Transfer of epileptogenesis between perirhinal cortex and amygdala induced by electrical kindling.
An interesting feature of the kindling phenomenon relates to the finding that kindling established in one region of the brain may reduce the number of stimulations required to establish the phenomenon in a second region. It has been proposed that this 'transfer' phenomenon reflects the extent to which seizures arising in two distinct regions share common underlying mechanisms. The perirhinal cortex (PRC) is currently receiving considerable attention with regard to its possible role in epileptogenesis. Although the role of this region in limbic seizures is unclear, the existence of reciprocal connections between the PRC and amygdala provides a possible neural substrate through which these two regions may influence one another. On the basis of this connectivity, one might expect a transfer between PRC kindling and amygdaloid kindling. Using kindling transfer, the present study was formulated to determine the nature of the relationship between electrical kindling of the PRC and amygdala. Animals previously kindled from the PRC to a cortico-generalised level displayed significantly more advanced behavioural seizures during the early stages of amygdaloid kindling than either controls or those partially kindled. This suggests that primary PRC kindling may facilitate amygdaloid access to systems responsible for the generation of motor seizures. Thus, in terms of kindling, the PRC and amygdala appear to be functionally related, with generalised seizures elicited from the PRC and amygdala sharing, at some level, common underlying mechanisms. Finally, the finding that seizures kindled from the dorsal component of the PRC tended to exhibit characteristics which were quite distinct from those elicited by ventral PRC kindling suggests that these two subregions may have different kindling characteristics and/or different patterns of connectivity with the amygdaloid complex.
Buchanan
J A
JA
Department of Psychology and the Neuroscience Research Centre, University of Otago, Dunedin, New Zealand. buchanan@austin.unimelb.edu.au
Bilkey
D K
DK
D000679:Amygdala / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology; D000818:Animals; D001931:Brain Mapping; D002540:Cerebral Cortex / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology; D004558:Electric Stimulation; D004827:Epilepsy / Q000473:pathology / Q000503:physiopathology*; D007696:Kindling, Neurologic / Q000502:physiology*; D008032:Limbic System / Q000473:pathology / Q000502:physiology* / Q000503:physiopathology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000503:physiopathology*