in hippocampal pyramidal neurons. Cell 105, 331–343 (2001).
Lüscher, C., Nicoll, R. A., Malenka, R. C. & Muller, D. Synaptic plasticity and dynamic modulation of the postsynaptic membrane. Nature Neurosci. 3, 545–550 (2000).
Shepherd, G. M. The dendritic spine: a multifunctional integrative unit. J. Neurophysiol. 75, 2197–2210 (1996).
Sabatini, B. L., Maravall, M. & Svoboda, K. Ca2+ signaling in dendritic spines. Curr. Opin. Neurobiol. 11, 349–356 (2001).
Volfovsky, N., Parnas, H., Segal, M. & Korkotian, E. Geometry of dendritic spines affects calcium dynamics in hippocampal neurons: theory and experiments. J. Neurophysiol. 82, 450–462 (1999).
Korkotian, E. & Segal, M. Structure–function relations in dendritic spines: is size important? Hippocampus 10, 587–595 (2000).
Majewska, A., Brown, E., Ross, J. & Yuste, R. Mechanisms of calcium decay kinetics in hippocampal spines: role of spine calcium pumps and calcium diffusion through the spine neck in biochemical compartmentalization. J. Neurosci. 20, 1722–1734 (2000).
Majewska, A., Tashiro, A. & Yuste, R. Regulation of spine calcium dynamics by rapid spine motility. J. Neurosci. 20, 8262–8268 (2000).
Yuste, R., Majewska, A. & Holthoff, K. From form to function: calcium compartmentalization in dendritic spines. Nature Neurosci. 3, 653–659 (2000).
Sabatini, B. L. & Svoboda, K. Analysis of calcium channels in single spines using optical fluctuation analysis. Nature 408, 589–593 (2000).
Dailey, M. E. & Smith, S. J. The dynamics of dendritic structure in developing hippocampal slices. J. Neurosci. 16, 2983–2994 (1996).
Ziv, N. E. & Smith, S. J. Evidence for a role of dendritic filopodia in synaptogenesis and spine formation. Neuron 17, 91–102 (1996).
Lendvai, B., Stern, E. A., Chen, B. & Svoboda, K. Experience-dependent plasticity of dendritic spines in the developing rat barrel cortex in vivo. Nature 404, 876–881 (2000).The first description of spine and filopodia motility in vivo . Motility was reduced after deprivation of sensory input, but only during a critical period in development. Afferent deprivation did not change spine density or shape, but perturbed the proper formation of sensory maps, indicating that spine/filopodia motility driven by sensory input might be important for the establishment and reorganization of neuronal circuits.
Okabe, S., Miwa, A. & Okado, H. Spine formation and correlated assembly of presynaptic and postsynaptic molecules. J. Neurosci. 21, 6105–6114 (2001).
Marrs, G. S., Green, S. H. & Dailey, M. E. Rapid formation and remodeling of postsynaptic densities in developing dendrites. Nature Neurosci. 4,1006–1113 (2001).
Yuste, R. & Bonhoeffer, T. Morphological changes in dendritic spines associated with long-term synaptic plasticity. Annu. Rev. Neurosci. 24, 1071–1089 (2001).
Fifkova, E. & Van Harreveld, A. Long-lasting morphological changes in dendritic spines of dentate granular cells following stimulation of the entorhinal area. J. Neurocytol. 6, 211–230 (1977).
Fifkova, E. & Anderson, C. L. Stimulation-induced changes in dimensions of stalks of dendritic spines in the dentate molecular layer. Exp. Neurol. 74, 621–627 (1981).
Desmond, N. L. & Levy, W. B. Changes in the numerical density of synaptic contacts with long-term potentiation in the hippocampal dentate gyrus. J. Comp. Neurol. 253, 466–475 (1986).
Lee, K. S., Schottler, F., Oliver, M. & Lynch, G. Brief bursts of high-frequency stimulation produce two types of structural change in rat hippocampus. J. Neurophysiol. 44, 247–258 (1980).
Trommald, M., Hulleberg, G. & Andersen, P. Long-term potentiation is associated with new excitatory spine synapses on rat dentate granule cells. Learn. Mem. 3, 218–228 (1996).
Sorra, K. E. & Harris, K. M. Stability in synapse number and size at 2 hr after long-term potentiation in hippocampal area CA1. J. Neurosci. 18, 658–671 (1998).
Hosokawa, T., Rusakov, D. A., Bliss, T. V. & Fine, A. Repeated confocal imaging of individual dendritic spines in the living hippocampal slice: evidence for changes in length and orientation associated with chemically induced LTP. J. Neurosci. 15, 5560–5573 (1995).
Engert, F. & Bonhoeffer, T. Dendritic spine changes associated with hippocampal long-term synaptic plasticity. Nature 399, 66–70 (1999).
Maletic-Savatic, M., Malinow, R. & Svoboda, K. Rapid dendritic morphogenesis in CA1 hippocampal dendrites induced by synaptic activity. Science 283, 1923–1927 (1999).References 43–45 were the first to report that spine-like protrusions formed in association with LTP-inducing stimuli.
Halpain, S., Hipolito, A. & Saffer, L. Regulation of F-actin stability in dendritic spines by glutamate receptors and calcineurin. J. Neurosci. 18, 9835–9844 (1998).
McKinney, R. A., Capogna, M., Durr, R., Gahwiler, B. H. & Thompson, S. M. Miniature synaptic events maintain dendritic spines via AMPA receptor activation. Nature Neurosci. 2, 44–49 (1999).
Fischer, M., Kaech, S., Wagner, U., Brinkhaus, H. & Matus, A. Glutamate receptors regulate actin-based plasticity in dendritic spines. Nature Neurosci. 3, 887–894 (2000).This paper shows that the actin-based motility of spines in hippocampal cultures is inhibited by the activation of AMPA and NMDA receptors, resulting in a stabilization of spines.
Korkotian, E. & Segal, M. Release of calcium from stores alters the morphology of dendritic spines in cultured hippocampal neurons. Proc. Natl Acad. Sci. USA 96, 12068–12072 (1999).
Segal, M., Korkotian, E. & Murphy, D. D. Dendritic spine formation and pruning: common cellular mechanisms? Trends Neurosci. 23, 53–57 (2000).
Das, S. et al. Increased NMDA current and spine density in mice lacking the NMDA receptor subunit NR3A. Nature 393, 377–381 (1998).
Rampon, C. et al. Enrichment induces structural changes and recovery from nonspatial memory deficits in CA1 NMDAR1-knockout mice. Nature Neurosci. 3, 238–244 (2000).
Fischer, M., Kaech, S., Knutti, D. & Matus, A. Rapid actin-based plasticity in dendritic spines. Neuron 20, 847–854 (1998).A seminal time-lapse imaging study that reported the rapid actin-based motility of spines in cultured hippocampal neurons transfected with actin–GFP.
Matus, A. Actin-based plasticity in dendritic spines. Science 290, 754–758 (2000).
Korkotian, E. & Segal, M. Regulation of dendritic spine motility in cultured hippocampal neurons. J. Neurosci. 21, 6115–6124 (2001).The authors describe an inverse correlation between spine motility and the presence of active presynaptic terminals contacting spines, indicating that presynaptic innervation reduces spine motility.
Kaech, S., Brinkhaus, H. & Matus, A. Volatile anesthetics block actin-based motility in dendritic spines. Proc. Natl Acad. Sci. USA 96, 10433–10437 (1999).
Dunaevsky, A., Blazeski, R., Yuste, R. & Mason, C. Spine motility with synaptic contact. Nature Neurosci. 4, 685–686 (2001).
Korkotian, E. & Segal, M. Spike-associated fast contraction of dendritic spines in cultured hippocampal neurons. Neuron 30, 751–758 (2001).
Kaech, S., Fischer, M., Doll, T. & Matus, A. Isoform specificity in the relationship of actin to dendritic spines. J. Neurosci. 17, 9565–9572 (1997).
Capani, F., Martone, M. E., Deerinck, T. J. & Ellisman, M. H. Selective localization of high concentrations of F-actin in subpopulations of dendritic spines in rat central nervous system: a three-dimensional electron microscopic study. J. Comp. Neurol. 435, 156–170 (2001).
Allison, D. W., Gelfand, V. I., Spector, I. & Craig, A. M. Role of actin in anchoring postsynaptic receptors in cultured hippocampal neurons: differential attachment of NMDA versus AMPA receptors. J. Neurosci. 18, 2423–2436 (1998).
Wyszynski, M. et al. Differential regional expression and ultrastructural localization of α-actinin-2, a putative NMDA receptor-anchoring protein, in rat brain. J. Neurosci. 18, 1383–1392 (1998).
Hayashi, K. & Shirao, T. Change in the shape of dendritic spines caused by overexpression of drebrin in cultured cortical neurons. J. Neurosci. 19, 3918–3925 (1999).
Allen, P. B., Ouimet, C. C. & Greengard, P. Spinophilin, a novel protein phosphatase 1 binding protein localized to dendritic spines. Proc. Natl Acad. Sci. USA 94, 9956–9961 (1997).
Satoh, A. et al. Neurabin-II/spinophilin. J. Biol. Chem. 273, 3470–3475 (1998).
Matsuoka, Y., Li, X. & Bennett, V. Adducin is an in vivo substrate for protein kinase C: phosphorylation in the MARCKS-related domain inhibits activity in promoting spectrin–actin complexes and occurs in many cells, including dendritic spines of neurons. J. Cell Biol. 142, 485–497 (1998).
Pak, D. T., Yang, S., Rudolph-Correia, S., Kim, E. & Sheng, M. Regulation of dendritic spine morphology by SPAR, a PSD-95-associated RapGAP. Neuron 31, 289–303 (2001).This study describes a postsynaptic RapGAP protein that interacts with PSD95 and F-actin, and which regulates dendritic spine size and complexity. Rap is implicated in spine elongation.
Naisbitt, S. et al. Shank, a novel family of postsynaptic density proteins that binds to the NMDA receptor/PSD-95/GKAP complex and cortactin. Neuron 23, 569–582 (1999).
Feng, J. et al. Spinophilin regulates the formation and function of dendritic spines. Proc. Natl Acad. Sci. USA 97, 9287–9292 (2000).
Luo, L. et al. Differential effects of the Rac GTPase on Purkinje cell axons and dendritic trunks and spines. Nature 379, 837–840 (1996).An important genetic study in mice, showing the effect of Rac on dendritic spine number and morphology in vivo.
Nakayama, A. Y., Harms, M. B. & Luo, L. Small GTPases Rac and Rho in the maintenance of dendritic spines and branches in hippocampal pyramidal neurons. J. Neurosci. 20, 5329–5338 (2000).
Tashiro, A., Minden, A. & Yuste, R. Regulation of dendritic spine morphology by the Rho family of small GTPases: antagonistic roles of Rac and Rho. Cereb. Cortex 10, 927–938 (2000).References 71 and 72 used the transfection of constitutively active and dominant-negative constructs of Rac GTPases to reveal the roles of these ubiquitous cytoskeletal regulators in spine morphogenesis.
Penzes, P. et al. The neuronal Rho-GEF kalirin-7 interacts with PDZ domain-containing proteins and regulates dendritic morphogenesis. Neuron 29, 229–242 (2001).Kalirin-7 — a GEF for Rac — is shown to bind PSD95, localize in spines and induce increased spine-like protrusions in neurons.
Wu, G. Y., Deisseroth, K. & Tsien, R. W. Spaced stimuli stabilize MAPK pathway activation and its effects on dendritic morphology. Nature Neurosci. 4, 151–158 (2001).
Husi, H., Ward, M., Choudhary, J., Blackstock, W. & Grant, S. Proteomic analysis of NMDA receptor-adhesion protein signaling complexes. Nature Neurosci. 3, 661–669 (2000).
Hsueh, Y.-P. et al. Direct interaction of CASK/LIN-2 and syndecan heparan sulfate proteoglycan and their overlapping distribution in neuronal synapses. J. Cell Biol. 142, 139–151 (1998).
Ethell, I. & Yamaguchi, Y. Cell surface heparan sulfate proteoglycan syndecan-2 induces the maturation of dendritic spines in rat hippocampal neurons. J. Cell Biol. 144, 575–586 (1999).This paper showed that overexpression of syndecan 2, a synaptic heparan-sulphate proteoglycan, induced the maturation of mushroom-like spines. This effect was dependent on the cytoplasmic carboxyl terminus of syndecan 2.
Ethell, I. M., Hagihara, K., Miura, Y., Irie, F. & Yamaguchi, Y. Synbindin, a novel syndecan-2-binding protein in neuronal dendritic spines. J. Cell Biol. 151, 53–68 (2000).
Sheng, M. & Pak, D. T. S. Ligand-gated ion channel interactions with cytoskeletal and signaling proteins. Annu. Rev. Physiol. 62, 755–778 (2000).
Sheng, M. & Sala, C. PDZ domains and the organization of supramolecular complexes. Annu. Rev. Neurosci. 24, 1–29 (2001).
El-Husseini, A. E., Schnell, E., Chetkovich, D. M., Nicoll, R. A. & Bredt, D. S. PSD-95 involvement in maturation of excitatory synapses. Science 290, 1364–1368 (2000).By the transfection of cultured neurons, this study showed that overexpression of PSD95 could stimulate the maturation of dendritic spines, which correlated with the recruitment of AMPA receptors to spines.
Tu, J. C. et al. Coupling of mGluR/Homer and PSD-95 complexes by the Shank family of postsynaptic density proteins. Neuron 23, 583–592 (1999).
Sala, C. et al. Regulation of dendritic spine morphology and synaptic function by Shank and Homer. Neuron 31, 115–130 (2001).Overexpression of two PSD proteins — Shank and Homer — is shown to induce a remarkable enlargement of the spine head and recruitment of InsP 3 R and smooth endoplasmic reticulum into the spine head. Dominant-negative Shank caused a loss of spines.
Svoboda, K. & Mainen, Z. F. Synaptic [Ca2+]: intracellular stores spill their guts. Neuron 22, 427–430 (1999).
Sheng, M. & Lee, S. H. AMPA receptor trafficking and the control of synaptic transmission. Cell 105, 825–828 (2001).
Steward, O. & Schuman, E. M. Protein synthesis at synaptic sites on dendrites. Annu. Rev. Neurosci. 24, 299–325 (2001).
Globus, A. & Scheibel, A. B. The effect of visual deprivation on cortical neurons: a Golgi study. Exp. Neurol. 19, 331–345 (1967).
Parnavelas, J. G., Globus, A. & Kaups, P. Continuous illumination from birth affects spine density of neurons in the visual cortex of the rat. Exp. Neurol. 40, 742–747 (1973).
Moser, M. B., Trommald, M., Egeland, T. & Andersen, P. Spatial training in a complex environment and isolation alter the spine distribution differently in rat CA1 pyramidal cells. J. Comp. Neurol. 380, 373–381 (1997).
Comery, T. A., Shah, R. & Greenough, W. T. Differential rearing alters spine density on medium-sized spiny neurons in the rat corpus striatum: evidence for association of morphological plasticity with early response gene expression. Neurobiol. Learn. Mem. 63, 217–219 (1995).
Popov, V. I. & Bocharova, L. S. Hibernation-induced structural changes in synaptic contacts between mossy fibres and hippocampal pyramidal neurons. Neuroscience 48, 53–62 (1992).
Mong, J. A., Roberts, R. C., Kelly, J. J. & McCarthy, M. M. Gonadal steroids reduce the density of axospinous synapses in the developing rat arcuate nucleus: an electron microscopy analysis. J. Comp. Neurol. 432, 259–267 (2001).
Shors, T. J., Chua, C. & Falduto, J. Sex differences and opposite effects of stress on dendritic spine density in the male versus female hippocampus. J. Neurosci. 21, 6292–6297 (2001).
Woolley, C. S. & McEwen, B. S. Estradiol mediates fluctuation in hippocampal synapse density during the estrous cycle in the adult rat. J. Neurosci. 12, 2549–2554 (1992).
Yankova, M., Hart, S. A. & Woolley, C. S. Estrogen increases synaptic connectivity between single presynaptic inputs and multiple postsynaptic CA1 pyramidal cells: a serial electron-microscopic study. Proc. Natl Acad. Sci. USA 98, 3525–3530 (2001).
Hinton, V. J., Brown, W. T., Wisniewski, K. & Rudelli, R. D. Analysis of neocortex in three males with the fragile X syndrome. Am. J. Med. Genet. 41, 289–294 (1991).
Irwin, S. A. et al. Abnormal dendritic spine characteristics in the temporal and visual cortices of patients with fragile-X syndrome: a quantitative examination. Am. J. Med. Genet. 98, 161–167 (2001).
Suetsugu, M. & Mehraein, P. Spine distribution along the apical dendrites of the pyramidal neurons in Down's syndrome. A quantitative Golgi study. Acta Neuropathol. (Berl.) 50, 207–210 (1980).
Ferrer, I. & Gullotta, F. Down's syndrome and Alzheimer's disease: dendritic spine counts in the hippocampus. Acta Neuropathol. (Berl.) 79, 680–685 (1990).
Swann, J. W., Al-Noori, S., Jiang, M. & Lee, C. L. Spine loss and other dendritic abnormalities in epilepsy. Hippocampus 10, 617–625 (2000).
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Glossary
- LONG-TERM POTENTIATION
-
A long-lasting increase in the efficacy of neurotransmission, which can be elicited by diverse patterns of synaptic activation.
- FILOPODIA
-
Long, thin protrusions at the periphery of migrating cells and growth cones. They are rich in bundles of F-actin.
- TWO-PHOTON MICROSCOPY
-
A form of microscopy in which a fluorochrome that would normally be excited by a single photon is stimulated quasi-simultaneously by two photons of lower energy. Under these conditions, fluorescence increases as a function of the square of the light intensity, and decreases approximately as the square of the distance from the focus. Because of this behaviour, only fluorochrome molecules near the plane of focus are excited, greatly reducing light scattering and photodamage of the sample.
- FRAGILE-X SYNDROME
-
A genetic condition commonly transmitted from mother to son, which is associated with mental retardation, abnormal facial features and enlarged testicles.
- TETRODOTOXIN
-
A potent marine neurotoxin that blocks voltage-gated sodium channels. Tetrodotoxin was originally isolated from the tetraodon pufferfish, and contains a positively charged guanidinium group and a pyrimidine ring.
- RHO/RAC/CDC42 GTPASES
-
Molecules related to the product of the oncogene Ras, which are involved in controlling the polymerization and subsequent organization of actin.
- LAMELLIPODIA
-
Flattened, sheet-like projections from the surface of a cell, which are often associated with cell migration.
- DOMINANT NEGATIVE
-
Describes a mutant molecule that can form a heteromeric complex with the normal molecule, knocking out the activity of the entire complex.
- PDZ DOMAIN
-
A peptide-binding domain that is important for the organization of membrane proteins, particularly at cell–cell junctions, including synapses. They can bind to the carboxyl termini of proteins, or can form dimers with other PDZ domains. PDZ domains are named after the proteins in which these sequence motifs were originally identified (PSD95, Discs-large, zona occludens 1).
- RAS PROTEINS
-
A group of small GTPases involved in growth, differentiation and cellular signalling that require the binding of GTP to enter into their active state.
- HEPARAN SULPHATE
-
A glycosaminoglycan that consists of repeated units of hexuronic acid and glucosamine residues. It usually attaches to proteins through a xylose residue to form proteoglycans.
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Hering, H., Sheng, M. Dentritic spines : structure, dynamics and regulation. Nat Rev Neurosci 2, 880–888 (2001). https://doi.org/10.1038/35104061
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DOI: https://doi.org/10.1038/35104061
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