Biomedical subjects

J S Gross

Publications and source records attributed to J S Gross.

At least 19 recordsLinked to original sources

PubMed2002

Synaptophysin in the cochlear nucleus following acoustic trauma.

Chinchillas are notable for a low-frequency hearing range similar to that of humans and a marked sensitivity to loud noise. A single noise exposure that produces cochlear damage may lead to progressive loss of synaptic endings in the cochlear nucleus, followed by new axonal growth. As an index of synaptic regulation during such changes, we have examined the expression of a synaptic vesicle protein, synaptophysin, in the cochlear nucleus following a damaging acoustic stimulus in adult chinchillas. With one ear protected by a plug, following a 3-h exposure to an octave-band noise of 108 dB sound pressure level, centered at 4 kHz, the unprotected cochlea and the cochlear nuclei exhibited degeneration of hair cells and axons over periods of 7, 14, 30, 90, and 150 days. Axonal degeneration, as revealed by a silver degeneration method, was heavy ipsilateral to the cochlear damage, but sparse degeneration also appeared on the contralateral, unexposed side. Synaptophysin immunostaining underwent a major, bilateral decline in the anteroventral and posteroventral cochlear nuclei, interrupted at intervening periods by transient increases in the numbers of stained structures. A distinction in staining between large perisomatic structures and smaller puncta in the neuropil and between the dorsal and the ventral zones of the ventral cochlear nuclei revealed some variations in the response and degree of recovery of synaptophysin staining. These findings could best be explained by degeneration of synaptic endings followed by new growth of terminals and by regulatory changes in the levels of synaptophysin expression and synaptic vesicle accumulation over time.

Acoustic Stimulation↗

PubMed1997

Synaptophysin immunoreactivity in the cochlear nucleus after unilateral cochlear or ossicular removal.

This study determined if unilateral cochlear removal in adult guinea pigs led to synaptic loss followed by synaptogenesis in the cochlear nucleus (CN) and if unilateral middle ear ossicle removal led to synaptic loss in the CN. Synaptic endings were identified immunohistochemically, using a monoclonal antibody to synaptophysin. Immunolabeling was quantified densitometrically in the CN 4-161 days after cochlear removal and 161 days after ossicle removal. Fiber degeneration was visualized with the Nauta-Rasmussen silver method. Tissue shrinkage was measured from drawings of CN sections. Compared to the contralateral side, immunolabeling density ipsilaterally was reduced by 4 days in the anterior division of the anteroventral CN (a-AVCN) and by 7 days in the anterior part of the posteroventral CN (a-PVCN). At 7 days, preterminal fiber degeneration was abundant in both areas. These findings were consistent with the loss of cochlear nerve endings and fibers. At later times, immunolabeling density recovered. In the a-AVCN, tissue shrinkage explained approximately half the recovery of staining density; the rest was attributed to synaptogenesis. In the a-PVCN, the entire recovery was attributed to tissue shrinkage. In the polymorphic layer of the dorsal CN, immunostaining density increased transiently at 4 days, while at 7 days preterminal fiber degeneration was abundant. A net loss of synaptic endings was not detected immunohistochemically. The increased immunostaining density may reflect a transient growth of immature processes or presynaptic endings. Ossicle removal produced a deficit in immunolabeling density only in the ipsilateral a-PVCN, without fiber degeneration, suggesting a loss of presynaptic endings or of synaptophysin expression.

Afferent Pathways↗

PubMed1997