Spreading cortical depression and audiogenic seizures in mice

doi:10.1016/0014-4886(71)90246-9

Experimental Neurology

Volume 31, Issue 3, June 1971, Pages 437-443

https://doi.org/10.1016/0014-4886(71)90246-9 Get rights and content

Abstract

Bilateral spreading cortical depression in mice susceptible to audiogenic seizure is associated with a slight increase in latency to seizure, with no detectable change in susceptibility. Bilateral cortical depression does not appear to affect the processes whereby insusceptible mice are placed at risk as a result of prior exposure to noise. Unilateral cortical depression is associated with asymmetrical convulsions, the mice falling to that side on which cortical depression produces ataxia.

References (18)

R.P. Kesner
Subcortical mechanisms of audiogenic seizure
Exp. Neurol.
(1966)
F.A. Beach et al.
Noise induced seizures in the rat and their modification by cerebral injury
J. Comp. Neurol.
(1947)
K.R. Carlson
Cortical spreading depression and subcotrical memory storage
J. Comp. Physiol.
(1967)
L. Chocholova
The role of the cerebral cortex in audiogenic seizures in the rat
Physiol. Bohemoslov.
(1962)
R.L. Collins
Unilateral inhibition of sound-induced convulsions in mice
Science
(1970)
R.L. Collins
A new genetic locus mapped from behavioral variation in mice: audiogenic seizure prone (asp)
Bchavior Genetics
(1970)
R.L. Collins et al.
Audiogenic seizure prone (asp): a gene affecting behavior in Linkage Group VIII of the mouse
Science
(1968)
J.L. Fuller et al.
Temporal parameters of sensitization for audiogenic seizures in $SJL J$ mice
Develop. Psychobiol.
(1968)
J.L. Fuller et al.
Mice unilaterally sensitized for audiogenic seizure
Science
(1968)

There are more references available in the full text version of this article.

Cited by (14)

Spreading depression: A review of the clinical relevance
2001, Brain Research Reviews
Spreading depression (SD), a transient reversible phenomenon with characteristic ionic, metabolic and hemodynamic changes, has been known for over 55 years. A vast number of studies into this mysterious experimental event provides evidence for SD involvement in brain pathophysiology. There is sufficient evidence to admit that SD plays an important role in some clinical disorders including migraine, cerebrovascular diseases, head injury and transient global amnesia. However, the exact pathophysiological mechanisms of SD are unknown and further studies are needed to demonstrate the involvement of SD in these clinical disorders. The purpose of this review is to collect different evidences and hypotheses which suggest a link between SD and clinical disorders. Learning more about the importance of SD may increase our understanding of SD associated disorders and improve our fundamental research strategies.
The relationship between callosal variation and lateralization in mice is genotype-dependent
1987, Brain Research
The relation between morphological variation of the corpus callosum and variation in the degree of paw preference was investigated in 129/J and BALB/cCF mice. A positive relationship explaining 24% of the variance of paw preference was found in 129/J mice; no such relationship exists in BALB/cCF mice. It is suggested that, since the genetic dissimilarity between these two inbred strains is comparable in magnitude with the genetic dissimilarity between unrelated human subjects, genetic variation may have been an uncontrolled source of heterogeneity in previous human neuropsychological studies.
VII. Neuroanatomical localization of structures responsible for seizures in the GEPR: Lesion studies
1986, Life Sciences
Identification of the neural substrates subserving audiogenic convulsions in the GEPR is an important task and while it is not yet complete, many laboratories employing various techniques have contributed importantly to our current understanding. The present review focuses on the use of lesions to identify the neural substrates of audiogenic convulsions. Lesions in brain stem nuclei appear to have a much greater ability to attenuate audiogenic convulsions than do forebrain lesions. In fact, some forebrain lesions (dorsal hippocampus, caudate, intralaminar thalamic nuclei) appear to enhance the severity of audiogenic seizures. On the other hand, bilateral lesions in the inferior colliculus (IC) have been shown to completely abolish audiogenic convulsions, while lesions in the pontine reticular formation (PRF nucleus) abolish all aspects except the running episode suggesting that these two brain stem structures are important neural substrates involved in the expression of audiogenic convulsions. Large bilateral lesions of the substantia nigra also appear to attenuate audiogenic convulsions. The effect of lesions on audiogenic convulsions is basically similar to their effect on other generalized seizure models and the data appear to support the hypothesis that there are two anatomical systems involved in the expression of all generalized convulsions: (1) a $forebrain system$ responsible for the expression of face and forelimb clonus; and (2) a $brain stem system$ responsible in the expression of running-bouncing clonus and tonus.
A comparison of short-latency auditory-evoked potentials in two strains of mice: possible neurophysiological correlates of susceptibility to audiogenic seizures?
1981, Brain Research
The short-latency auditory-evoked response was recorded from adult (over 8 wk) and young (16–22 day) mice of the audiogenic seizure-prone DBA/2J (D2) and seizure-resistant C57BL/6J (C6) strains. An auditory complex made up of eleven peaks and troughs was found within the first 20 ms after click stimuli. The latencies of the potentials tended to be shorter in the C6 mice and in the adults of both strains. The ratio of amplitude differences of late to early peaks (‘amplitude index’) was much larger(P<0.01) in D2 mice. The data are consistent with greater neuronal recruitment to acoustic stimuli in the higher-order auditory centers of D2 mice.
Midbrain pathways of audiogenic seizures in DBA/2 mice
1980, Experimental Neurology
The effects on audiogenic seizures of bilateral electrolytic lesions at levels of the inferior colliculus (IC), superior colliculus (SC), or medial geniculate body were determined for inbred $DBA 2$ mice. Of 88 control mice (surgical and nonsurgical), 82% displayed the full seizure syndrome when exposed to intense sound: wildrunning attacks progressed to clonic convulsions and then tonic convulsions. All remaining control animals displayed at least wild-running attacks. In 27 of 49 mice with IC-level lesions, either no seizure activity was observed or the syndrome terminated at the wild-running stage. In these mice, lesions consistently damaged the central IC nucleus (ICC) and sometimes adjacent midbrain tegmentum. In the 12 IC-lesion mice that displayed the full seizure syndrome, IC damage was generally lateral, primarily involving the external IC nucleus (ICX). In SC-lesion mice, absence of wild-running was observed in only 3 of 23 mice, but termination of seizures at wild-running or clonic stages was often seen (14 of 23 mice). Attenuation of seizure activity was correlated with damage to the deep SC and tegmentum, including the central gray. Little or no effect on audiogenic seizures was found with lesions of the dorsal SC or medial geniculate body. Analysis of the time course of components of the seizure syndrome revealed that IC-lesion mice attaining only the wild-running stage had increased latencies to onset of this behavior. In SC-lesion mice, time to onset of wild-running did not differ significantly from controls. Progression from wild-running attacks to onset of clonic convulsions was slowed by lesions at both IC and SC levels. The data indicate that the primary pathway of audiogenic seizure activity includes the ICC, deep SC, and adjacent tegmentum. Wild-running attacks appear to be mediated at the IC level, whereas progression to clonic and tonic convulsions may require more rostral levels.
Influence of the cribriform degeneration (cri) mutation on audiogenic seizures in DBA/2J mice
1979, Experimental Neurology

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²: Dr. Ward is supported by the Scottish Rite Committee on Research in Schizophrenia. The treatment of animals at this Laboratory is governed by those principles advocated by the National Society for Medical Research.

¹: This work was supported by Research Grant No. MH 11327 from the National Institute of Mental Health and by Training Grant No. GY 7614 from the National Science Foundation, and was carried out while Mr. Sinnett was a member of the National Science Foundation Undergraduate Training Programme.

View full text

Spreading cortical depression and audiogenic seizures in mice

Abstract

Exp. Neurol.

Noise induced seizures in the rat and their modification by cerebral injury

J. Comp. Neurol.

Cortical spreading depression and subcotrical memory storage

J. Comp. Physiol.

The role of the cerebral cortex in audiogenic seizures in the rat

Physiol. Bohemoslov.

Unilateral inhibition of sound-induced convulsions in mice

Science

A new genetic locus mapped from behavioral variation in mice: audiogenic seizure prone (asp)

Bchavior Genetics

Audiogenic seizure prone (asp): a gene affecting behavior in Linkage Group VIII of the mouse

Science

Temporal parameters of sensitization for audiogenic seizures in SJLJ mice

Develop. Psychobiol.

Mice unilaterally sensitized for audiogenic seizure

Science

Temporal parameters of sensitization for audiogenic seizures in $SJL J$ mice