title: Unilateral low-frequency stimulation of central piriform cortex delays seizure development induced by amygdaloid kindling in rats.
abstract: Low-frequency stimulation of the kindling site interferes with the course of kindling epileptogenesis. The present study examined the effect of unilateral low-frequency stimulation of the central piriform cortex on seizure development induced by amygdaloid kindling in rats. The ipsilateral or contralateral central piriform cortex received low-frequency stimulation (15 min train of 0.1 ms pulses at 1 Hz and 50-150 muA) immediately after termination of once daily kindling stimulation (2 s train of 1 ms pulses at 60 Hz and 150-300 microA) in the right amygdala for 30 days. Low-frequency stimulation of either the ipsilateral or contralateral central piriform cortex significantly suppressed the progression of seizure stages and reduced afterdischarge duration throughout the course of amygdaloid kindling. The marked suppression induced by low-frequency stimulation of the central piriform cortex on either side was predominantly due to the significant retardation of progression from stage 0 to stage 1 and stage 3 to stage 4 seizures. In addition, the suppressive effect of low-frequency stimulation did not disappear when the stimulation was stopped; it could persist for at least 10 days. These findings indicate that brain areas other than the kindling focus, such as the central piriform cortex on both sides, can also be used as reasonable targets for low-frequency stimulation to retard seizure development induced by amygdaloid kindling. Secondly, like the ipsilateral central piriform cortex, the contralateral central piriform cortex may also participate in the progression and secondary generalization of focal seizures. The study suggests that unilateral low-frequency stimulation of the central piriform cortex may have a significant antiepileptogenic effect, and may be helpful for exploring effective and long-lasting therapies for human temporal lobe epilepsy.
authors.affiliation: Department of Pharmacology and Neurobiology, School of Medicine, Zhejiang University, Hangzhou, China 310031.
authors.forename: L-X
authors.initials: LX
authors.lastname: Yang
authors.forename: C-L
authors.initials: CL
authors.lastname: Jin
authors.forename: Z-B
authors.initials: ZB
authors.lastname: Zhu-Ge
authors.forename: S
authors.initials: S
authors.lastname: Wang
authors.forename: E-Q
authors.initials: EQ
authors.lastname: Wei
authors.forename: I C
authors.initials: IC
authors.lastname: Bruce
authors.forename: Z
authors.initials: Z
authors.lastname: Chen
mesh_terms: D000679:Amygdala / Q000503:physiopathology*; D000818:Animals; D004195:Disease Models, Animal; D004599:Electric Stimulation Therapy / Q000379:methods*; D004827:Epilepsy / Q000503:physiopathology / Q000628:therapy*; D007839:Functional Laterality / Q000502:physiology; D007696:Kindling, Neurologic / Q000502:physiology*; D036881:Long-Term Synaptic Depression / Q000502:physiology; D008297:Male; D009433:Neural Inhibition / Q000502:physiology; D009434:Neural Pathways / Q000503:physiopathology*; D009833:Olfactory Pathways / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D016896:Treatment Outcome