Evoked potentials in rats with misonidazole neurotoxicity

Edwards, Michael S. B.; Powers, Stephen K.; Baringer, Richard A.; Jewett, Don L.; Bolger, Catherine A.; Phillips, Theodore L.

doi:10.1007/bf00182956

Cited by 8 publications

(7 citation statements)

References 25 publications

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“…1~ Table 1). Rats in this study tolerated significantly higher total doses of MISO than rats in the previous study (4). Clinical signs of toxicity began to appear at approximately the time of the 33rd injection (X = 4.455 g MISO) (Fig.…”

Section: Latencymentioning

confidence: 54%

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Misonidazole neurotoxicity in rats: Part I

Edwards¹,

Gordon²,

Levin³

et al. 1984

J Neuro-Oncol

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The effects of misonidazole (MISO) on brain stem evoked potentials (BAEPs) and cortical evoked potentials (CEPs) were evaluated in 16 Sprague-Dawley rats !reated with the agent. As found in previous studies, serial BAEPvalues were diagnostic of the onset of MISO toxicity before clinical signs and symptoms appeared. However, MISO had no effects on CEPs, which remained essentially unchanged through the course of the experiment. At histologic examination, significant changes were found in the area of the brain stem, but there was no histologic evidence of damage to cortical or subcortical structures caused by MISO administration. The results of this study suggest that the neurotoxic effects of MISO are species-specific, and that while the rat model may be useful for comparison of the relative toxic effects of nitroimidazole radiosensitizers, it is not a model suited for measurement of neurotoxicity caused by MISO in humans and nonhuman primates.A ddressfor reprints: Dr Edwards, c/o the Editorial Office,

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Section: Latencymentioning

confidence: 54%

“…Recordings were performed as described (4). Potentials were amplified by a gain of 10,000 with bandpass filtration of 30 HZ-3 KHz for BAEP recordings and 5 100 Hz for CEP recordings.…”

Section: Recording Of Baep and Cepmentioning

confidence: 99%

Misonidazole neurotoxicity in rats: Part I

Edwards¹,

Gordon²,

Levin³

et al. 1984

J Neuro-Oncol

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“…In rats, it has been shown that following exposure to misonidazole neurotoxicity, Peaks I and I1 were the only peaks not affected (17). In the same study, histologic examination showed consistent necrosis in the cochlear nuclei, leading the authors to suggest that the generator for Peak I1 is the auditory nerve.…”

Section: Discussionmentioning

confidence: 87%

“…Although the generator site for Peak I1 was once thought to be the cochlear nucleus, more recent evidence suggests that it is the auditory nerve ( 17,18). In rats, it has been shown that following exposure to misonidazole neurotoxicity, Peaks I and I1 were the only peaks not affected (17).…”

Section: Discussionmentioning

confidence: 97%

Cranial Nerve Dysfunction in Conscious Galactosemic Rats as Measured by the Auditory-Evoked Brainstem Response

Notvest

Inserra

Emrey

et al. 1990

Experimental Biology and Medicine

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The purpose of this study was to extend our previous work with the auditory-evoked brainstem response and determine whether galactosemia would produce a functional neuropathy similar to that previously seen in streptozocin-induced diabetic rats. Sprague-Dawley male rats implanted with cortical electrodes received either normal chow (n = 17) or a 50% galactose diet (n = 17) for 5 weeks. Peak II latency of the auditory-evoked brainstem response, interpreted as a functional measure of the auditory nerve (VIII cranial) in rats, was significantly prolonged in galactose-fed rats relative to controls (P less than 0.05). These results demonstrate a functional deficit in the auditory nerves of galactosemic rats. The deficit in the auditory-evoked brainstem response of galactosemic rats is similar to our previous finding in streptozocin-induced diabetic rats.

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“…In independent studies, Rebert and ourselves have shown that the brain stem conduction time of the BAEP (wave I to wave IV interpeak latency) is prolonged after chronic administration of MISO (1,5). This is expected, because lesions involving the cochlear and vestibular nuclei and other periventricular brain stem nuclei brain are typically produced in rats by MISO.…”

Section: Discussionmentioning

confidence: 93%

Evoked potentials in rats with misonidazole neurotoxicity

1983

Self Cite

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Spinal and cortical somatosensory potentials were recorded weekly in rats treated with misonidazole at a dose of 300 mg/kg/day until clinical signs of severe neurotoxicity developed. After sacrifice, the brains, spinal cords and sciatic nerves were examined. All treated rats developed necrotic brain stem lesions identical to those previously described by Griffin and by us. Two rats had mild demyelination of spinal cord white matter tracts, but only one of these rats had changes in the SEPs. Interestingly, changes in the cervical and cortical SEP from this rat were only transient. We conclude that misonidazole neurotoxicity in the rat predominantly affects the brain stem nuclei adjacent to the fourth ventricle without involving the lemniscal pathways that are situated ventromedially in the brain stem. Therefore, somatosensory evoked potentials (SEPs) are not useful for the diagnosis of MISO neurotoxicity.

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Evoked potentials in rats with misonidazole neurotoxicity

Cited by 8 publications

References 25 publications

Misonidazole neurotoxicity in rats: Part I

Misonidazole neurotoxicity in rats: Part I

Cranial Nerve Dysfunction in Conscious Galactosemic Rats as Measured by the Auditory-Evoked Brainstem Response

Evoked potentials in rats with misonidazole neurotoxicity

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