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Biomedical subjects

M A Sikora

Publications and source records attributed to M A Sikora.

12 recordsLinked to original sources
PubMed2001

Structure and functional connections of presynaptic terminals in the vertebrate retina revealed by activity-dependent dyes and confocal microscopy.

The fluorescent dyes sulforhodamine 101 (SR 101) and FM1-43 were used as activity-dependent dyes (ADDs) to label presynaptic terminals in the retinas of a broad range of animals, including amphibians, mammals, fish, and turtles. The pattern of dye uptake was studied in live retinal preparations by using brightfield, fluorescence, and confocal microscopy. When bath-applied to the retina-eyecup, these dyes were avidly sequestered by the presynaptic terminals of virtually all rods, cones, and bipolar and amacrine cells; ganglion cell dendrites and horizontal cells lacked significant dye accumulation. Other structures stained with these dyes included pigment epithelial cells, cone outer segments, and Müller cell end-feet. Studies of dye uptake in dark- and light-adapted preparations showed significant differences in the dye accumulation pattern in the inner plexiform layer (IPL), suggesting a dynamic, light-modulated control of endocytotic activity. Presynaptic terminals in the IPL could be segregated on the basis of volume: bipolar varicosities in the IPL were typically larger than those of amacrine cells. The combination of retrograde labeling of ganglion cells and presynaptic terminal labeling with ADDs served as the experimental preparation for three-dimensional reconstruction of both structures, based on dual detector, confocal microscopy. Our results demonstrate a new approach for studying synaptic interactions in retinal function. These findings provide new insights into the likely number and position of functional connections from amacrine and bipolar cell terminals onto ganglion cell dendrites.

Adaptation, Ocular↗
PubMed1985

Sensorineural hearing loss in experimental purulent otitis media due to Streptococcus pneumoniae.

Sensorineural hearing loss (SNHL) has been described clinically following chronic otitis media with effusion, but to the best of our knowledge, no studies have demonstrated SNHL in an animal model of otitis media. Using the chinchilla model of pneumococcal otitis media, significant SNHL was demonstrated after purulent otitis media, especially at higher frequencies. Animals with otitis media received penicillin G procaine treatment for five days after otitis media with effusion (OME) was first documented; resolution of middle ear infection was confirmed by middle ear effusion culture in all animals. Both the inoculated and uninoculated ears were examined by tone burst-elicited compound action potential at threshold. The inoculated ear showed a marked hearing loss of 13 to 36 dB three to four days after OME was first documented; a hearing loss up to 24 dB persisted two to five weeks after inoculation. The change in the compound action potential was highly significant at all frequencies studied. Conductive losses were largely ruled out because there was no middle ear effusion at death and the tympanogram was normal. Purulent labyrinthitis was ruled out by histopathological study. These results indicate that purulent pneumococcal otitis media in the chinchilla model causes significant SNHL and suggest that the pathogenesis of SNHL associated with chronic OME in humans may be studied in this model.

Animals↗
PubMed1983

Compound action potential input-output decruitment. Effect of topically applied antiseptics.

The ototoxic effect of povidone-iodine antiseptics topically applied to the chinchilla round window was examined with particular emphasis on the action potential (AP) input-output function at 2 and 4 kHz. A group of chinchillas exhibited a marked elevation of AP threshold at 8 and 12 kHz, with only a slight threshold elevation at 2 and 4 kHz. A distinct decruitment (less than normal growth of response with increasing sound intensity) of the AP input-output function was, however, found at the lower frequencies. There are implications of an ototoxically induced high-frequency hearing loss on speech frequencies.

Action Potentials↗
PubMed1983

N1 latency following acute pure-tone trauma.

The latency of the N1 component of tone burst evoked compound action potentials was examined in chinchilla following acute pure-tone trauma. At and below the trauma frequency (4 kHz) the N1 latency at threshold generally increased, while above the trauma frequency it decreased; tonotopically paralleling pitch shifts observed in humans following pure-tone trauma. When N1 latency at threshold is considered across animals as a linear function of dB SPL at threshold, after trauma a high degree of linear correlation was found at 6 and 8 kHz, while a low degree of linear correlation was found at 4 kHz. An interpretation and the significance of the data are discussed.

Animals↗
PubMed1983

Tympanostomy tubes and otic drops.

Otic drops have been proposed as a form of prophylaxis against the otitis media which follows middle ear contamination by water in patients with tympanostomy tubes. The potential adverse effects of this form of therapy were studied in chinchillas with tympanostomy tubes; 31 chinchillas underwent bilateral tympanostomy tube insertion. Seven animals had a mixture of green dye and Cortisporin otic suspension placed in both external auditory canals 24 hours following the placement of tympanostomy tubes and were sacrificed 30 minutes later for gross examination; 3 of these animals had previous eustachian tube obstruction with Silastic sponge. Twenty-one animals had Cortisporin otic suspension placed in the right external auditory canal on postoperative days 3, 4, 5, 6 and 7. No otic drops were placed in the left ear. Ten of these 20 animals had VIIIth nerve action potentials measured on postoperative day 17 and the other 11 animals had VIIIth nerve action potentials measured on postoperative day 42 followed by immediate sacrifice for histological examination and scanning electronmicroscopy. The remaining 3 animals had VIIIth nerve action potentials measured 21 days following tympanostomy tube insertion and served as electrophysiological controls. The 8 ears receiving Cortisporin otic drops mixed with green dye from animals with normal eustachian tubes showed staining of the round window membrane at sacrifice, while the 6 ears receiving Cortisporin otic suspension and green dye from animals with eustachian tube obstruction demonstrated no dye in the middle ear. All animals receiving Cortisporin otic drops in the right ear showed an intra-aural difference in action potentials with the right ear being attenuated by an average of 10.3 dB at 2,000 Hz, 12 dB at 4,000 Hz, 21 dB and 8,000 Hz, and 26 dB at 12,000 Hz. Morphological study revealed hair cell loss in the hook portion of the cochlea in those animals receiving Cortisporin otic drops. It was concluded from this study that, in patients with patent tympanostomy tubes in place, potentially ototoxic topical agents should be used with caution.

Action Potentials↗
PubMedDate not supplied

Neurophysiologic assessment of endolymphatic hydrops.

An electrophysiological method for assessing endolymphatic hydrops of the cochlea in an animal model of Meniere's disease is described. Eighth nerve gross action potentials (AP) were evoked by tone bursts presented at discrete phases of a simultaneously delivered 50-Hz pure tone. Hydropic cochleas showed significantly less modulation of AP amplitude and latency than normal cochleas. This method may be useful in objectively evaluating Meniere's disease with electrocochleography.

Animals↗
PubMedDate not supplied

Measurement of action potential thresholds in experimental endolymphatic hydrops.

Unilateral experimental endolymphatic hydrops was created by endolymphatic sac and duct obstruction in guinea pigs. Studies of action potential (AP) threshold were then performed and compared with histologic findings. Action potential thresholds were significantly increased in the hydrops ears. The close relationship between AP changes and hydrops was sufficient to allow the detection of hydrops by AP threshold measurements alone. The AP threshold changes were positively related to the degree of hydrops and postoperative interval in a manner consistent with hearing changes seen in Meniere's disease. Based upon the foregoing, experimental endolymphatic hydrops appears to be a valid and usable model for the study of the cochlear aspects of Meniere's disease.

Action Potentials↗
PubMedDate not supplied

Experimental hypercholesterolemia and auditory function in the chinchilla.

Possible harmful effects of a high-cholesterol diet on auditory function were suggested by our previous work in rabbits, in which evoked potentials were measured from a chronic electrode inserted into the inferior colliculus. However, serum cholesterol levels in those rabbits tended to be extraordinarily high, i.e., more than 1,500 mg/dL. Chinchillas were used in the present work as an animal model to study the relationship between hypercholesterolemia and auditory dysfunction. One percent cholesterol in standard Chinchow was fed to chinchillas for three months. The experimental groups showed a high mean cholesterol level of 437 +/- 394 mg/dL (N = 9). Isopotential curve of the cochlear microphonics, threshold of action potentials (AP), and endocochlear DC potential did not differ from those in the control group. When moderately intense sound (12 kHz, 95 dB SPL) was given for ten minutes, however, the reduction in AP threshold was significantly greater (P = .036) in the cholesterol group. It is postulated that hypercholesterolemia may be one of the factors involved in differential susceptibility to noise.

Animals↗
PubMedDate not supplied

Ototoxicity of ethanol in the tympanic cleft in animals.

This work was undertaken to study the ototoxicity of topically applied ethanol in quantitative terms. Using guinea pigs, ethanol was administered (1) on the round window for 10 min, (2) instilled in the middle ear cavity for 24 hours, and (3) perfused into the cochlear canal (into the scala tympani) at the rat of 10 microliter/min for 10 min. Cochlear microphonics from the electrode on the round window were recorded. The critical concentration (the maximum dilution ratio) of the ethanol that appears to be ototoxic in the experimental condition mentioned above was determined to be (1) 50%, (2) 10%, (3) 0.1% respectively. Using chinchillas, the effect of ethanol with round window application on the Endocochlear Potential (EP) was studied. Simultaneous recording of EP from the 1st and 3rd turn of the cochlea showed a more marked decline in EP in the 1st turn. 70% ethanol caused an irreversible, plateauing decline in EPO, while 35% ethanol caused a reversible decline in EP.

Action Potentials↗
PubMedDate not supplied

Hyperlipidemia and noise in the chinchilla.

Chinchillas were maintained on a 1% cholesterol diet for 6 months. Auditory Brainstem Response (ABR) measurements were obtained before and at 1, 3, 5, and 6 months after initiation of diet. Compound Action Potential (AP) measurements were obtained at sacrifice at 6 months. A significant reduction in ABR was seen at 5 months-on-diet. At 5 months, the animals were exposed to a 2 octave bandpass noise centered at 1 kHz at 105 dB for 220 min. One month following noise exposure, the cholesterol-fed animals exhibited a greater ABR latency shift at low intensities, and an elevated AP threshold at higher frequencies, vis-à-vis a control group.

Animals↗
PubMedDate not supplied

Diet-induced hyperlipidemia and auditory dysfunction.

Chinchillas rendered hyperlipidemic by a 1% cholesterol diet or maintained on a normal diet were either exposed to a 2-octave bandpass noise (700-2,800 Hz for 220 min at 105 or 114 dB) or else not exposed to noise. The animals were assessed with tone-burst (2-16 kHz) elicited compound action potentials (CAP). Compared with normal diet animals, the hyperlipidemic animals: not exposed to noise exhibited elevated thresholds at 8 kHz and higher frequencies; exposed to 105-dB noise exhibited elevated thresholds at 16 kHz; and exposed to 114-dB noise exhibited elevated thresholds at 2-16 kH. Surface preparations were made of the left cochleae of all noise-exposed animals. There was essentially no difference in hair cell counts between hyperlipidemic animals exposed to the 105-dB noise and normal animals similarly exposed. The hyperlipidemic animals exposed to the 114-dB noise exhibited a greater hair cell loss in the first turn of the cochlea than did similarly exposed normal animals. We conclude that maintenance on a high-cholesterol diet can cause a high-frequency hearing loss, probably due to vascular pathology resulting from a hyperlipidemic state. Furthermore, maintenance on a high-cholesterol diet can increase susceptibility to noise-induced hearing losses.

Animals↗