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The Journal of General Psychology Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vgen20
Recovery of Susceptibility Following Audiogenic Seizure in Mice a
Howard M. Reid & Jean L. Muench
a
a
Department of Psychology , SUNY College , Buffalo, USA Published online: 06 Jul 2010.
To cite this article: Howard M. Reid & Jean L. Muench (1991) Recovery of Susceptibility Following Audiogenic Seizure in Mice, The Journal of General Psychology, 118:3, 285-290, DOI: 10.1080/00221309.1991.9917787 To link to this article: http://dx.doi.org/10.1080/00221309.1991.9917787
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content.
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This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/terms-and-conditions
The Journal of General Psychology. f f8(3).285-289
Downloaded by [McMaster University] at 07:18 05 February 2015
Recovery of Susceptibility Following Audiogenic Seizure in Mice HOWARD M. REID JEAN L. MUENCH Department of Psychology S U M College at Bufalo
ABSTRACT. The rate at which SJUJ mice recover susceptibilityfollowingan initial sound-induced seizure was examined. Fewer than 15% of the subjects seized when retested after a 2-min delay, and only 50% reseized after a 10-min delay. The likelihood of a second s e i m was enhanced if the initial seizure exhibited a rapid progression to clonus. During the retest, seizures progressed more slowly than during the initial test, which indicates that recovery was not complete even if a second seizure was induced. Finally, recovery of seizure susceptibilitywas prevented as long as the subject continued to be exposed to intense auditory stimulation following the initial convulsion, an effect previously noted by Alexander and Kopeloff (1980). The findings are discussed in terms of a recently proposed central inhibitory model of the recovery of audiogenic seizure susceptibility.
SOUND-INDUCED SEIZURE IN LABORATORY ANIMALS is one of a number of experimental models of human convulsive disorders. Noted in a variety of species, these generalized convulsions have been extensively studied using rats and mice. Fuller and Collins (1968) and Henry (1967) have determined that whereas some genetic strains of mice are susceptible during an initial exposure to loud auditory stimulation, other strains of mice only exhibit seizures during subsequent exposure. The data suggest that the initial exposure to the auditory stimulus leads to supersensitivity to loud sounds (Chen, 1978; Henry, 1972). Regardless of the strain of mouse used, the seizure progression invariably begins with a burst@)of rapid running that is followed by clonic and frequently tonic levels of seizure activity. Most mice regain coordinated locomotor activity within 60 s of the onset of clonus, thus appearing to recover quickly. It has been reported, however, that the mice Requests for reprints should be sent to Howard M . Reid, Department of Psychology, State University of New York College at Buffalo, Buffalo, NY 14222. 285
Downloaded by [McMaster University] at 07:18 05 February 2015
286
The Journul of General Psychology
remain seizure resistant for an extended period. Ward (1971), for instance, found that only 30% of SJUJ mice would reseize 60 min following the initial test. A similar effect was reported for DBN2 mice (Boggan, 1973; Willott & Henry, 1976). In addition, Boggan (1973) found that recovery occurred in progressive steps, so that the running behavior was elicited while subjects remained refractory to the clonic and tonic stages of seizure activity. More recent studies have found a considerably shorter refractory period. Reid and Collins (1990) reported that virtually all of their SJL/J subjects would reseize after only a 4-min delay between tests; their subjects however, were monaurally tested, which might be a factor in a shorter refractory period. Ward (197 l ) found a much more extensive refractory period using the same strain and a similar procedure. Alexander and Kopeloff (1980) also noted that recovery occurred within only a few minutes. However, their finding might have been influenced by their choice of subject, the CW mouse, a strain that has not been employed in other recovery studies. Alexander and Kopeloffs study also found that seizure recovery was completely prevented as long as the intense acoustic stimulation continued uninterrupted following the initial seizure. However, this effect, which was observed for up to 20 min following the initial seizure, has not been replicated. Our study was designed to clarify a number of issues concerning the audiogenic seizure recovery process, among them, the rate at which audiogenic seizure susceptibility returns following an initial seizure. Mice were chosen from a strain that had been used previously so that we would be able to make comparisons more effectively. Data were collected to determine if Boggan’s (1973) finding of recovery by seize stage could be generalized to include another strain of mouse. Our study also reexamined Alexander and Kopeloffs (1980) finding that continued acoustic stimulation prevents recovery. Finally, our study examined asymmetries of run and fall direction reported during audiogenic seizure (Reid & Collins, 1982) for both the initial and retest seizures to determine if they would be affected by the recovery process.
Method Subjects The data reported are from 60 SJUJ mice. The SJUJ mouse has been found to be susceptible to sound-induced (audiogenic) seizures following exposure to a loud sound (sensitization) (Fuller & Collins, 1968). Apparatus and Procedure We sensitized the SJUJ mice at 21 days of age by placing them in a clear cylinder (30.5cm in diameter, 30 cm in height) within a sound-deadened box.
Downloaded by [McMaster University] at 07:18 05 February 2015
Reid & Muench
287
We then exposed them to the ringing of an electric bell (Trine 204A, measured to have a peak intensity of 116 db with a reference pressure level of .0002 dyne/cm2) for 30 s. When the mice were 23 days of age, we randomly assigned them to one of four experimental groups and reexposed them to the acoustic stimulation. Any subject that did not seize during the initial 60 s was discarded. For the 60 mice that did seize, the bell was turned off at the onset of clonus. We retested one group of subjects by turning the bell on again as soon as the mice had righted themselves. The bell remained on for 11 min or until clonus occurred (bell-on group). For the other mice, the bell remained off for 2,5, or 10 min following the subject’s righting itself (backgroundnoise level was measured to be 60 db with a reference pressure level of .0002 dyne/ cm2). Then the bell was turned on for 1 min unless clonus occurred (groups quiet-2, quiet-5, and quiet-10, respectively).
Results Fourteen of the 60 subjects that initially seized, seized again during the retest. The probability of reseizing depended upon properties of the initial seizure as well as the group to which a subject was assigned. Specifically, subjects that seized during both tests exhibited a faster seizure progression during the initial test than subjects that did not subsequently seize. This was found for the latency to the burst of running preceding clonus (M = 21.5 s vs. 32.2 s, (23) = 2.30, p < .05) as well as the latency to falling at the onset of clonus (M = 27.7 s vs. 39.0 s, t(24) = 2.31, p < .05). It was also determined through the use of a series of Fisher Exact tests that the bell-on group had a lower retest seizure rate than either the quiet-5 or quiet-10 groups (p < .05 and p < .002, respectively) but did not differ from the quiet-2 group (p > .05) (Table 1). We found that the mice in the quiet-2 group had a lower seizure rate than the mice assigned to the quiet-I0 condition (p < .05). In addition, all the mice that exhibited a burst of running during the retest proceeded to clonus within the 60-s test period. We noted several similarities between the initial and retest seizures. In both cases, if clonus occurred during the first half of the 60-s test period it
TABLE 1 Frequency of Undergoing a Sound-Induced Seizure During the Retest Group Bell-on Quiet-2 Quiet-5 Quiet-10
Seized
Did not seize 15 14 10 7
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The Journal of General Psychology
was usually preceded by a single burst of running, whereas if clonus occurred during the second half of the test period, it was usually preceded by two bursts of running. Thus, of the 60 seizures we observed during the initial test, 26 reached clonus during the first 30 s, and 23 of these were preceded by a single burst of running. Of the 34 seizures that reached clonus after 30 s, 20 were preceded by two bursts of running xz (1, N = 60) = 13.9, p C .001. The same pattern was evident in the 14 seizures during the retest. One subject’s data was omitted because the subject fell at 30 s. Four of the remaining 13 subjects reached clonus before 30 s, and 3 of these exhibited only a single burst of running. In 8 of the 9 subjects that reached clonus after more than 30 s had elapsed, clonus was preceded by two bursts of running (Fisher Exact Test, p < .05). We also noted that the 9 out of 14 subjects that seized in both the initial and retest trial5 tended to fall onto the same side during clonus on each test, but this effect was not statistically significant. The initial and retest seizures were not identical, however. When subjects seized on both trials, the second seizure progressed more slowly than the first. Thus, a longer latency was noted before both the burst of running ~ .01) and the fall preceding clonus (M = 32.4 s vs. 21.5 s, r(13) = 3 . 3 3 , < to one side during clonus (M = 40.7 s vs. 27.7 s, r(13) = 3.75, p < .005). In the initial seizures, subjects that fell onto their left side during clonus (19 of 26 subjects) had usually been running in a counterclockwise direction, whereas mice that fell onto their right side (17 of 32 subjects, two subjects were excluded due to missing data) showed a weak tendency to have been running in a clockwise direction x2 ( 1 , N = 58) = 4.06, p < .05. We saw an effect in the same direction in the retest seizures, but it was not statistically significant. Finally, 5 of the bell-on subjects were tested a third time, 2 to 5 days after the second test. All of these mice seized.
Discussion The results of our study reconfirmed that there is a substantial period of recovery following an audiogenic seizure. Thus, fewer than 15%of the subjects seized when retested after a 2-min delay and only 50% reseized after a 10min delay. These data indicate a recovery that is much faster than the recovery that has usually been reported (e.g., Boggan, 1973; Ward, 1971; Willott & Henry, 1976) but considerably slower than what was reported by Reid and Collins (1990). We also found that the likelihood of a second seizure was dependent upon the rate at which the initial seizure progressed; a rapid progression to clonus during the first test increased the probability of seizures during the retest. Reid and Collins (1989) reported that seizures that progress rapidly to clonus (clonus occurs after less than 30 s of acoustic stimulation) are gener-
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289
ally preceded by a single burst of running, whereas seizures that progress more slowly (clonus occurs after more than 30 s of acoustic stimulation) are characteristically preceded by two such bursts. We observed both of these effects in the initial seizures and in the retest. We also observed a linkage (first noted by Reid and Collins in 1982) between the side of fall during clonus and the direction of the preceding burst of running. There was no evidence in our study of a progression in the seizure recovery beginning with running behavior and ending with clonic-tonic seizures, as was noted by Boggan (1973). All subjects in our study that exhibited a burst of wild running during the retest also attained a clonic level of seizure activity. However, seizures that occurred during the retest progressed more slowly, as was indicated by a longer latency to reach both the preceding burst of running and clonus. This finding suggests that recovery was not complete, even in the mice that seized during the retest. Finally, as Alexander and Kopeloff reported in 1980, recovery of seizure susceptibility was prevented as long as the subject was exposed to intense auditory stimulation following the initial convulsion (bell-on group), even though the subject appeared normal in other respects and would subsequently seize if exposed to a quiet period. Reid and Collins (1990) concluded that neither auditory fatigue nor anoxia can account for the extended recovery period that was found to follow an audiogenic seizure. Instead, they proposed that a central, inhibitory process is responsible for this refractory period. Our results r e c o n h that a quiet period is necessary for the termination of whatever process is involved. We also note that the post-seizure level of acoustic stimulation was not reported in the studies that found a greatly extended refractory period (e.g., Boggan, 1973; Ward, 1971; Willott & Henry, 1976). If the postseizure level of acoustic stimulation was substantial, it might provide an explanation for the longer recovery times reported in these studies and the pattern of progressive recovery described by Boggan (1973). REFERENCES Alexander, G. J., & Kopeloff, L. M. (1980). Post-ictal resistance to audiogenic seizures in inbred mice. Neurobehavioral Toxicology, 2, 79-80. Boggan, W. 0. (1973). Recovery of susceptibility after audiogenic seizure. Experimental Neurology, 40, 25 1-253. Chen, C. S. (1978). Acoustic trauma-induced developmental change in the acoustic startle response and audiogenic seizures in mice. Experimental Neurology, 60, 400-403. Fuller, J. L. & Collins, R. L. (1968). Temporal parameters of sensitizations for audiogenic seizures in SJUJ mice. Developmental Psychobiology, 1, 185-188. Henry, K. R. (1967). Audiogenic seizure susceptibility induced in C57BU6J mice by prior auditory exposure. Science, 158,938-940. Henry, K. R. (1972). Unilateral increase of auditory sensitivity following early auditory exposure. Science, 176, 689-690.
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The Journal of General Psychology
Reid, H. M. & Collins, R. L. (1982). Audiogenic seizures in mice: Asymmetries of the preconvulsive running pattern and subsequent seizure. Animal Learning and Behavior, 10, 321-324. Reid, H. M. & Collins, R. L. (1989). Monaural and binaural audiogenic seizures in mice. Behavioral and Neural Biology, 51, 136-144. Reid, H. M. & Collins, R. L. (1990, March). Recovery of suscepribilify to audiogenic seizure in mice. Paper presented at the Eastern Psychological Association Convention, Philadelphia, PA. Ward, R. (1971). Recovery of susceptibility after audiogenic seizure. Nature New Biology, 233, 56-57. Willott, J. F. & Henry, K. R. (1976). Roles of anoxia and noise-induced hearing loss in the postictal refractory period for audiogenic seizures in mice. Journal of Compararive and Physiological Psychology, 90, 373-38 1 .
Received October 9, 1990
ERRATA An error was printed in the appendix of the article by Irwin Nahinsky, “Belief That Experiments Work and Equal Distribution of Ignorance: What Happens When These Tendencies Compete?” published in the January 1991 issue. The sentence that read “These surfaces are (a) much less likely, (b) somewhat less likely, (c) as likely, (d) somewhat more’likely, or (e) much more likely (1) to exhibit rust and (2) to not exhibit rust as those surfaces not given the compound.” should have read “These surfaces are (a) much less likely, (b) somewhat less likely, (c) as likely, (d) somewhat more likely, or (e) much more likely to exhibit rust than not exhibit rust during this period. These surfaces are (a) much less likely, (b) somewhat less likely, (c) as likely, (d) somewhat more likely, or (e) much more likely to exhibit rust as those surfaces not given the compound.”
The Journal of General Psychology Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/vgen20
Recovery of Susceptibility Following Audiogenic Seizure in Mice a
Howard M. Reid & Jean L. Muench
a
a
Department of Psychology , SUNY College , Buffalo, USA Published online: 06 Jul 2010.
To cite this article: Howard M. Reid & Jean L. Muench (1991) Recovery of Susceptibility Following Audiogenic Seizure in Mice, The Journal of General Psychology, 118:3, 285-290, DOI: 10.1080/00221309.1991.9917787 To link to this article: http://dx.doi.org/10.1080/00221309.1991.9917787
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content.
Downloaded by [McMaster University] at 07:18 05 February 2015
This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http://www.tandfonline.com/page/terms-and-conditions
The Journal of General Psychology. f f8(3).285-289
Downloaded by [McMaster University] at 07:18 05 February 2015
Recovery of Susceptibility Following Audiogenic Seizure in Mice HOWARD M. REID JEAN L. MUENCH Department of Psychology S U M College at Bufalo
ABSTRACT. The rate at which SJUJ mice recover susceptibilityfollowingan initial sound-induced seizure was examined. Fewer than 15% of the subjects seized when retested after a 2-min delay, and only 50% reseized after a 10-min delay. The likelihood of a second s e i m was enhanced if the initial seizure exhibited a rapid progression to clonus. During the retest, seizures progressed more slowly than during the initial test, which indicates that recovery was not complete even if a second seizure was induced. Finally, recovery of seizure susceptibilitywas prevented as long as the subject continued to be exposed to intense auditory stimulation following the initial convulsion, an effect previously noted by Alexander and Kopeloff (1980). The findings are discussed in terms of a recently proposed central inhibitory model of the recovery of audiogenic seizure susceptibility.
SOUND-INDUCED SEIZURE IN LABORATORY ANIMALS is one of a number of experimental models of human convulsive disorders. Noted in a variety of species, these generalized convulsions have been extensively studied using rats and mice. Fuller and Collins (1968) and Henry (1967) have determined that whereas some genetic strains of mice are susceptible during an initial exposure to loud auditory stimulation, other strains of mice only exhibit seizures during subsequent exposure. The data suggest that the initial exposure to the auditory stimulus leads to supersensitivity to loud sounds (Chen, 1978; Henry, 1972). Regardless of the strain of mouse used, the seizure progression invariably begins with a burst@)of rapid running that is followed by clonic and frequently tonic levels of seizure activity. Most mice regain coordinated locomotor activity within 60 s of the onset of clonus, thus appearing to recover quickly. It has been reported, however, that the mice Requests for reprints should be sent to Howard M . Reid, Department of Psychology, State University of New York College at Buffalo, Buffalo, NY 14222. 285
Downloaded by [McMaster University] at 07:18 05 February 2015
286
The Journul of General Psychology
remain seizure resistant for an extended period. Ward (1971), for instance, found that only 30% of SJUJ mice would reseize 60 min following the initial test. A similar effect was reported for DBN2 mice (Boggan, 1973; Willott & Henry, 1976). In addition, Boggan (1973) found that recovery occurred in progressive steps, so that the running behavior was elicited while subjects remained refractory to the clonic and tonic stages of seizure activity. More recent studies have found a considerably shorter refractory period. Reid and Collins (1990) reported that virtually all of their SJL/J subjects would reseize after only a 4-min delay between tests; their subjects however, were monaurally tested, which might be a factor in a shorter refractory period. Ward (197 l ) found a much more extensive refractory period using the same strain and a similar procedure. Alexander and Kopeloff (1980) also noted that recovery occurred within only a few minutes. However, their finding might have been influenced by their choice of subject, the CW mouse, a strain that has not been employed in other recovery studies. Alexander and Kopeloffs study also found that seizure recovery was completely prevented as long as the intense acoustic stimulation continued uninterrupted following the initial seizure. However, this effect, which was observed for up to 20 min following the initial seizure, has not been replicated. Our study was designed to clarify a number of issues concerning the audiogenic seizure recovery process, among them, the rate at which audiogenic seizure susceptibility returns following an initial seizure. Mice were chosen from a strain that had been used previously so that we would be able to make comparisons more effectively. Data were collected to determine if Boggan’s (1973) finding of recovery by seize stage could be generalized to include another strain of mouse. Our study also reexamined Alexander and Kopeloffs (1980) finding that continued acoustic stimulation prevents recovery. Finally, our study examined asymmetries of run and fall direction reported during audiogenic seizure (Reid & Collins, 1982) for both the initial and retest seizures to determine if they would be affected by the recovery process.
Method Subjects The data reported are from 60 SJUJ mice. The SJUJ mouse has been found to be susceptible to sound-induced (audiogenic) seizures following exposure to a loud sound (sensitization) (Fuller & Collins, 1968). Apparatus and Procedure We sensitized the SJUJ mice at 21 days of age by placing them in a clear cylinder (30.5cm in diameter, 30 cm in height) within a sound-deadened box.
Downloaded by [McMaster University] at 07:18 05 February 2015
Reid & Muench
287
We then exposed them to the ringing of an electric bell (Trine 204A, measured to have a peak intensity of 116 db with a reference pressure level of .0002 dyne/cm2) for 30 s. When the mice were 23 days of age, we randomly assigned them to one of four experimental groups and reexposed them to the acoustic stimulation. Any subject that did not seize during the initial 60 s was discarded. For the 60 mice that did seize, the bell was turned off at the onset of clonus. We retested one group of subjects by turning the bell on again as soon as the mice had righted themselves. The bell remained on for 11 min or until clonus occurred (bell-on group). For the other mice, the bell remained off for 2,5, or 10 min following the subject’s righting itself (backgroundnoise level was measured to be 60 db with a reference pressure level of .0002 dyne/ cm2). Then the bell was turned on for 1 min unless clonus occurred (groups quiet-2, quiet-5, and quiet-10, respectively).
Results Fourteen of the 60 subjects that initially seized, seized again during the retest. The probability of reseizing depended upon properties of the initial seizure as well as the group to which a subject was assigned. Specifically, subjects that seized during both tests exhibited a faster seizure progression during the initial test than subjects that did not subsequently seize. This was found for the latency to the burst of running preceding clonus (M = 21.5 s vs. 32.2 s, (23) = 2.30, p < .05) as well as the latency to falling at the onset of clonus (M = 27.7 s vs. 39.0 s, t(24) = 2.31, p < .05). It was also determined through the use of a series of Fisher Exact tests that the bell-on group had a lower retest seizure rate than either the quiet-5 or quiet-10 groups (p < .05 and p < .002, respectively) but did not differ from the quiet-2 group (p > .05) (Table 1). We found that the mice in the quiet-2 group had a lower seizure rate than the mice assigned to the quiet-I0 condition (p < .05). In addition, all the mice that exhibited a burst of running during the retest proceeded to clonus within the 60-s test period. We noted several similarities between the initial and retest seizures. In both cases, if clonus occurred during the first half of the 60-s test period it
TABLE 1 Frequency of Undergoing a Sound-Induced Seizure During the Retest Group Bell-on Quiet-2 Quiet-5 Quiet-10
Seized
Did not seize 15 14 10 7
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The Journal of General Psychology
was usually preceded by a single burst of running, whereas if clonus occurred during the second half of the test period, it was usually preceded by two bursts of running. Thus, of the 60 seizures we observed during the initial test, 26 reached clonus during the first 30 s, and 23 of these were preceded by a single burst of running. Of the 34 seizures that reached clonus after 30 s, 20 were preceded by two bursts of running xz (1, N = 60) = 13.9, p C .001. The same pattern was evident in the 14 seizures during the retest. One subject’s data was omitted because the subject fell at 30 s. Four of the remaining 13 subjects reached clonus before 30 s, and 3 of these exhibited only a single burst of running. In 8 of the 9 subjects that reached clonus after more than 30 s had elapsed, clonus was preceded by two bursts of running (Fisher Exact Test, p < .05). We also noted that the 9 out of 14 subjects that seized in both the initial and retest trial5 tended to fall onto the same side during clonus on each test, but this effect was not statistically significant. The initial and retest seizures were not identical, however. When subjects seized on both trials, the second seizure progressed more slowly than the first. Thus, a longer latency was noted before both the burst of running ~ .01) and the fall preceding clonus (M = 32.4 s vs. 21.5 s, r(13) = 3 . 3 3 , < to one side during clonus (M = 40.7 s vs. 27.7 s, r(13) = 3.75, p < .005). In the initial seizures, subjects that fell onto their left side during clonus (19 of 26 subjects) had usually been running in a counterclockwise direction, whereas mice that fell onto their right side (17 of 32 subjects, two subjects were excluded due to missing data) showed a weak tendency to have been running in a clockwise direction x2 ( 1 , N = 58) = 4.06, p < .05. We saw an effect in the same direction in the retest seizures, but it was not statistically significant. Finally, 5 of the bell-on subjects were tested a third time, 2 to 5 days after the second test. All of these mice seized.
Discussion The results of our study reconfirmed that there is a substantial period of recovery following an audiogenic seizure. Thus, fewer than 15%of the subjects seized when retested after a 2-min delay and only 50% reseized after a 10min delay. These data indicate a recovery that is much faster than the recovery that has usually been reported (e.g., Boggan, 1973; Ward, 1971; Willott & Henry, 1976) but considerably slower than what was reported by Reid and Collins (1990). We also found that the likelihood of a second seizure was dependent upon the rate at which the initial seizure progressed; a rapid progression to clonus during the first test increased the probability of seizures during the retest. Reid and Collins (1989) reported that seizures that progress rapidly to clonus (clonus occurs after less than 30 s of acoustic stimulation) are gener-
Downloaded by [McMaster University] at 07:18 05 February 2015
Reid & Muench
289
ally preceded by a single burst of running, whereas seizures that progress more slowly (clonus occurs after more than 30 s of acoustic stimulation) are characteristically preceded by two such bursts. We observed both of these effects in the initial seizures and in the retest. We also observed a linkage (first noted by Reid and Collins in 1982) between the side of fall during clonus and the direction of the preceding burst of running. There was no evidence in our study of a progression in the seizure recovery beginning with running behavior and ending with clonic-tonic seizures, as was noted by Boggan (1973). All subjects in our study that exhibited a burst of wild running during the retest also attained a clonic level of seizure activity. However, seizures that occurred during the retest progressed more slowly, as was indicated by a longer latency to reach both the preceding burst of running and clonus. This finding suggests that recovery was not complete, even in the mice that seized during the retest. Finally, as Alexander and Kopeloff reported in 1980, recovery of seizure susceptibility was prevented as long as the subject was exposed to intense auditory stimulation following the initial convulsion (bell-on group), even though the subject appeared normal in other respects and would subsequently seize if exposed to a quiet period. Reid and Collins (1990) concluded that neither auditory fatigue nor anoxia can account for the extended recovery period that was found to follow an audiogenic seizure. Instead, they proposed that a central, inhibitory process is responsible for this refractory period. Our results r e c o n h that a quiet period is necessary for the termination of whatever process is involved. We also note that the post-seizure level of acoustic stimulation was not reported in the studies that found a greatly extended refractory period (e.g., Boggan, 1973; Ward, 1971; Willott & Henry, 1976). If the postseizure level of acoustic stimulation was substantial, it might provide an explanation for the longer recovery times reported in these studies and the pattern of progressive recovery described by Boggan (1973). REFERENCES Alexander, G. J., & Kopeloff, L. M. (1980). Post-ictal resistance to audiogenic seizures in inbred mice. Neurobehavioral Toxicology, 2, 79-80. Boggan, W. 0. (1973). Recovery of susceptibility after audiogenic seizure. Experimental Neurology, 40, 25 1-253. Chen, C. S. (1978). Acoustic trauma-induced developmental change in the acoustic startle response and audiogenic seizures in mice. Experimental Neurology, 60, 400-403. Fuller, J. L. & Collins, R. L. (1968). Temporal parameters of sensitizations for audiogenic seizures in SJUJ mice. Developmental Psychobiology, 1, 185-188. Henry, K. R. (1967). Audiogenic seizure susceptibility induced in C57BU6J mice by prior auditory exposure. Science, 158,938-940. Henry, K. R. (1972). Unilateral increase of auditory sensitivity following early auditory exposure. Science, 176, 689-690.
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The Journal of General Psychology
Reid, H. M. & Collins, R. L. (1982). Audiogenic seizures in mice: Asymmetries of the preconvulsive running pattern and subsequent seizure. Animal Learning and Behavior, 10, 321-324. Reid, H. M. & Collins, R. L. (1989). Monaural and binaural audiogenic seizures in mice. Behavioral and Neural Biology, 51, 136-144. Reid, H. M. & Collins, R. L. (1990, March). Recovery of suscepribilify to audiogenic seizure in mice. Paper presented at the Eastern Psychological Association Convention, Philadelphia, PA. Ward, R. (1971). Recovery of susceptibility after audiogenic seizure. Nature New Biology, 233, 56-57. Willott, J. F. & Henry, K. R. (1976). Roles of anoxia and noise-induced hearing loss in the postictal refractory period for audiogenic seizures in mice. Journal of Compararive and Physiological Psychology, 90, 373-38 1 .
Received October 9, 1990
ERRATA An error was printed in the appendix of the article by Irwin Nahinsky, “Belief That Experiments Work and Equal Distribution of Ignorance: What Happens When These Tendencies Compete?” published in the January 1991 issue. The sentence that read “These surfaces are (a) much less likely, (b) somewhat less likely, (c) as likely, (d) somewhat more’likely, or (e) much more likely (1) to exhibit rust and (2) to not exhibit rust as those surfaces not given the compound.” should have read “These surfaces are (a) much less likely, (b) somewhat less likely, (c) as likely, (d) somewhat more likely, or (e) much more likely to exhibit rust than not exhibit rust during this period. These surfaces are (a) much less likely, (b) somewhat less likely, (c) as likely, (d) somewhat more likely, or (e) much more likely to exhibit rust as those surfaces not given the compound.”
