The effects of congenital deafness on auditory nerve synapses and globular bushy cells in cats.

It is well known that auditory deprivation affects the structure and function of the central nervous system. Congenital deafness represents one form of deprivation, and in the adult white cat, it has been shown to have a clear effect upon the synaptic interface between endbulbs of Held and spherical bushy cells. It is not known, however, whether all primary synapses are affected and/or whether they are affected in the same way and to the same extent. Thus, we studied a second neuronal circuit in the deaf white cat involving modified (small) endbulbs and globular bushy cells. Compared to normal hearing cats, modified endbulbs of congenitally deaf cats were 52.2% smaller but unchanged in structural complexity. There was also a striking loss of extracellular space between ending and cell body. The somata of postsynaptic globular bushy cells were 13.4% smaller and had enlarged postsynaptic densities. These data reveal that axosomatic synapses demonstrate abnormal structure as a consequence of deafness and that the extent of the abnormalities can vary with respect to the circuits involved. The implication of these observations is that synaptic anomalies would introduce differential delays within separate circuits, thereby desynchronizing neural activity from sound stimuli. This loss of synchronization could in turn disrupt temporal processing and compromise a host of related functions, including language comprehension.

Minimally invasive device to effect vocal fold lateralization.

Despite many operative procedures focused on vocal fold lateralization, none has achieved an acceptable level of dependability. Bilateral vocal fold abductor paralysis is treated by arytenoidectomy, cordotomy, suture lateralization, or partial cordectomy. Tracheotomy remains the gold standard for maximizing the airway and preserving phonatory function. We have developed a device that is minimally invasive, tunable, and reversible, with the potential for lateralization or medialization of the vocal process. The device consists of a polyethylene collar, a Vitallium cam, and a double-helix core for engaging soft tissue. It is introduced through a circular opening in the thyroid cartilage by a modified thyroplasty approach. Both the first and second iterations of this device have been evaluated for clinical effectiveness in 9 sheep by means of photographic and video documentation. Effectiveness in humans is currently being assessed. The results of the animal study permit us to have substantial optimism with respect to the clinical application of this device.

Therapeutic hypothermia is cytoprotective without attenuating the traumatic brain injury-induced elevations in interstitial concentrations of aspartate and glutamate.

Moderate hypothermia has been shown to have therapeutic utility in the treatment of cerebral ischemia and to attenuate the rise in interstitial concentrations of the excitatory amino acid neurotransmitter L-glutamate. In this study, the influence of hypothermia on traumatic brain injury (TBI) was assessed using a controlled cortical impact model. Rats were cooled to 32.0-33.0 degrees C at least 30 min before injury and maintained at this temperature for 2 h after injury. The influence of hypothermia on the immediate increase in interstitial concentrations of aspartate and glutamate and the volume of the resultant lesion 14 days after TBI was then determined. The volume of the lesion (mean +/- SEM) in hypothermic animals (8.2 +/- 1.3 mm3, n = 9) was significantly smaller than that of normothermic animals (13.2 +/- 1.7 mm3, n = 8). By contrast, TBI-induced increases in dialysate concentrations of aspartate and glutamate were similar at the two temperatures. Thus, aspartate content (nmol/10 min) in animals maintained at 37.0-37.5 degrees C (n = 6) and 32.0-33.0 degrees C (n = 6) increased from respective mean preinjury values of 0.05 +/- 0.02 and 0.08 +/- 0.02 to much larger peak values (0.78 +/- 0.13 and 0.71 +/- 0.09, respectively). Similarly, under normothermic conditions glutamate content (nmol/10 min) increased from 0.13 +/- 0.03 to 3.08 +/- 0.52 and from 0.19 +/- 0.06 to a peak value of 3.09 +/- 0.26 under hypothermic conditions. These data clearly demonstrate the cytoprotective action of moderate hypothermia and further suggest that this action is not mediated by attenuation of the rise in interstitial concentrations of aspartate and glutamate.