Experimental neurology
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Experimental neurology · Jan 1992
Video-enhanced DIC images of the noise-damaged and regenerated chick tectorial membrane.
Exposure of the chick cochlea to acoustic overstimulation results in a loss of hair cells and a disruption of the tectorial membrane. With time, new hair cells are produced to replace those that are lost and, concurrently, a new tectorial membrane is regenerated. Previous studies of tectorial membrane regeneration examined tissues that were fixed and processed for scanning and transmission electron microscopy. ⋯ Examination of the unfixed membrane immediately after noise exposure shows that the damage to the tectorial membrane is actually caused by the acoustic trauma and is not an artifact of fixation. After 14 days of recovery, a thick, honeycomb of new matrix has grown from the supporting cells in the basilar papilla and has formed new connections with the stereocilia of surviving and regenerating hair cells. Moreover, this new honeycomb has fused with the remainder of the surrounding, undamaged tectorial membrane, thus reestablishing a continuity in the structure of the membrane across both the damaged and undamaged regions of the basilar papilla.
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Experimental neurology · Jan 1992
The structural and functional aspects of hair cell regeneration in the chick as a result of exposure to intense sound.
This paper summarizes the structural and functional damage caused by intense sound exposure in neonatal chicks. Scanning electron microscopy has been used to follow the structural changes to the papilla and their subsequent repair. Pure-tone exposures produced a localized lesion consisting of tectorial membrane destruction, changes in surface organization of the papilla, and hair cell loss. ⋯ Auditory function returned to near normal levels within 3 days postexposure. The inescapable conclusion from these observations was that hair cell regeneration had little to do with the functional recovery observed during the first 3 days. Tectorial membrane regeneration and the restoration of cochlear micromechanics were combined to form a hypothesis to account for the restoration of auditory function.
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Experimental neurology · Sep 1991
Loss of intensity-induced inhibition in inferior colliculus neurons leads to audiogenic seizure susceptibility in behaving genetically epilepsy-prone rats.
The genetically epilepsy-prone rat (GEPR) exhibits elevated seizure sensitivity and audiogenic seizures (AGS). The inferior colliculus (IC) is the most critical brain region for AGS initiation. The present study evaluated IC neuronal firing and convulsive behavior simultaneously in freely moving GEPRs. ⋯ The diminished efficacy of these forms of GABA-mediated acoustically evoked inhibition in the GEPR IC extends previous results, showing reduced effectiveness of exogenously applied GABA and benzodiazepine in GEPR IC neurons. This reduced effectiveness of GABA-mediated inhibition along with excess excitant amino acids in GEPR IC, previously reported, appear to be vital neurotransmitter mechanisms, subserving the exaggerated output of IC neurons at high acoustic intensities. This exaggerated IC firing may be instrumental in seizure initiation in this epilepsy model.
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Experimental neurology · Sep 1990
Trophic influence of the distal nerve segment on GABAA receptor expression in axotomized adult sensory neurons.
The depolarizing action of gamma-aminobutyric acid (GABA), or the GABAA receptor agonist muscimol, on rat dorsal root (L4 and L5) fibers is attenuated following transection, but not crush, of the sciatic nerve. Following discrete nerve crush, axons actively regenerate and contact both the distal nerve segment and the peripheral target tissues. The aim of the present study was to distinguish between these two regions as possible sources of trophic support for retrograde maintenance of dorsal root GABA receptor sensitivity. ⋯ Under these conditions, the injury-induced decrement in the dorsal root GABA response, observed between 12 and 21 postoperative days, was significantly attenuated relative to that of ligated nerves, in which regeneration into the distal stump does not occur. The data suggest that nerve transection by ligation restricts trophic support for maintenance of GABA receptor expression in dorsal root ganglion (DRG) neurons. Furthermore, during regeneration the denervated distal nerve segment assumes a neurotrophic role in the maintenance of dorsal root GABA sensitivity, consistent with the hypothesis that growth factors derived from reactive Schwann cells may positively regulate the expression of receptors on axotomized sensory neurons.
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Experimental neurology · Jan 1989
Correlative analyses of lesion development and functional status after graded spinal cord contusive injuries in the rat.
The development of both histopathological changes and functional deficits was quantitatively assessed after mild, moderate, and severe spinal cord contusive injuries. The cross-sectional area of the spinal cord at the epicenter (region of maximal damage) and the areas of hemorrhage, lesion, and remaining gray and white matter were determined from 15 min to 8 weeks after injury. From 24 h to 8 weeks after injury, functional deficits were quantified using a combined behavioral score (CBS) based on the results from a number of behavioral tests of function. ⋯ The development of stable functional deficits was observed beginning at 3 weeks after injury. There was a significant correlation between residual white matter and the degree of initial injury at 24 h after injury and all subsequent time points. However, a significant correlation between residual white matter and functional deficit, as measured by the CBS, was not observed at 24 h or 1 week but did develop by 4 weeks after injury.