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Biomedical subjects

J F Willott

Publications and source records attributed to J F Willott.

72 records · Page 4Linked to original sources
PubMed1979

Development of inferior colliculus response properties in C57BL/6J mouse pups.

Response properties of inferior colliculus (IC) neurons were studied in traquilized C57BL/6J mice during a period of rapid auditory system development between 12 and 17 days of age. In IC units of the youngest mice, spontaneous activity was absent, a disproportionate number of onset responses was observed, and many units were not securely driven by sound. Frequency response ranges were restricted to relatively low frequencies, sharpness of tuning was poor, and thresholds at best frequencies (BFs) were quite high. Dynamic intensity ranges were restricted, but nonmonotonic functions were observed. By 15--17 days of age, spontaneous activity was appreciable, incidences of response patterns were near adult proportions, and most units in the ventrolateral nucleus were securely driven by tones. Response ranges had expanded markedly to include high frequencies, sharpness of tuning increased, and thresholds had decreased. Dynamic intensity ranges and intensity functions were similar to those observed in adult mice.

Acoustic Stimulation↗
PubMed1979

Changes in brain levels of NE and 5-HT are not responsible for attenuation of audiogenic seizures by spinal cordotomy.

Spinal cord transection affords protection from audiogenic seizures (anterior to paralysis) in 21 day-old DBA/2J mice. To test the possibility that altered brain levels of NE or 5-HT are involved in mediating this effect, whole brain levels of these amines were assayed in cordotomized and control DBA/2J mice, aged 21 days. The assay revealed no significant differences between cordotomized and control mice. Therefore, cordotomy protects mice from seizures by mechanisms other than altering brain levels of NE or 5-HT.

Acoustic Stimulation↗
PubMed1977

Audiogenic seizures in curarized mice.

Previous experiments have indicated that interference with somatosensory feedback from convulsive movements may lessen the severity of audiogenic seizures in susceptible rodents. For further investigation of this phenomenon, mice were partially immobilized with tubocurarine chloride to attenuate convulsive movements and somatosensory input associated with such movements. In Experiment 1, seizures of mice injected with .15 mg/kg were evaluated behaviorally and compared with seizures of saline-injected litter-mates. The likelihood of clonic-tonic seizures in curarized mice was as high as that of control mice, although convulsive movements were somewhat less violent and seizure fatalities were markedly reduced. In Experiment 2, seizures of mice given .25 mg/kg were evaluated with electroencephalography, and records were compared with those of controls. Despite the near absence of behavioral signs of convulsions, electroencephalograms of curarized mice showed that audiogenic seizures readily occurred. The findings suggest that audiogenic seizures are centrally "programmed" and do not require feedback from convulsive movements. However, it may be possible to disrupt the central "program" by introducing appropriate somatosensory input not normally encountered during audiogenic seizures.

Acoustic Stimulation↗
PubMed1976

Roles of anoxia and noise-induced hearing loss in the postictal refractory period for audiogenic seizures in mice.

The present series of experiments demonstrated a postictal refractory period for audiogenic seizures in DBA/2J mice, which was not related to hearing loss but apparently was related to anoxia. Unlike many previous studies, Experiment 1 controlled for the effects of noise exposure upon hearing sensitivity and demonstrated reduced susceptibility to subsequent audiogenic seizures for at least 1 hr after initial clonic-tonic convulsions. The postictal refractory period was shown to result from the occurrence of seizures per se, not from noise exposure alone. Experiment 2 demonstrated deficiencies of sensorimotor functions that accompanied reduced postictal seizure susceptibility. The two phenomena had similar time courses of recovery, which suggested a common mechanism, probably anoxia, associated with the initial convulsions. In support of this view, Experiment 3 showed that recovery from both phenomena was expedited by allowing subjects to breathe increased O2. The role of anoxia in fatal convulsions was suggested by the finding that subjects experiencing clonic-tonic convulsions in a high-O2 environment survived without exception. In contrast, seizures of air-breathing controls were almost always fatal. Taken together, the data indicate that the postictal reduced susceptibility to audiogenic seizures was closely related to metabolic depletion (in particular, anoxia). The pattern of recovery of susceptibility further suggests that the effects of anoxia impair the spread of seizure activity through the central nervous system, although the initiation of seizures is also affected for a short time.

Anesthesia, Inhalation↗
PubMedDate not supplied

Ultrastructural features of neurons in the C57BL/6J mouse anteroventral cochlear nucleus: young mice versus old mice with chronic presbycusis.

Transmission electron microscopy was used to examine "bushy" and "multipolar" neurons in the anteroventral cochlear nucleus (AVCN) of young (2-month-old) and old (2-year-old) C57BL/6J mice, a strain that develops profound peripheral sensorineural auditory impairment during the second year of life. Two features differed with age irrespective of cell type or location within the AVCN: there was an increase in the incidence of neurons with heterochromatic nuclei and an increase in the percent of the neuron occupied by lipofuscin. Two features differed with age in multipolar cells only: there was a decrease in the roundness of nuclei and an increase in the number of nuclear invaginations. Some features differed with age to a greater extent in the dorsal portion of the AVCN: there were decreases in the length of terminals on bushy cells, and in the percentage of soma surface apposed by terminals, and increases in the incidence of neurons contacted by myelinated axons, in mean synaptic vesicle density, and in the amount of lipofuscin in bushy cells. Some features did not differ with age: the mean area of mitochondria, percentage of cytoplasm occupied by mitochondria, size of dense synaptic junctions, and for bushy cells only, nuclear shape and invaginations and width of perinuclear cisternae. Aging per se, chronic presbycusis, and neuronal type play roles in determining age-related changes in AVCN neurons.

Age Factors↗
PubMedDate not supplied

Morphology of the inferior colliculus in C57BL/6J and CBA/J mice across the life span.

Basic anatomical features were evaluated in the inferior colliculus (IC) of C57BL/6J and CBA/J mice across the adult life span (1.5 to 30 months of age). C57BL/6J mice exhibit progressive age-related cochlear pathology and become severely hearing-impaired during the second year of life; CBA/J mice exhibit little hearing loss as they age. Age had little effect on the size of the IC, the size of IC neurons, or the packing density of IC neurons and there was no evidence of age-related neuron loss. However, old CBA/J mice developed numerous spongiform lesions throughout the brainstem. The absence of morphological changes in the IC of hearing-impaired C57BL/6J mice supports the hypothesis that features such as the size of neurons, survival of neurons, and volume of the neuropil are not affected by chronic sensorineural pathology in central auditory nuclei (e.g., as the IC) that do not receive direct input from primary afferent fibers. The data from both strains taken together indicate that certain basic anatomical properties of the mouse IC persist in the face of aging.

Aging↗
PubMedDate not supplied

Modulation of presbycusis: current status and future directions.

Literature and ideas are reviewed concerning the modulation of presbycusis - the influence of variables that can alter the severity and/or time course of presbycusis or counteract its negative aspects. Eleven topics are identified: variables related to biological aging; genetics; noise-induced hearing loss; moderately augmented acoustic environment; neural plasticity and the central auditory system; neural plasticity and hearing aids; socioeconomic and cultural barriers to hearing aid use; lifestyle (diet, exercise, etc.); medical variables; pharmaceutical interventions for presbycusis, and cognitive variables. It is concluded that the field of otogerontology will best be served by a comprehensive, integrative interaction among basic researchers and clinical scientists who will continue to learn how the auditory problems associated with presbycusis can be intentionally modulated in beneficial ways.

Age Factors↗