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Hippocampus (brain).jpg
Subiculum labeled at center left.
CA1 to subiculum4.jpg
Subiculum to CA1 transition Artist Don Cooper and Leah Leverich
Part of Temporal lobe
Posterior cerebral
Anterior choroidal
Acronym(s) S
MeSH A08.186.211.577.405
NeuroNames hier-170
NeuroLex ID Subiculum
TA A14.1.09.326
FMA 74414
Anatomical terms of neuroanatomy

The subiculum (Latin for "support") is the most inferior component of the hippocampal formation. It lies between the entorhinal cortex and the CA1 subfield of the hippocampus proper.


It receives input from CA1 and entorhinal cortical layer III pyramidal neurons and is the main output of the hippocampus. The pyramidal neurons send projections to the nucleus accumbens, septal nuclei, prefrontal cortex, lateral hypothalamus, nucleus reuniens, mammillary nuclei, entorhinal cortex and amygdala.

The pyramidal neurons in the subiculum exhibit transitions between two modes of action potential output: bursting and single spiking.[1] The transitions between these two modes is thought to be important for routing information out of the hippocampus.


It is believed to play a role in some cases of human epilepsy.[2][3]

It has also been implicated in working memory[4] and drug addiction.[5]

It has been suggested that the dorsal subiculum is involved in spatial relations, and the ventral subiculum regulates the hypothalamic-pituitary-adrenal axis.[6]

Clinical significance[edit]

Potential role in Alzheimer's Disease[edit]

Rat studies indicate that lesioning of the subiculum decreases the spread of amyloid-beta in rat models of Alzheimer's disease. Alzheimer's disease pathology is thought to have prion-like properties. The disease tends to spread in characteristic sequence from the entorhinal cortex through the subiculum.[7]

Additional images[edit]


  1. ^ Donald C. Cooper, Sungkwon Chung, Nelson Spruston, "Output-Mode Transitions Are Controlled by Prolonged Inactivation of Sodium Channels in Pyramidal Neurons of Subiculum," PLoS Biology, 3(6):e175, 2005 June.
  2. ^ Knopp A, Frahm C, Fidzinski P, Witte OW, Behr J (June 2008). "Loss of GABAergic neurons in the subiculum and its functional implications in temporal lobe epilepsy". Brain 131 (Pt 6): 1516–27. doi:10.1093/brain/awn095. PMID 18504292. 
  3. ^ Stafstrom CE (2005). "The role of the subiculum in epilepsy and epileptogenesis". Epilepsy Curr 5 (4): 121–9. doi:10.1111/j.1535-7511.2005.00049.x. PMC 1198740. PMID 16151518. 
  4. ^ Riegert C, Galani R, Heilig S, Lazarus C, Cosquer B, Cassel JC (June 2004). "Electrolytic lesions of the ventral subiculum weakly alter spatial memory but potentiate amphetamine-induced locomotion". Behav. Brain Res. 152 (1): 23–34. doi:10.1016/j.bbr.2003.09.011. PMID 15135966. 
  5. ^ Martin-Fardon R, Ciccocioppo R, Aujla H, Weiss F (July 2008). "The dorsal subiculum mediates the acquisition of conditioned reinstatement of cocaine-seeking". Neuropsychopharmacology 33 (8): 1827–34. doi:10.1038/sj.npp.1301589. PMID 17957218. 
  6. ^ O'Mara S (September 2005). "The subiculum: what it does, what it might do, and what neuroanatomy has yet to tell us". J. Anat. 207 (3): 271–82. doi:10.1111/j.1469-7580.2005.00446.x. PMC 1571536. PMID 16185252. 
  7. ^ George, Sonia; Annica Rönnbäck; Gunnar K Gouras; Géraldine H Petit; Fiona Grueninger; Bengt Winblad; Caroline Graff; Patrik Brundin (2014). "Lesion of the subiculum reduces the spread of amyloid beta pathology to interconnected brain regions in a mouse model of Alzheimer’s disease". Acta Neuropathologica Communications 2 (1): 17. doi:10.1186/2051-5960-2-17. ISSN 2051-5960. PMID 24517102. 

External links[edit]