Biomedical subjects

D J Creel

Publications and source records attributed to D J Creel.

At least 37 records · Page 2Linked to original sources

PubMed1986

Reduced neuronal size and dendritic length in the medial superior olivary nucleus of albino rabbits.

We have previously demonstrated that circumscribed structural and functional abnormalities exist in the brainstem auditory system of albino cats. Anomalies in the auditory brainstem evoked response of albino cats were correlated with anatomical defects in the medial superior olivary nucleus (MSO) of the same animals. To examine whether a similar syndrome is present in other albino mammals, we studied the MSO of albino and pigmented rabbits using both Nissl-stained and Golgi-impregnated material. Neurons in the MSO of the albinos were significantly smaller (24%) than those in the pigmented rabbits and there was no overlap in the size distributions between the two groups. Neurons in the abducens nucleus of the albinos were also 14% smaller than in the pigmented rabbits, but this difference was not statistically reliable. The broad overlap in the distributions of neuronal size in the abducens nucleus between groups indicated that not all cells in the albino brainstem are significantly smaller than normal. In the Golgi-impregnated material, the mean total dendritic length for the 'marginal' cell type in the MSO was 39% shorter in albinos than in the pigmented animals. The branching density of dendrites was also significantly reduced in the albinos. Mean total dendritic length for cerebellar granule cells was a statistically insignificant 6% longer in the albinos, demonstrating that dendritic structure is not uniformly affected in all regions of the albino brain. The demonstration of similar anatomical differences in albino rabbits and cats indicates that whatever process produces these effects is not species-specific and may be common to the albinos of other mammalian species. The evidence that the amount of cochlear melanin may be related to differences in auditory function further suggests that the differences in the MSO of the albinos may ultimately be related to absence of inner ear pigmentation and not to other gene effects.

Albinism↗

PubMed1986

Differential susceptibility to noise-induced permanent threshold shift between albino and pigmented guinea pigs.

Evidence that reduced levels of cochlear melanin are associated with increased auditory sensitivity, increased levels of auditory fatigue and an increased susceptibility to noise-induced hearing loss led us to investigate the effects of noise exposure on the cochlear microphonic (CM) in albino and pigmented English shorthair guinea pigs. CMs were recorded from the round window prior to and at 90 min and 7 days after exposure to 45 min of 126 dB noise. Thresholds for the first detectable elicitation of the CM for four pure tones were determined and the output voltage of each cochlea was measured in 10 dB steps through intensity levels which produced a maximum voltage amplitude in the CM and voltage rollover. This analysis demonstrated that: albino guinea pigs displayed significantly lower auditory thresholds than did pigmented animals before exposure to noise; thresholds were elevated to comparable levels in both groups 90 min after noise exposure; pigmented guinea pigs showed a reliable recovery in CM thresholds 7 days after exposure to noise while thresholds in the albinos remained elevated to the same degree at both 90 min and 7 days after noise; 90 min after noise exposure, the maximum voltage output of albino cochleas was significantly less than that recorded from the cochleas of the pigmented guinea pigs. These results demonstrate that albino guinea pigs are more susceptible to the ototoxic effects of high intensity noise than pigmented guinea pigs. Converging evidence indicates that some aspects of cochlear function involve melanin pigment and that its absence may produce auditory abnormalities. Reduced melanin pigmentation may also contribute to such phenomena as noise-induced threshold shifts and individual differences in noise-induced hearing loss.

Albinism↗

PubMed1985

Abnormal visual pathways in normally pigmented cats that are heterozygous for albinism.

The various forms of albinism affect about one in 10,000 births in the United States. An additional 1 to 2 percent of the population has normal pigmentation but is heterozygous and carries a recessive allele for albinism. The retinogeniculocortical pathways were studied in normally pigmented cats that carry a recessive allele for albinism. The cats exhibited abnormalities in their visual pathways similar to those present in homozygous albinos. These results imply that visual anomalies like those found in albinos may be present in 1 to 2 percent of the human population.

Albinism↗

PubMed1985

Identification of minimal expression of myotonic dystrophy using electroretinography.

The electroretinograms (ERGs) of patients with definite myotonic dystrophy were studied as well as neurologically asymptomatic patients with minimal expression of myotonic dystrophy. Children in 4 families exhibited definite myotonic dystrophy when neither parent exhibited clinical or electromyographic signs of myotonic dystrophy. Myotonic dystrophy is dominantly inherited. We were able to identify the asymptomatic parent with the gene in these families. This study suggests that ERG testing, which includes scotopically balanced dim blue and red flashes, will identify some asymptomatic adults minimally expressing the gene for myotonic dystrophy.

Adolescent↗

PubMed1985

Retinal projections and functional architecture of cortical areas 17 and 18 in the tyrosinase-negative albino cat.

The visual field representation and functional architecture of cortical areas 17 and 18 in albino cats were studied. In the same animals the distributions of ipsilaterally and contralaterally projecting retinal ganglion cells were determined by injecting horseradish peroxidase into the dorsal lateral geniculate nucleus or optic tract. All cats were tyrosinase-negative albinos (cc), not deaf white cats (W). The proportion of ipsilaterally projecting ganglion cells in the temporal retina of the albino cat was found to be much smaller than in the normal cat or in the Siamese cat. In the albino cat less than 5% of ganglion cells in temporal retina project ipsilaterally. Recordings from areas 17 and 18 provided evidence of a substantial representation of the ipsilateral hemifield in albino visual cortex; cells representing the contralateral and ipsilateral hemifields were often segregated into alternating zones in area 17 and were always segregated in area 18. Cells recorded at the borders of zones representing the ipsilateral and contralateral hemifields often had abnormal properties. Some border cells had two receptive fields separated by as much as 60 degrees of azimuth; one field subserved the contralateral hemifield (contralateral nasal retina) and the other subserved the mirror-symmetric part of ipsilateral hemifield (contralateral temporal retina). Receptive fields of cells subserving the two hemifields did not differ in size. The preferred orientations, preferred velocities, and other characteristics of the two fields were approximately the same; preferred orientation changed gradually and systematically across the borders of zones representing the two hemifields. Our results indicate that afferents representing nasal and temporal regions of retina of the same eye can segregate and form "hemiretina" domains in albino visual cortex. These afferents can also converge upon individual cortical cells in a fashion reminiscent of convergence of afferents from the two eyes upon binocular cells in the normal cortex. The organization of albino visual cortex is therefore different from the organization of Siamese visual cortex. This may be because, in the albino cat but not the Siamese cat, nearly all cells in temporal retina project contralaterally; afferents representing contralateral temporal retina are not at a significant competitive disadvantage in the albino.

Albinism↗

PubMed1985

Effects of glycine on hemodynamic responses and visual evoked potentials in the dog.

To study the potential contribution of glycine toxicity in the transurethral resection syndrome, we evaluated hemodynamic and visual evoked potential responses to glycine infusion (1 g/kg) in 22 dogs anesthetized with halothane (1.0-1.2% end tidal. Three dogs received 5% glucose in normal saline without glycine; three received arginine (4 mg/kg) in normal saline without glycine; three received arginine (4 mg/kg) in normal saline without glycine; 10 received glycine (1 g/kg), then arginine (4 mg/kg) 120 min after the completion of glycine infusion; and six received arginine 30 min after the completion of glycine infusion. Arginine was infused to evaluate potential antagonistic effects of glycine toxicity. Blood levels of glycine, ammonia, arginine, urea, and formate were determined after infusions of glycine or arginine. All animals received about 5 ml X kg-1 X hr-1 of normal saline during the 2-4 hr of study. Immediately after glycine infusion, cardiac output increased 57%, whereas systemic vascular resistance and mean arterial pressure decreased 32% and 8%, respectively. Later cardiac output and mean arterial pressure were 41% and 18% less than control levels, whereas systemic vascular resistance returned to control levels. Both amplitude and latency of visual evoked potential waveforms were altered in the animals receiving glycine infusion but not in the control animals. These responses were associated with elevations of blood glycine (149 +/- 5 to 9591 +/- 809 microM/L, mean + SEM) and blood NH3 (10.5 +/- 2.8 to 100.0 +/- 13.6 microM/L), but not with formate levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonia↗

PubMed1984

Auditory brainstem anomalies in albino cats: II. Neuronal atrophy in the superior olive.

In a previous paper (Brain Res., 260:1-9, 1983) we reported that albino cats show abnormal auditory brainstem evoked responses that appear to arise from structural defects in or near the superior olivary complex. In the present study, neuronal cross-sectional area in brainstem nuclei was compared in albino and normally pigmented adult cats. The albinos were true tyrosinase-negative (cc) and should not be confused with the deaf white cat (W); the albinos are not deaf. Neurons in the medial superior olivary nucleus (MSO) of albinos were, on average, 41% smaller than in pigmented animals; there was no overlap in the neuronal size distributions for the two groups of animals. Cell size in the lateral superior olive, medial nucleus of the trapezoid body, ventral nucleus of the lateral lemniscus, anteroventral cochlear nucleus, dorsal cochlear nucleus, and facial nucleus was also smaller (by 9-21%) in albinos than in pigmented animals but none of these differences was statistically reliable. In the abducens nucleus, neurons were 12% larger in albinos than in pigmented animals, demonstrating that neuronal size in the albinos is not uniformly smaller. Several lines of evidence suggest that the auditory system defects in albinos are related to abnormal pigmentation rather than to other gene effects. It is possible that a subtle pigment-related disruption of inner ear development in albinos results in a central cascade of atrophic changes along the auditory pathway.

Animals↗

PubMed1984

Auditory brain-stem responses in Marcus Gunn ptosis.

The auditory brain-stem response (ABR) can detect anomalies both in the auditory pathways and in structures adjacent to these pathways. Patients with Duane's retraction syndrome, associated with hypoplasia of the abducens nerve in the brain-stem, and patients with hemifacial spasm, due to compression of the facial nerve in the brain-stem, have been found to have abnormal ABRs. Marcus Gunn ptosis with 'jaw winking' is considered to be due to misconnection of oculomotor, trigeminal and other cranial nerves. Suspecting that perhaps some 'jaw-winking' phenomena may be due to detectable brain-stem anomalies we tested 7 patients with Marcus Gunn ptosis. Three of the patients demonstrated abnormal ABRs indicative of pontine pathology.

Adolescent↗

PubMed1974