Cherylea Browne - Academia.edu (original) (raw)
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Southern Illinois University School of Medicine
Southern Illinois University School of Medicine
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Papers by Cherylea Browne
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2010
Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We te... more Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We tested the hypothesis that nicotine increases expression of the nicotinic acetylcholine receptor (nAChR) subunits alpha7 and beta2 in a piglet model. Piglets exposed to 2mg/kg/day nicotine for 14 days postnatally (n=14) were compared to non-exposed controls (n=14), (equal gender proportions). Immunohistochemistry was performed to identify and quantify changes in, alpha7 and beta2 nAChR subunits in 8 nuclei of the medulla at both the rostral and caudal levels. Compared to controls, nicotine exposed piglets had decreased alpha7 in the rostral dorsal motor nucleus of the vagus (rDMNV) (p=0.01), and increased beta2 in the caudal DMNV (cDMNV) (p=0.05), caudal nucleus of the spinal trigeminal tract (cNSTT) (p=0.03) and caudal nucleus of the solitary tract (cNTS) (p=0.04). Analysis by gender showed that in the control group, compared to males, females had higher beta2 in the caudal hypoglossal (c...
PloS one, 2012
Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These patholog... more Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We ...
International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience, 2010
Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We te... more Exposure to cigarette smoke is a major risk factor for sudden infant death syndrome (SIDS). We tested the hypothesis that nicotine increases expression of the nicotinic acetylcholine receptor (nAChR) subunits alpha7 and beta2 in a piglet model. Piglets exposed to 2mg/kg/day nicotine for 14 days postnatally (n=14) were compared to non-exposed controls (n=14), (equal gender proportions). Immunohistochemistry was performed to identify and quantify changes in, alpha7 and beta2 nAChR subunits in 8 nuclei of the medulla at both the rostral and caudal levels. Compared to controls, nicotine exposed piglets had decreased alpha7 in the rostral dorsal motor nucleus of the vagus (rDMNV) (p=0.01), and increased beta2 in the caudal DMNV (cDMNV) (p=0.05), caudal nucleus of the spinal trigeminal tract (cNSTT) (p=0.03) and caudal nucleus of the solitary tract (cNTS) (p=0.04). Analysis by gender showed that in the control group, compared to males, females had higher beta2 in the caudal hypoglossal (c...
PloS one, 2012
Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These patholog... more Excessive exposure to loud noise can damage the cochlea and create a hearing loss. These pathologies coincide with a range of CNS changes including reorganisation of frequency representation, alterations in the pattern of spontaneous activity and changed expression of excitatory and inhibitory neurotransmitters. Moreover, damage to the cochlea is often accompanied by acoustic disorders such as hyperacusis and tinnitus, suggesting that one or more of these neuronal changes may be involved in these disorders, although the mechanisms remain unknown. We tested the hypothesis that excessive noise exposure increases expression of markers of excitation and plasticity, and decreases expression of inhibitory markers over a 32-day recovery period. Adult rats (n = 25) were monaurally exposed to a loud noise (16 kHz, 1/10(th) octave band pass (115 dB SPL)) for 1-hour, or left as non-exposed controls (n = 5). Animals were euthanased at either 0, 4, 8, 16 or 32 days following acoustic trauma. We ...