The differing effects of partial seizures on neurobehavioral recovery follo
wing anteromedial cortex (AMC) injury in rats have previously been reported
. Specifically, convulsive Stage 1 seizures evoked ipsilateral to the lesio
n during the 6-day post-lesion critical period delayed recovery, while non-
convulsive Stage 0 seizures were neutral. The present study was designed to
elaborate on that research by examining several potential mechanisms for t
he seizure-associated difference observed in functional outcome. Anesthetiz
ed rats sustained unilateral AMC lesions followed by implantation of a stim
ulating electrode in the amygdala ipsilateral (Expt. 1) or contralateral (E
xpt. 2) to the lesion. Beginning 48 h after surgery, animals were kindled t
o evoke Stage 0 or Stage 1 seizure activity during the critical period. Kin
dling trials and afterdischarge (AD) were controlled to ascertain their rol
e in functional outcome. Recovery from somatosensory deficits was assessed
over a two-month period. The results revealed that (i) Stage 0 seizures did
not impact recovery regardless of whether initiated ipsilateral or contral
ateral to the lesion, (ii) Stage 1 seizures prevented recovery only when in
itiated in the ipsilateral hemisphere during the post-lesion critical perio
d, and (iii) the detrimental effect of Stage 1 seizures appears to be indep
endent of the number of kindling trials provided and cumulative AD. Thus, t
o determine why Stage 1 seizures evoked in the hemisphere ipsilateral to th
e lesion impeded recovery, a separate group of animals (Expt. 3) were kindl
ed accordingly and processed for c-Fos and basic fibroblast growth factor (
bFGF) immunohistochemistry. It was hypothesized that Stage 1 seizures evoke
d in the injured hemisphere prevent recovery by blocking lesion-induced bFG
F expression in structures shown to he important for recovery after cortex
lesions (e.g., striatum). The results confirmed our hypothesis and suggest
that thr seizure-associated inhibition of lesion-induced bFGF may alter the
growth factor-mediated plasticity necessary for functional recovery. (C) 2
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