SEIZURE-INDUCED SYNAPTIC PLASTICITY: UNDERSTANDING SYNAPTIC REORGANIZATION - Synaptic Plasticity: New Research - page 172

identify which plastic changes are desirable and which are not before treatment strategies can
be developed and attempted.
One may think that seizure activity is too variable and that each seizure model is too
different to yield consistent results when evaluating seizure-induced gene expression. On the
contrary, if one examines the neurotrophins, which are normally expressed in granule cells of
the hippocampus and change their expression dramatically after limbic seizures, one finds
that in spite of the model used (kindling, pilocarpine, kainic acid, or even brain injury models
using trauma or ischemia) neurotrophins, such BDNF, are increased in every model tested.
Furthermore, a number of past studies have shown that BDNF is also associated with LTP,
thus potentially linking plastic processes with epileptogenesis. Given these sorts of results,
the future of molecular studies involving seizure-induced gene expression and plastic
responses hold great promise.
R EFERENCES
[1] Duncan, J.S., and Sagar, H.J. (1987). Seizure characteristics, pathology, and outcome
after temporal lobectomy . Neurology , 37(3), p. 405-9.
[2] Morimoto, K., Fahnestock, M., and Racine, R.J. (2004). Kindling and status epilepticus
models of epilepsy: rewiring the brain . Prog Neurobiol , 73(1), p. 1-60.
[3] Bruton, C.J. (1988). The neuropathology of temporal lobe epilepsy. Oxford, UK:
Oxford University Press (Maudsley Monographs).
[4] Sommer, W. (1880). Erkrankung des Ammonshornes als aetiologisches Moment der
Epilepsie. Arch Psychiatr Nervenkr , 10, p. 631-675.
[5] Bernard, C., Marsden, D.P., and Wheal, H.V. (2001). Changes in neuronal excitability
and synaptic function in a chronic model of temporal lobe epilepsy . Neuroscience ,
103(1), p. 17-26.
[6] Wong, R.K., Miles, R., and Traub, R.D. (1984). Local circuit interactions in
synchronization of cortical neurones . J Exp Biol , 112, p. 169-78.
[7] Scharfman, H.E. (2002). Epilepsy as an example of neural plasticity . Neuroscientist ,
8(2), p. 154-73.
[8] Teyler, T.J. et al. (2001). Synaptic plasticity and secondary epileptogenesis . Int Rev
Neurobiol , 45, p. 253-67.
[9] Sutula, T. et al. (1989). Mossy fiber synaptic reorganization in the epileptic human
temporal lobe . Ann Neurol , 26(3), p. 321-30.
[10] Koyama, R., and Ikegaya, Y. (2004). Mossy fiber sprouting as a potential therapeutic
target for epilepsy . Curr Neurovasc Res , 1(1), p. 3-10.
[11] Bliss, T.V., and Collingridge, G.L. (1993). A synaptic model of memory: long-term
potentiation in the hippocampus . Nature , 361(6407), p. 31-9.
[12] Neves, G., Cooke, S.F., and Bliss, T.V. (2008). Synaptic plasticity, memory and the
hippocampus: a neural network approach to causality . Nat Rev Neurosci , 9(1), p. 65-75.
[13] Leung, L.S., and Wu, C. (2003). Kindling suppresses primed-burst-induced long-term
potentiation in hippocampal CA1 . Neuroreport , 14(2), p. 211-4.
[14] Anderson, P. et al. (2007). The Hippocampal Formation in The Hippocampus Book , P.
Anderson, et al. Editors. Oxford University Press: New York. p. 3-8.