title: Distinctive amygdala kindled seizures differentially affect neurobehavioral recovery and lesion-induced basic fibroblast growth factor (bFGF) expression.
abstract: The differing effects of partial seizures on neurobehavioral recovery following anteromedial cortex (AMC) injury in rats have previously been reported. Specifically, convulsive Stage 1 seizures evoked ipsilateral to the lesion 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 the seizure-associated difference observed in functional outcome. Anesthetized rats sustained unilateral AMC lesions followed by implantation of a stimulating electrode in the amygdala ipsilateral (Expt. 1) or contralateral (Expt. 2) to the lesion. Beginning 48 h after surgery, animals were kindled to evoke Stage 0 or Stage 1 seizure activity during the critical period. Kindling trials and afterdischarge (AD) were controlled to ascertain their role 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 contralateral to the lesion, (ii) Stage 1 seizures prevented recovery only when initiated in the ipsilateral hemisphere during the post-lesion critical period, and (iii) the detrimental effect of Stage 1 seizures appears to be independent of the number of kindling trials provided and cumulative AD. Thus, to determine why Stage 1 seizures evoked in the hemisphere ipsilateral to the lesion impeded recovery, a separate group of animals (Expt. 3) were kindled accordingly and processed for c-Fos and basic fibroblast growth factor (bFGF) immunohistochemistry. It was hypothesized that Stage 1 seizures evoked in the injured hemisphere prevent recovery by blocking lesion-induced bFGF expression in structures shown to be important for recovery after cortex lesions (e.g., striatum). The results confirmed our hypothesis and suggest that the seizure-associated inhibition of lesion-induced bFGF may alter the growth factor-mediated plasticity necessary for functional recovery.
authors.affiliation: Behavioral Neuroscience Program, Department of Psychology, University of Colorado, Campus Box 345, Boulder, CO 80309-0345, USA.
authors.forename: A E
authors.initials: AE
authors.lastname: Kline
authors.forename: S
authors.initials: S
authors.lastname: Montañez
authors.forename: H A
authors.initials: HA
authors.lastname: Bradley
authors.forename: C J
authors.initials: CJ
authors.lastname: Millar
authors.forename: T D
authors.initials: TD
authors.lastname: Hernandez
mesh_terms: D000679:Amygdala / Q000502:physiology* / Q000503:physiopathology; D000704:Analysis of Variance; D000818:Animals; D002540:Cerebral Cortex / Q000502:physiology* / Q000503:physiopathology; D016222:Fibroblast Growth Factor 2 / Q000235:genetics*; D007839:Functional Laterality; D005786:Gene Expression Regulation / Q000502:physiology*; D016762:Genes, fos; D007696:Kindling, Neurologic / Q000502:physiology*; D008297:Male; D016760:Proto-Oncogene Proteins c-fos / Q000032:analysis / Q000235:genetics; D051381:Rats; D020318:Rats, Long-Evans; D012640:Seizures / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D016222:Fibroblast Growth Factor 2