Mild carbon monoxide exposure and auditory function in the developing rat

Stockard-Sullivan, Janet; Korsak, Rose A.; Webber, Douglas S.; Edmond, John

doi:10.1002/jnr.10808

Cited by 19 publications

(22 citation statements)

References 63 publications

(88 reference statements)

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“…For example, Huttenlocher and de Courten [25] found that the greatest increases in synaptogenesis in the occipital cortex occur between 2.5 and 8 postnatal months; however, this process is relatively slower in the frontal cortex where synapse formation does not reach its maximum density until after 15 postnatal months. Third, influences of myelin development on the morphology of waveforms have been demonstrated in animal studies [26], showing that brain responses can be impaired if the brain is exposed to carbon monoxide during the developmental stage of myelination [27]. Moreover, the number of neurons involved in the sensory processes may vary at different ages.…”

Section: Morphological Changes Of Erp Componentsmentioning

confidence: 99%

Brain responses to tonal changes in the first two years of life

Jing

Benasich

2006

Brain and Development

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Maturation of auditory perceptual and discrimination process within the first two years of life is investigated in healthy infants by examining event-related potentials (ERPs). High-density EEG signals were recorded from the scalp monthly between 3 and 24 months of age. Two types of stimuli (100 vs. 100 Hz for standard stimuli; 100 vs. 300 Hz for deviant stimuli; occurrence rate: 85:15%) were presented using an oddball paradigm. Latencies and amplitudes were compared across development. The results showed that latencies of P 150 , N 250 , P 350 , and N 450 components gradually decreased with increasing age. Amplitudes of the N 250 and P 350 components gradually increased and reached the maximum at 9 months, and then gradually decreased with the increase of age. Mismatch negativity was not obvious at 3 months of age, but was seen at 4-5 months and became robust after 6 months. Robust late positivity was recorded at all ages. These mismatch responses were noticeable in the frontal, central, and parietal areas, and the maximal MMN amplitude distribution gradually moved from the parietal area to the frontal area across the age range. Two important periods-one around 6 months and the other around 9 months are suggested in the maturation of auditory central system. Dynamical changes in the underlying source strengths and orientations may be principal contributors to ERP morphological changes in infants within the first 24 months.

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Section: Morphological Changes Of Erp Componentsmentioning

confidence: 99%

Brain responses to tonal changes in the first two years of life

Jing

Benasich

2006

Brain and Development

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“…Chronic mild postnatal CO exposure has also been shown to impair the developing auditory system (Lopez, 2003; Stockard-Sullivan, 2003; Webber, 2003). Expression of c-Fos, an indicator of neuronal activation following sound stimulation, was found to be significantly decreased in the central nucleus of the inferior colliculus in 27 day old rats following chronic postnatal exposure to between 12 and 50 ppm CO beginning on the eighth day of life (Webber, 2003).…”

Section: Low Concentration Co Exposure and Subclinical Neurotoxicitymentioning

confidence: 99%

“…Expression of c-Fos, an indicator of neuronal activation following sound stimulation, was found to be significantly decreased in the central nucleus of the inferior colliculus in 27 day old rats following chronic postnatal exposure to between 12 and 50 ppm CO beginning on the eighth day of life (Webber, 2003). In addition, chronic postnatal exposure to 50 ppm CO beginning at the onset of myelination was shown to attenuate the amplitude of conduction of the eighth cranial nerve in newborn rats (Stockard-Sullivan, 2003). Interestingly, exposure to 100 ppm CO, yielding a mean COHb level of 10.2%, had no effect on eighth cranial nerve conduction suggesting that lower levels of CO exposure were responsible for the pathologic effects (Stockard-Sullivan, 2003).…”

Section: Low Concentration Co Exposure and Subclinical Neurotoxicitymentioning

confidence: 99%

“…In addition, chronic postnatal exposure to 50 ppm CO beginning at the onset of myelination was shown to attenuate the amplitude of conduction of the eighth cranial nerve in newborn rats (Stockard-Sullivan, 2003). Interestingly, exposure to 100 ppm CO, yielding a mean COHb level of 10.2%, had no effect on eighth cranial nerve conduction suggesting that lower levels of CO exposure were responsible for the pathologic effects (Stockard-Sullivan, 2003). In both of these studies, CO-induced defects persisted into adulthood and failed to recover completely, however, the exact mechanisms remain unknown (Stockard-Sullivan, 2003; Webber, 2003).…”

Section: Low Concentration Co Exposure and Subclinical Neurotoxicitymentioning

confidence: 99%

“…Interestingly, exposure to 100 ppm CO, yielding a mean COHb level of 10.2%, had no effect on eighth cranial nerve conduction suggesting that lower levels of CO exposure were responsible for the pathologic effects (Stockard-Sullivan, 2003). In both of these studies, CO-induced defects persisted into adulthood and failed to recover completely, however, the exact mechanisms remain unknown (Stockard-Sullivan, 2003; Webber, 2003). The authors of these investigations concluded that their results may have implications for auditory neuropathy acquired by children born to tobacco smoking mothers (Stockard-Sullivan, 2003).…”

Section: Low Concentration Co Exposure and Subclinical Neurotoxicitymentioning

confidence: 99%

See 2 more Smart Citations

Carbon monoxide pollution and neurodevelopment: A public health concern

Levy¹

2015

Neurotoxicology and Teratology

119

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Although an association between air pollution and adverse systemic health effects has been known for years, the effect of pollutants on neurodevelopment has been underappreciated. Recent evidence suggests a possible link between air pollution and neurocognitive impairment and behavioral disorders in children, however, the exact nature of this relationship remains poorly understood. Infants and children are uniquely vulnerable due to the potential for exposure in both the fetal and postnatal environments during critical periods in development. Carbon monoxide (CO), a common component of indoor and outdoor air pollution, can cross the placenta to gain access to the fetal circulation and the developing brain. Thus, CO is of particular interest as a known neurotoxin and a potential public health threat. Here we review overt CO toxicity and the policies regulating CO exposure, detail the evidence suggesting a potential link between CO-associated ambient air pollution, tobacco smoke, and learning and behavioral abnormalities in children, describe the effects of subclinical CO exposure on the brain during development, and provide mechanistic insight into a potential connection between CO exposure and neurodevelopmental outcome. CO can disrupt a number of critical processes in the developing brain, providing a better understanding of how this specific neurotoxin may impair neurodevelopment. However, further investigation is needed to better define the effects of perinatal CO exposure on the immature brain. Current policies regarding CO standards were established based on evidence of cardiovascular risk in adults with pre-existing comorbidities. Thus, recent and emerging data highlighted in this review regarding CO exposure in the fetus and developing child may be important to consider when the standards and guidelines are evaluated and revised in the future.

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Mild carbon monoxide exposure impairs the developing auditory system of the rat

Webber

Korsak

Sininger

et al. 2003

J of Neuroscience Research

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The object of this study was to determine if chronic exposure to mild concentrations of CO in air caused changes in the integrity of the inferior colliculus during the most active period of synaptogenesis/auditory development. We examined all subregions of the inferior colliculus (IC) of rats by immunocytochemical approaches after pups were exposed chronically to CO concentrations of, 0, 12.5, 25, and 50 ppm in air starting at Day 8 through 20-22 days of age. Mother-reared pups were compared to the gastrostomy-reared pups with or without CO exposure for basal neural activity, using c-Fos immunoreactivity as a marker. Half the rats were examined at 27 days of age, 5 days after the end of CO exposure, and the other half were examined 50 days later at 75-77 days of age. In the central nucleus of the IC, the number of cells expressing a basal level of c-Fos was decreased significantly in the CO-exposed animals when compared to controls; however, there was little or no difference in the number of cells expressing c-Fos in the other subregions of the IC. We conclude that the central nucleus of the inferior colliculus is affected selectively by mild CO exposure (0.0012% in air) and that this reduction in neuronal activity persists into adulthood.

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Mild carbon monoxide exposure and auditory function in the developing rat

Cited by 19 publications

References 63 publications

Brain responses to tonal changes in the first two years of life

Brain responses to tonal changes in the first two years of life

Carbon monoxide pollution and neurodevelopment: A public health concern

Mild carbon monoxide exposure impairs the developing auditory system of the rat

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