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. Author manuscript; available in PMC: 2011 Sep 1.
Published in final edited form as: Semin Pediatr Neurol. 2010 Sep;17(3):136–143. doi: 10.1016/j.spen.2010.06.002

Table 2.

A summation of the consequences of SE based on age and model.

Rat age SE model Neuropathology Behavioral impact in adulthood Susceptibility to seizures and development of epilepsy in adulthood Reference
P3 – P8 Pilocarpine No apparent injury None Do not develop epilepsy 36
KA No apparent injury ↑ anxiety, deficits in short and long term learning and memory* Do not develop epilepsy 38, 89, 90, 91
P8 – P10 Pilocarpine Mild loss in dorsal hippocampus (CA4, CA1), septum, amygdala, thalamus, neocortex, hypothalamus ↑ aggression to handling; deficits in auditory discrimination, and visual spatial memory Develop epilepsy ++ 36, 37, 103, 104, 105
Li Pilo No apparent injury ↓ threshold to KA (but not GABAergic antagonist) induced seizures; but do not develop epilepsy 92, 93
KA ? Reversible – all hippocampal sub fields ↑ anxiety, may have deficits in short and long term memory Do not develop epilepsy 38, 89, 91, 94, 95
PTZ No injury / Mossy fiber sprouting None or memory deficits†† Do not develop epilepsy 80, 95, 96, 97
Hyperthermia induced SE Reversible – lateral amygdala; hippocampus (CA1, CA3) Reference and working memory deficits ↓ threshold to KA induced seizures; Develop epilepsy 34, 35, 98, 99, 100, 101, 102
P11 – P24 Pilocarpine Similar to P11 – P20 animals; but damage extends into the ventral hippocampus Memory deficits Develop epilepsy +++ 19, 22, 36, 37
Li Pilo Similar to pilocarpine; but extensive cell loss in hippocampus (CA1 and DG) and associated mossy fiber sprouting. No CA3 loss Spatial memory deficits ↑ susceptibility to kindling, develop epilepsy + 32, 106, 107, 108, 109, 110,
KA Reversible CA1 injury in pups < P18; in those P18 and above, irreversible CA1–CA3 damage, amygdala, lateral septum, mild damage to thalamus, hypothalamus and neocortex ↑ anxiety, deficits in short and long term memory Do not (systemic administration) or can develop (focal application) epilepsy 38, 89, 91, 94, 111, 112
PTZ No injury None Do not develop epilepsy 74, 80
ES Develop epilepsy + 33
P25 – P35 Pilocarpine Similar to P25 – P30 pilocarpine treated animals ↑ aggression, deficits in learning and memory, deficits in auditory discrimination Develop epilepsy +++ 19, 36, 103, 104, 115
Li – Pilo Similar to pilocarpine Memory deficits Develop epilepsy +++ 111
KA Similar to P11 – P20 KA treated pups; but with increasing severity of damage ↑ anxiety, deficits in short and long term memory ↑ susceptibility to kindling; and develop epilepsy +++ 38, 83, 84, 114
PTZ No injury None Do not develop epilepsy 95
ES Develop epilepsy +++ 32
>P60 Li – Pilo Similar to pilocarpine treated animals Develop epilepsy +++ 20, 22
KA Similar to P25 – P30 KA treated animals; but with greater severity ↑ anxiety, deficits in short and long term memory ↑ susceptibility to kindling, and develop epilepsy +++ 38, 89
PTZ None None / Transient learning deficit Do not develop epilepsy 74, 115
*

Observed following focal administration of KA (see ref. 90)

But see ref. 97

††

Observed following repeated PTZ induced SE (see ref. 116)