Effect of Midbrain and Pontine Tegmental Lesions on Audiogenic Seizures in Genetically Epilepsy‐Prone Rats

Abstract

A bilateral mechanical lesion of the midbrain and pontine tegmentum was found to abolish completely the tonic components of sound-induced seizures in genetically epilepsy-prone rats (GEPR) that display tonic-clonic seizures. Correlations between varied lesions placements and effects on maximal audiogenic seizures provided evidence that damage to the nucleus reticularis pontis oralis (RPO) of the midbrain and pontine reticular formation (RF) was responsible for the seizure-attenuating effects. Moreover, electrolytic lesions of the pontine RF involving the RPO nucleus were found to abolish the tonic components of the maximal audiogenic seizure. Additionally, bilateral mechanical lesions involving the RPO nucleus were found to attenuate the clonic components of sound-induced seizures in GEPR that display only running seizures and clonus. These findings are consistent with previous studies showing that pontine tegmental lesions attenuate the tonic components of maximal electroshock- and pentylenetetrazol-induced seizures, and lend further support to the hypothesis that all generalized tonic seizures share a common neural substrate. The role of the brainstem RF in tonic versus clonic convulsions is discussed in light of the present findings.

Anatomy and physiology of multipolar cells in the rat inferior collicular cortex using the in vitro brain slice technique

“…Some IC cortical cells project to deep layers of the superior colliculus (Tokunaga et al, 1984;Coleman and Clerici, 1987) and may be involved in the circuit mediating the appropriate orientation of head, eyes, and pinna movements (see Aitkin, 1985). Lesion and stimulation studies of the deep superior colliculus indicate that IC output generating the major components of the seizure behavior probably does not use this route (Wada et al, 1970;McCown et al, 1984;Browning et al, 1985;Browning, 1986). Other cells in the IC cortex form a "descending" projection to the pons and medulla, and it is interesting to note that bilateral lesions of a region of the pons called nucleus reticularis pontis oralis (RPO) significantly attenuates audiogenic convulsions (Browning et al, 1985).…”

“…Lesion and stimulation studies of the deep superior colliculus indicate that IC output generating the major components of the seizure behavior probably does not use this route (Wada et al, 1970;McCown et al, 1984;Browning et al, 1985;Browning, 1986). Other cells in the IC cortex form a "descending" projection to the pons and medulla, and it is interesting to note that bilateral lesions of a region of the pons called nucleus reticularis pontis oralis (RPO) significantly attenuates audiogenic convulsions (Browning et al, 1985). This would seem to implicate this descending pathway in seizure initiation; however, RPO is not the pontine region where colliculopontine fibers terminate (Bume et al, 1981;Faye-Lund, 1986).…”

Effects of Stimulation of the Inferior Colliculi in Krushinskii–Molodkina Rats

“…Similar phenomena consisting of increases in the proportion of fast-wave sleep, linked with activation of the inferior colliculi, have been seen in rats, cats, and humans after repeated sessions of rhythmic auditory stimulation [19,20]. All these points provide grounds for the conclusion that the inferior colliculi in rats, acting via the relevant projections [22,28,34], may have a modulatory effect on the functioning of the centers triggering fast-wave sleep located in the area of the pons [30,37]. As demonstrated in our studies, the nature of these infl uences is far from unambiguous.…”

Audiogenic kindling and secondary subcortico-cortical epileptogenesis: Behavioral correlates and electrographic features

“…In nonkindled rodents, full-blown audiogenic seizures do not usually induce epileptiform activity in the cortex [7,8,30,59,60], confirming the subcortical origin of these seizures. Acutely induced audiogenic seizures of moderate severity (i.e., generalized clonic seizures) are not accompanied by distinct cortical epileptiform activity [30], though the amygdala has been shown to be involved in the network of the clonic form of AS even in nonkindled GEPR-3s [61].…”