Bilateral lesions of the central but not anterior or posterior parts of the piriform cortex retard amygdala kindling in rats.
The piriform cortex is thought to be involved in temporal lobe seizure propagation, such as that occurring during kindling of the amygdala or hippocampus. A number of observations suggested that the circuits of the piriform cortex might act as a critical pathway for limbic seizure discharges to assess motor systems, but direct evidence for this suggestion is scarce. Furthermore, the piriform cortex is not a homogeneous structure, which complicates studies on its role in limbic epileptogenesis. We have previously reported data indicating that the central part of the piriform cortex might be particularly involved during amygdala kindling. In order to further evaluate the role of different parts of the piriform cortex during kindling development, we bilaterally destroyed either the central, anterior or posterior piriform cortex by microinjections of ibotenate two weeks before onset of amygdala kindling. Lesions of the anterior piriform cortex hardly affected kindling acquisition, except that fewer animals exhibited stage 3 (unilateral forelimb) seizures compared to sham controls. Lesions of the central piriform cortex significantly retarded kindling, which was due to a decreased progression from stage 3 to stage 4/5 seizures, i.e. the lesioned rats needed significantly longer for the acquisition of generalized clonic seizures in the late stages of kindling development. Lesions of the posterior piriform cortex did not significantly affect kindling development. The data demonstrate that different parts of the piriform cortex mediate qualitatively different effects on amygdala kindling. The central piriform cortex seems to be a neural substrate involved in the continuous development of kindling from stage 3 to stages 4/5, indicating that this part of the piriform cortex may have preferred access, either directly or indirectly, to structures capable of supporting generalized kindled seizure expression.
Schwabe
K
K
Department of Pharmacology, Toxicology and Pharmacy, School of Veterinary Medicine, Bünteweg 17, D-30559, Hannover, Germany.
Ebert
U
U
Löscher
W
W
D000679:Amygdala / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D007051:Ibotenic Acid / Q000009:adverse effects; D007696:Kindling, Neurologic / Q000473:pathology / Q000502:physiology*; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology*; D009833:Olfactory Pathways / Q000473:pathology / Q000503:physiopathology*; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*
D007051:Ibotenic Acid