Spine apparatus

The spine apparatus (SA) is a specialized form of endoplasmic reticulum (ER) that is found in a subpopulation of dendritic spines in central neurons. It was discovered by E. G. Gray in 1959 when he applied electron microscopy to fixed cortical tissue.[1] The SA consists of a series of stacked discs that are thought to be connected to each other and to the dendritic system of ER-tubules.[2] The actin binding protein synaptopodin (which has originally been described in podocytes of the kidney) is an essential component of the SA.[3] Mice that lack the gene for synaptopodin do not form a spine apparatus.[4] The SA is believed to play a critical role in learning and memory.

Contents

Morphology

In CA1 pyramidal cells of the hippocampus, a spine apparatus is found in about 20% of all dendritic spines.[4] The SA is mostly found in large mushroom-shaped spines which are thought to carry strong synapses. Not all spiny cells form a SA: Purkinje cells of the cerebellum, for example, have many dendritic spines, but no spine apparatus.

Function

Dendritic spines in cortical neurons contain ion channels that are capable of releasing calcium from the endoplasmic reticulum (ryanodine receptors and IP3 receptors). Therefore, it has long been speculated that the spine apparatus might be involved in calcium signaling inside the spine. A knockout mouse lacking synaptopodin provided the first evidence for an involvement of the spine apparatus in synaptic plasticity.[4] These mice, which had no spine apparatus, had impaired long-term potentiation in the hippocampus and also deficits in spatial learning. Recent studies have shown that synapses on spines with a spine apparatus are stronger and display enhanced long-term plasticity.[5] A specific form of long-term depression (mGluR-dependent LTD) is only supported by spines with spine apparatus and seems to be triggered by calcium release from this structure.[6] In summary, an important function of the spine apparatus is the regulation of plasticity at individual synapses, a process known as metaplasticity.

References

  1. ^ Gray (1959). "Electron microscopy of synaptic contacts on dendrite spines of the cerebral cortex". Nature 183 (4675): 1592–3. doi:10.1038/1831592a0. PMID 13666826. 
  2. ^ Cooney; Hurlburt, JL; Selig, DK; Harris, KM; Fiala, JC (2002). "Endosomal compartments serve multiple hippocampal dendritic spines from a widespread rather than a local store of recycling membrane". Journal of Neuroscience 22 (6): 2215–24. PMID 11896161. 
  3. ^ Deller; Merten, T; Roth, SU; Mundel, P; Frotscher, M (2000). "Actin-associated protein synaptopodin in the rat hippocampal formation: localization in the spine neck and close association with the spine apparatus of principal neurons". The Journal of Comparative Neurology 418 (2): 164–81. doi:10.1002/(SICI)1096-9861(20000306)418:2<164::AID-CNE4>3.0.CO;2-0. PMID 10701442. 
  4. ^ a b c Deller; Korte, M; Chabanis, S; Drakew, A; Schwegler, H; Stefani, GG; Zuniga, A; Schwarz, K et al. (2003). "Synaptopodin-deficient mice lack a spine apparatus and show deficits in synaptic plasticity". Proceedings of the National Academy of Sciences of the United States of America 100 (18): 10494–9. doi:10.1073/pnas.1832384100. PMC 193589. PMID 12928494. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=193589. 
  5. ^ Vlachos, A.; Korkotian, E.; Schonfeld, E.; Copanaki, E.; Deller, T.; Segal, M. (2009). "Synaptopodin Regulates Plasticity of Dendritic Spines in Hippocampal Neurons". Journal of Neuroscience 29 (4): 1017–33. doi:10.1523/JNEUROSCI.5528-08.2009. PMID 19176811. 
  6. ^ Holbro, N.; Grunditz, A.; Oertner, T. G. (2009). "Differential distribution of endoplasmic reticulum controls metabotropic signaling and plasticity at hippocampal synapses". Proceedings of the National Academy of Sciences 106 (35): 15055. doi:10.1073/pnas.0905110106. 

External links