Pediatric arytenoid dislocation: diagnosis and treatment.

Arytenoid dislocation and subluxation are well-described injuries in adults but are poorly documented in children. The most commonly cited etiology is intubation trauma although external blunt trauma also is recognized. Symptoms include dysphonia, vocal fatigue, loss of vocal control, breathiness, odynophagia, dysphagia, dyspnea, and cough. Prompt diagnosis and treatment lead to the best chance for recovery, and delayed treatment is likely to result in scarring and possibly ankylosis. The mean age of our study group was 12.3 years and consisted of six males (55%) and five females (45%). The most commonly presenting symptom was hoarseness (81.8%). Six of the 11 patients underwent surgical correction of the dislocated arytenoid cartilage. Four patients refused any treatment and one patient received voice therapy alone. Two patients who refused surgical intervention had spontaneous reduction of their dislocations. After surgical intervention, one patient regained normal voice, four patients had substantial voice improvement without return to preinjury vocal function, and one patient had only slight voice improvement. Pediatric symptoms are similar to these in adults, yet these may be less noticeable to the patient and clinician. A high index of suspicion is needed to diagnose and treat pediatric arytenoid dislocation.

Group S8A serine proteases, including a novel enzyme cadeprin, induce long-lasting, metabotropic glutamate receptor-dependent synaptic depression in rat hippocampal slices.

Long-term potentiation and long-term depression (LTD) are forms of synaptic plasticity in the central nervous system. We now report that a group of chymotrypsin-like serine proteases, especially members of the S8A subfamily, induce LTD of evoked potentials in rat hippocampal slices. The proteolytic activity of these enzymes is required for the induction of LTD, as serine protease inhibitors prevent the effect. The depression is partly mediated by the suppression of transmitter release from glutamatergic terminals but also involves an elevation of action potential threshold with no change of post-synaptic membrane potential or input resistance. We have also isolated a novel and more potent related enzyme, cadeprin, from Aspergillus. The LTD produced by all of these proteases is not dependent on receptors for several transmitter systems, including N-methyl-d-aspartate or adenosine receptors, but is prevented by blocking group I metabotropic glutamate receptors. The activity of cadeprin, subtilisin and other S8A serine proteases may shed light on the mechanisms of LTD and a related endogenous molecule could have a physiological or pathological role as a modulator of synaptic plasticity in the mammalian hippocampus.

Selective subunit antagonists suggest an inhibitory relationship between NR2B and NR2A-subunit containing N-methyl-D: -aspartate receptors in hippocampal slices.

Glutamate receptors responding to N-methyl-D: -aspartate (NMDA) are involved in neural development, excitotoxicity and neuronal plasticity. Each receptor includes at least two NR2 subunits. Here, we have examined the effects of selective antagonists of NR2A and NR2B subunits (NVP-AAM07 and Ro25-6981 respectively) on the effects of NMDA in the CA1 field of rat hippocampal slices. We have observed that Ro25-6981 potentiates, rather than blocks, the effects of NMD on field EPSPs and paired-pulse interactions (indicators of presynaptic effects) and on postsynaptic depolarisation in hippocampal slices. The NR2A subunit antagonist NVP-AAM077 blocks the effects of NMDA alone, or after potentiation by Ro25-6981. The potentiation of NMDA by Ro25-6981 was not prevented by staurosporine (protein kinase inhibitor), okadaic acid (an inhibitor of serine/threonine protein phosphatases) or anisomycin (protein synthesis inhibitor), but was prevented by cyclosporin A, which inhibits Ca2+/calmodulin-dependent phosphatase 2B [calcineurin]. NMDA-dependent long-term potentiation (LTP) induced by electrical stimulation was not prevented by Ro25-6981 but was prevented by selective blockade of the NR2A subunit. The results suggest that, at both presynaptic and postsynaptic sites in the rat hippocampus, NR2B-subunit-containing receptors limit NMDA receptor function by inhibitory restraint over NR2A-subunit-containing receptors, via calcineurin activation, and that LTP induction critically involves primarily receptors containing the NR2A subunit. Endogenous factors or drugs that modify this NR2B/NR2A interaction could have a major influence on synaptic transmission and plasticity in the brain.