Diabetic retrobulbar optic neuropathy

The authors describe a case of retrobulbar optic neuropathy in a patient with type 1 Diabetes mellitus. In spite of good metabolic control, there has been a slow but progressive functional visual decline. Worthy of note is the abnormal precocity of the appearance of the functional damage of the optic nerve compared to the involvement of the peripheral system.     

A proposed classification of swollen legs

The subject of enlarged legs is vast and complex. Up to now there has been no organic classification of the clinical picture involved. The basic problem is that of the criterion on which to base the classification. Literature on this subject has opted for the pathogenic criterion because it seems to facilitate the formulation of a classification which is of use to the doctor. One possibility would be to divide the syndrome into vascular and non-vascular swollen legs. The first group could in turn be separated into macro-circulating and micro-circulatory. The micro-circulatory forms can be primitive or secondary. Amongst the secondary micro-circulatory forms, two other groups can be singled out: secondary forms with local cause and secondary forms caused by organic pathology. However, there are clinical forms which are on the periphery of these different groups and these forms are subject to discussion regarding nosographic localization.     

A comparison of sensory loss tests and histopathology in the diagnosis of leprosy

Three different sensory loss tests, for anaesthesia to light touch, for diminished pain sensation and for loss of thermosensation, were compared with histopathological examination results in the diagnosis of suspected tuberculoid leprosy in 120 individuals with 126 lesions. Though none of the 3 tests used in this study was found to be strikingly superior to any of the others, the results indicate potentially important differences in their usefulness in different subgroups of suspected patients. The methodological problems inherent in such studies are discussed.     

Death of sensory ganglion neurons after acute withdrawal of nerve growth factor in dissociated cell cultures

The time course of dependence on nerve growth factor (NGF) for survival in sensory neurons in vitro was examined with microscopic and biochemical methods. Primary dorsal root ganglion (DRG) cultures from embryonic-day-15 (E-15) and day-19 (E-19) rats were maintained with standard dissociated cell culture techniques in the absence of most non-neuronal cells. After various times in culture, neurons were acutely deprived of neurotrophic support by changing to NGF-free medium and adding NGF antiserum to eliminate any residual NGF. Neuronal cultures were examined with phase microscopy; and, their metabolic activity was measured with a protein assay at various time points after NGF deprivation. E-15 neurons grown in culture for 5 days were exquisitely sensitive to acute NGF deprivation. By 12 h after NGF deprivation, neuronal morphology was severely disrupted and the majority of neurons appeared dead. E-15 neurons grown in culture for 8 or 11 days showed progressively less dependence on NGF for survival. These older neurons did not die until 24 and 48 h, respectively, following NGF withdrawal. Neurons grown in culture for 20 days did not show any morphologic changes by phase microscopy up to 4 days after NGF deprivation. Protein incorporation progressively decreased between 12 and 48 h after NGF withdrawal in E-15 neurons grown in culture for 5, 8, or 11 days.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cytoplasmic loop of beta-adrenergic receptors: synaptic and intracellular localization and relation to catecholaminergic neurons in the nuclei of the solitary tracts

Pharmacological studies suggest that beta-adrenergic receptors (beta AR) in the medial nuclei of the solitary tracts (m-NTS) facilitate presynaptic release of catecholamines and also function at postsynaptic sites. We have localized the antigenic sites for a monoclonal antibody against a peptide corresponding to amino acids 226-239 of beta AR in the m-NTS of rat brain. By light microscopy, immunoperoxidase labeling for this antibody was detected in somata and proximal processes of many small cells that were distributed throughout the rostrocaudal extent of the m-NTS. Electron microscopy confirmed the cytoplasmic localization of beta AR in perikarya and proximal dendrites of neurons. Immunoreactivity occurred as discrete patches associated with cytoplasmic surfaces of plasma membrane and with irregularly-shaped saccules with clear lumen in the immediate vicinity. Select regions of nuclear envelopes, mitochondrial membranes, and rough endoplasmic reticulum were also immunoreactive along their cytoplasmic surfaces. In contrast, the Golgi apparatus was labeled, but infrequently. Immunoreactivity was also detected at numerous post- and occasional presynaptic membrane specializations of select axodendritic junctions. Dual labeling for the beta AR-antibody by the immunoperoxidase method and for a rabbit antiserum against the catecholamine-synthesizing enzyme, tyrosine hydroxylase (TH), by the immunoautoradiographic method within the same sections, further established the precise cellular relations between beta AR and catecholaminergic neurons. Immunoreactivity for beta AR was detected in numerous perikarya and proximal dendrites that did not show detectable levels of TH. However, a few cells were dually labeled for both antigens, as seen by both light and electron microscopy. The TH-labeled terminals formed synapses at junctions both with and without beta AR-like immunoreactivity. These results from the single and dual labeling studies: (1) confirm biochemical predictions that amino acids 226-239 of beta AR protein reside intracellularly; (2) provide the first ultrastructural evidence for beta AR localization within both pre- and postsynaptic membrane specializations of a subset of catecholaminergic synapses; and (3) suggest select intracellular sites that may be involved with synthesis and/or internalization and degradation of the receptor protein.