Kindling model
Kindling is a commonly used model for the development of seizures and epilepsy in which the duration and behavioral involvement of induced seizures increases after seizures are induced repeatedly.[1] The kindling model was first proposed in the late 1960s by Goddard and colleagues.[2] Although kindling is a widely used model, its applicability to human epilepsy is controversial.[1]
The word kindling is a metaphor: the increase in response to small stimuli is similar to the way small burning twigs can produce a large fire.[3] It is used by scientists to study the effects of repeated seizures on the brain.[1] A seizure may increase the likelihood that more seizures will occur; an old saying in epilepsy research is "seizures beget seizures".[1] Repeated stimulation "lowers the threshold" for more seizures to occur.[4]
The brains of experimental animals are repeatedly stimulated, usually with electricity, to induce the seizures.[1] Chemicals may also be used to induce seizures.[3] The seizure that occurs after the first such electrical stimulation lasts a short time and is accompanied by a small amount of behavioral effects compared with seizures that result from repeated stimulations.[1] With further seizures, the accompanying behavior intensifies, for example progressing from freezing in early stimulations to convulsions in later ones.[5] The lengthening of duration and intensification of behavioral accompaniment eventually reaches a plateau after repeated stimulation.[1] Even if animals are left unstimulated for as long as 12 weeks, the effect remains; the response to stimulation remains higher than it had been before.[3]
It has been reported that repeated seizure stimulation can result in spontaneous seizures, but studies have had conflicting findings on this question.[1] In humans, some seizure disorders come to an end by themselves even after large numbers of seizures.[1] However, in both human epilepsy and in some animal models, evidence suggests that a process like that found in kindling does occur.[1]
[edit] See also
- Kindling (substance withdrawal)
- Epileptogenesis
- Racine Stages (a method by which seizure severity is quantified in animal models of epilepsy)
[edit] References
- ^ a b c d e f g h i j Bertram E (2007). "The relevance of kindling for human epilepsy". Epilepsia 48 (Supplement 2): 65–74. doi:10.1111/j.1528-1167.2007.01068.x. PMID 17571354.
- ^ Sato M (2008). "Kindling: An experimental model of epilepsy" (PDF). Psychiatry and Clinical Neurosciences 36 (4): 440–441. doi:10.1111/j.1440-1819.1982.tb03123.x. http://www3.interscience.wiley.com/cgi-bin/fulltext/120156204/PDFSTART.
- ^ a b c Abel MS, McCandless DW (1992). "The kindling model of epilepsy". In Adams RN, Baker GB, Baker JM, Bateson AN, Boisvert DPJ, Boulton AA, et al.. Neuromethods: Animal Models of Neurological Disease. Totowa, NJ: Humana Press. pp. 153–155. ISBN 0-89603-211-6.
- ^ PK Sahoo, KI Mathai, GV Ramdas, MN Swamy (2007). "The pathophysiology of post traumatic epilepsy" (PDF). Indian Journal of Neurotrauma 4 (1): 11–14. http://www.ijntonline.com/June07/abstracts/03.PDF. Temkin NR, Jarell AD, Anderson GD (2001). "Antiepileptogenic agents: how close are we?". Drugs 61 (8): 1045–55. PMID 11465868.
- ^ Morimoto K, Fahnestock M, Racine RJ (May 2004). "Kindling and status epilepticus models of epilepsy: Rewiring the brain". Prog. Neurobiol. 73 (1): 1–60. doi:10.1016/j.pneurobio.2004.03.009. PMID 15193778.
