GABA and glycine as inhibitory neurotransmitters in the vestibuloocular reflex.
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Biomedical subjects
Publications and source records attributed to R F Spencer.
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Hair cells of the avian inner ear have been shown to regenerate following acoustic or ototoxic insult. The consequences of this regeneration on the acoustic nerve have yet to be defined. The purpose of the present study was to use TEM analysis following cochlear damage and hair cell regeneration to describe afferent and efferent neural terminals on hair cells in the newly repopulated sensory epithelium. Following acoustic overstimulation (12 h, 115 dB SPL, 1500 Hz) adult quail were sacrificed immediately (0 day), or at 2, 12, or 24 weeks. Serial thin sections were taken from the embedded papilla in a plane tangential to the basilar membrane in the area consistent with regenerative activity. Immediately following noise exposure very few hair cells could be seen within the epithelia; afferent terminals on remaining cells appeared normal. Two weeks later afferent terminals showed signs of degeneration; efferent terminals were rarely seen on tall hair cells but remained relatively normal on short hair cells. Three to six months later afferent terminals had regained a more normal appearance but were less numerous on tall hair cells; some return of efferent-like terminals was seen often contacting two tall hair cells. Large normal appearing, efferent terminals remained on short hair cells. These results suggest that regenerated hair cells are likely to receive neural innervation. It would appear that some degeneration of afferent terminals takes place prior to final innervation of new hair cells.
We describe a case of combined volar dislocation of the lunate and dorsal dislocation of the remainder of the carpus. Such a combination is probably very rare and the possible mechanism of injury is discussed.
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1. The biochemical basis for the human renal Fanconi syndrome, including glucosuria, phosphaturia and aminoaciduria, remains enigmatic. This is due, in part, to the lack of an appropriate animal model. Since there is an association between the human genetic disease hereditary tyrosinaemia, for which urinary excretion of the compound succinylacetone constitutes a biochemical marker, and a renal Fanconi syndrome, we have examined the relationship between succinylacetone and renal tubular function in the rat. 2. Intraperitoneal injection of succinylacetone for 3 consecutive days into adult male Sprague-Dawley rats resulted in succinylacetone plasma concentration of 3 mmol/l. This concentration was associated with glucosuria, aminoaciduria, polyuria, reduced renal phosphate reabsorption and normal creatinine clearance. In addition, urinary porphobilinogen and total porphyrin excretions were markedly reduced. In animals permitted to recover for 7 days after succinylacetone administration, these renal functional changes remitted partially or completely. Ultrastructural examination of the kidneys after the 3 days of treatment showed no fine structural changes. 3. We conclude that the physiological alterations produced in normal rat renal tubules by succinylacetone provide the basis for the study of the biochemical changes underlying the human renal Fanconi syndrome.
The postnatal development of cholinergic afferents to the superior colliculus in neonatal cats was studied by using acetylcholinesterase (AChE) histochemistry, choline acetyltransferase (ChAT) immunohistochemistry, and retrograde transport of horseradish peroxidase (HRP). In the adult cat, the pattern of AChE staining was laminar specific. AChE was distributed continuously in the stratum griseum superficiale (SGS) but was organized as patches in the stratum griseum intermediate (SGI). Diffuse AChE staining also was present in the stratum griseum profundum (SGP) and the dorsolateral periaqueductal gray (PAG). At birth, however, AChE staining was barely detectable in the SGS and, aside from a few isolated labeled neurons, was absent from the SGI, SGP, and PAG. By 7 days postnatal (dpn), staining in the SGS was more apparent but did not change appreciably in the deeper laminae. A substantial increase in AChE staining occurred in the SGS at 14 dpn (several days after eye opening), at which time patches in the SGI first became apparent. By 28 dpn, the complete laminar-specific adult AChE staining pattern was present, though the staining intensity did not reach the adult level until 56 dpn. A protracted maturation of both AChE staining and ChAT immunoreactivity also was observed in the sources of cholinergic afferents to the superior colliculus, which include the parabigeminal nucleus, and the pedunculopontine (PPN) and lateral dorsal tegmental (LDTN) nuclei. AChE and ChAT-immunoreactive staining in each nucleus was weak at birth but increased during the ensuing 2 weeks. At 21 dpn, however, ChAT immunoreactivity virtually disappeared in the parabigeminal nucleus and significantly decreased in PPN and LDTN. The ChAT immunoreactivity in these nuclei then gradually increased reaching maximum levels by 28 dpn. At 35 dpn, AChE staining showed a significant, though temporary (4 weeks), decrease in the parabigeminal nucleus, but not in the PPN and LDTN, that subsequently increased to the adult level of staining at 70 dpn. The absence of AChE in the SGI in neonatal animals was correlated, at least in part, with a paucity of neurons in the brainstem cholinergic cell groups labeled by retrograde transport of HRP from the superior colliculus. Injections of HRP into the superior colliculus retrogradely labeled many neurons in the parabigeminal nucleus, but few, if any, neurons in the PPN or LDTN at 1 dpn. Retrogradely labeled neurons also were observed in the substantia nigra pars reticulata, albeit fewer in neonates than in adults.(ABSTRACT TRUNCATED AT 400 WORDS)
A total of 39 fractures of the diaphyses of long bones in 31 children were subjected to operative fixation. Indications for surgery included concomitant severe head injury, multiple injuries, patients nearing skeletal maturity, inability to obtain a satisfactory reduction by conservative means, severe soft-tissue injury with or without vascular trauma, long-standing neurological disorder with incapacity and contractures, malunion, and delayed union. Although long-bone diaphyseal fractures in children are generally managed non-operatively, the use of fixation may be indicated in certain cases.
A case of successful four-level anterior decompression for paraplegia due to metastatic breast carcinoma is reported. Posterior instrumentation carried out shortly afterwards provided sufficient additional stability for the patient to stand and walk. It is suggested that this form of aggressive management may provide excellent palliation in certain cases of extensive metastatic neoplastic disease.
We report three cases of progressive ulnar nerve palsy following fractures of the distal radius. One was an open injury and one involved dorsal displacement of the nerve through a dislocated distal radio-ulnar joint. All were associated with dense scar tissue formation around the nerve. Early surgical decompression was successful in all cases. An anatomical study indicated that the relative immunity of the nerve to injury in this region may be due to its greater excursion and mobility compared with the median nerve.
A case of digital periarticular heterotopic ossification is described. Such cases are extremely rare and diagnosis may be delayed. Spasticity, possibly in association with minor trauma, may contribute to the development of the process. Little experience exists of the management of such problems and a mobile joint may be difficult to achieve.
The inhibitory neurotransmitter gamma-aminobutyric acid (GABA) is found in the superior colliculus (SC) of many mammalian species. In cat, several distinct classes of putative GABAergic neuron have been identified using antibodies directed against the neurotransmitter. It is not known whether these classes are found in other species. To study this, we examined the distribution, morphology, ultrastructure, and synaptic organization of GABA immunoreactive neurons in the SC of the Rhesus monkey (Macaca mulatta). Antibody-labeled neurons were distributed throughout the monkey SC, but were most densely concentrated within the zonal and superficial gray layers (32.5% of the total). These neurons were all small cells ranging from 6.6-16.3 microns in average diameter, and had granule, pyriform, and horizontal morphologies. Four types of labeled profile were identified in single ultrathin sections with the electron microscope. Presynaptic dendrites (PSDs) contained pleomorphic vesicles, received synaptic input from unlabeled axon terminals, and sometimes formed symmetric synaptic contacts with postsynaptic profiles. Two subtypes were found. One type contained loose accumulations of synaptic vesicles throughout the profile and had a distinctive varicose shape. The other type contained small discrete clusters of synaptic vesicles near the site of synaptic apposition. The former were much more common. Profiles with typical axon terminal morphology were also found. These profiles usually contained numerous flattened vesicles and formed symmetric synapses with postsynaptic profiles, both dendrites and cell bodies. Some conventional dendrites and myelinated axons were also labeled. Serial ultrathin section reconstructions revealed that PSDs formed complex synaptic relationships with other elements. Retinal terminals, identified by their characteristic pale mitochondria, established synaptic contacts with both types of PSD. These PSDs also established contact with each other, providing a possible anatomical substrate for disinhibition. We conclude that the monkey SC has multiple GABAergic cell types, similar to those found in cat, and may represent an organization common to both mammals and some other vertebrate species. The circuitry established by these cell types may provide a mechanism for disinhibition as well as inhibition in the mammalian SC.
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A case of complete transection of the posterior tibial nerve complicating a closed mid-shaft fracture of the tibia is reported. Early surgical exploration and repair resulted in return of function within 6 months. Such injuries are not common, but the case described highlights the importance of vigilance in assessment of all limb fractures.
The concentration of 18 alpha-amino acids (AAs) in plasma and renal cortical cell water were measured 3 or 24 hr after 1 hr of unilateral renal artery clamping or 24 or 48 hr after 15 mg/kg body weight HgCl2 injection sc as a test of epithelial integrity. Cellular glycine (Gly), hydroxyproline (Hpr), ornithine (Orn), phenylalanine (Phe), serine (Ser), and tryptophan (Trp) concentrations were depressed 24 hr after HgCl2 (p less than 0.05), but the remaining 12 AAs were not distinguishable from control despite the presence of severe renal failure. ARginine (Arg), glutamic acid (Glu), and valine (Val) also were decreased (P less than 0.05) 24 hr later, but concentrations of half of all measured AAs were still normal. Cellular alanine (Ala), Arg, Glu, Gly, Phe, and Ser concentrations were decreased 3 hr after ischemia, p less than 0.05, but 12 AAs were unchanged and only Arg, Phe, Ser, and threonine (Thr) were reduced 24 hr after ischemia was reversed. Concentrations of even the most affected AAs remained notably higher than in plasma in both forms of acute renal failure (ARF). Total loss of AAs from a small proportion of tubular cells would be hidden by essentially normal concentrations in the rest, and such losses may well have occurred. Unless cellular AAs in ARF are almost completely bound, however, the well-maintained cell:plasma AA concentration ratios indicate that cellular energetics were adequate for AA uptake and that epithelial permeability to AAs in the vast majority of cells was not greatly disturbed. Such findings suggest that most of the epithelium, although seriously damaged, had remained viable.
A review of 283 patients with late effects of poliomyelitis affecting the limbs revealed no evidence of heterotopic new bone formation, or of greater than normal callus/new bone formation around fractures and osteotomies. It is suggested, in contradiction to the published tradition, that poliomyelitis does not encourage the formation of new bone to any significant extent.
Using a feline model, the effects of stereotaxic brain lesions producing unilateral spasticity on bilateral fibular osteotomies were observed. Healing in spastic limbs occurred with more new bone formation than on the contralateral (control) side. Union appeared to be slightly faster in spastic limbs. Histomorphometric analysis of resected fibular specimens following union revealed little difference between spastic and non-spastic limbs. When these brain-lesioned animals were compared with a group with identical osteotomies but no brain lesions in respect of various systemic biochemical and endocrine parameters, no differences were found.
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Ten patients with neural injury who demonstrated very large amounts of new bone formation around fractures are reported. Eight patients displayed clear evidence of spasticity in the affected limbs. It is suggested that there may be a relationship between the two conditions.