title: The relationship between audiogenic seizure (AGS) susceptibility and forebrain tone-responsiveness in genetically AGS-prone Wistar rats.
abstract: The present study characterized the intensity-response functions of extracellular field responsiveness of different cortical/subcortical structures of the forebrain following the free-field presentation of tone stimuli, within a population of genetically audiogenic seizure (AGS)-prone KM-Wistar rats. The neural response properties of each case were compared to its propensity to exhibit AGSs during the continuous tone stimulation (15 kHz, 90 s at max.). The amplitudes or slope components of the evoked responses and their peak latencies showed significant positive (amplitude and slope) and negative (peak latency) Bolzmann's sigmoid relationships with the onset-latency of AGS. These relationships, with areal differences in the slopes of saturation functions, applied for the three different data sets recorded simultaneously from the stratum radiatum dendritic layer of the hippocampal CA1 area, primary auditory cortex layers II-IV, and frontal cortex surface. In addition, the similar type of functions between the evoked response variables and AGS onset latency held when all the areas were considered together. These data suggest that the neural responsiveness to acoustic stimulation of the primary sensory, multimodal and association cortices of the forebrain may altogether contribute to the seizure initiation by that modality in the genetically AGS-prone rats. It has been previously shown that there exist abundant and dispersed auditory projections from these forebrain areas to the brain stem and spinal cord, structures that are generally considered to be the key predisposing factors in the generation of AGS. Hence, the types of correlation found reflect the subject-specific stage of forebrain responsiveness, being either related or unrelated to genetic AGS-specific changes, and possibly its triggering impact upon the lower brain AGS network. Accordingly, the mere comparison of forebrain response measures of these AGS-prone animals with those of the AGS-resistant ones could not reveal the result presented.
authors.affiliation: Department of Pharmacology and Toxicology, University of Kuopio, P.O. B. 1627, SF-70210, Kuopio, Finland. antti.valjakka@uku.fi
authors.forename: A
authors.initials: A
authors.lastname: Valjakka
authors.forename: M
authors.initials: M
authors.lastname: Jaakkola
authors.forename: J
authors.initials: J
authors.lastname: Vartiainen
authors.forename: H
authors.initials: H
authors.lastname: Olkkonen
authors.forename: A
authors.initials: A
authors.lastname: Semiokhina
authors.forename: I
authors.initials: I
authors.lastname: Fedotova
authors.forename: J
authors.initials: J
authors.lastname: Virkkala
authors.forename: J
authors.initials: J
authors.lastname: Ylikoski
authors.forename: L
authors.initials: L
authors.lastname: Tuomisto
mesh_terms: D000161:Acoustic Stimulation; D000818:Animals; D001303:Auditory Cortex / Q000166:cytology / Q000502:physiology; D003712:Dendrites / Q000502:physiology; D004594:Electrophysiology; D005072:Evoked Potentials, Auditory / Q000502:physiology; D006624:Hippocampus / Q000166:cytology / Q000502:physiology; D016548:Prosencephalon / Q000166:cytology / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000235:genetics* / Q000503:physiopathology*