Granule cell dispersion is one of the abnormal structural changes that has been shown in brains of patients with temporal lobe epilepsy. It has also been shown in different animal models, such as the kainic acid model,[1] pilocarpine model,[2] and kindling model. But granule cell dispersion was not found by using perforant pathway stimulation.[3]

It was first described by Houser.[4] In a normal situation, the granule cells in dentate gyrus should be tightly packed. But in granule cell dispersion, the compact formation was lost, and the axons need to extend longer to reach the neighboring granule cells.

Mechanism of formation

There are currently two hypotheses for the mechanism. It might be a consequence of a migration disorder, and the first hypothesis considers an initial injury that release toxin(s) that affect the normal migration of granule cells. The second hypothesis concerns the role of reelin (see below).

Reelin role in temporal lobe epilepsy

Reelin is required for normal neuronal lamination humans, and the lack of this expression can lead to migration defect associated with temporal lobe epilepsy[5]

Effect toward dentate gyrus excitability

References

  1. ↑ Murphy, Brian L; Rylon D. Hofacer; Christian N Faulkner; Andreas W Loepke; Steve C Danzer (May 2012). "Abnormalities of granule cell dendritic structure are a prominent feature of the intrahippocampal kainic acid model of epilepsy despite reduced post-injury neurogenesis". Epilepsia. 53 (5): 908–921. doi:10.1111/j.1528-1167.2012.03463.x. PMC 3340618. PMID 22533643.
  2. ↑ Mello, L; Cavalheiro, E.; Tan, A.; Pretorius, J.; Babb, T.; Finch, D. (1992). "Granule cell dispersion in relation to mossy fiber sprouting, hippocampal cell loss, silent period and seizure frequency in the pilocarpine model of epilepsy". Epilepsy Resesarch. 9: 51–60. PMID 1285914.
  3. ↑ Sloviter, Robert S; Friederike Kienzler; Braxton A. Norwood (10 July 2009). "Hippocampal injury, atrophy, synaptic reorganization, and epileptogenesis after perforant pathway stimulation-induced status epilepticus in the mouse". Journal of Comparative Neurology. 515 (2): 181–196. doi:10.1002/cne.22059. PMC 2705826. PMID 19412934.
  4. ↑ Houser, Carolyn R (December 1990). "Granule cell dispersion in the dentate gyrus of humans with temporal lobe epilepsy". Brain Research. 535 (2): 195–204. doi:10.1016/0006-8993(90)91601-c. PMID 1705855. S2CID 7510030.
  5. ↑ Hass, Carola A; Oliver Dudeck; Matthias Kirsch; Csaba Huszka; Gunda Kann; Stefan Pollak; Josef Zentner; Michael Frotscher (15 July 2002). "Role for Reelin in the Development of Granule Cell Dispersion in Temporal Lobe Epilepsy". The Journal of Neuroscience. 22 (14): 5797–5802. doi:10.1523/JNEUROSCI.22-14-05797.2002. PMC 6757930. PMID 12122039.
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