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A very short hemoglobin (CerHb; 109 amino acids) binds O(2) cooperatively in the nerve tissue of the nemertean worm Cerebratulus lacteus to sustain neural activity during anoxia. Sequence analysis suggests that CerHb tertiary structure may be unique among the known globin fold evolutionary variants. The X-ray structure of oxygenated CerHb (R factor 15.3%, at 1.5 A resolution) displays deletion of the globin N-terminal A helix, an extended GH region, a very short H helix, and heme solvent shielding based on specific aromatic residues. The heme-bound O(2) is stabilized by hydrogen bonds to the distal TyrB10-GlnE7 pair. Ligand access to heme may take place through a wide protein matrix tunnel connecting the distal site to a surface cleft located between the E and H helices.
By means of electron holographic visualization of detailed electric potential distribution around sciatic nerve tissues coated with C and OsO(4), we show that the steady state of these specimens subjected to intense charging with electron irradiation is accompanied with a dynamic motion of collective secondary electrons; the secondary electrons emitted from the coated specimens revolve around the positively charged specimens forming stationary orbits. Further, this study clarified the possibility of the direct visualization of a part of the orbits of the collective secondary electrons without disturbing their motions.
Two methods for freeze-cleaving of thin tissue layers are presented. Whereas a simple technique can be employed to fracture continuous, relatively firm tissue layers, a more sophisticated technique employing special carriers is needed to fracture very thin and incomplete layers, e.g., the fiber outgrowth of cultured nerve tissue or sparsely seeded isolated cells. Both methods basically consist of freezing the specimens sandwiched between two small metal carriers which are then fractured apart so that the cleavage plane runs through the tissue. In the resulting replicas of such thin specimens, large membrane areas are exposed, and new information is provided on the topography of membrane properties in entire cells or cell processes. The technique should also be useful for studies on the interactions of cells grown in culture.
The implication of insulin-like growth factor I (IGF-I) in the myelination and the repair of myelin that occur after a demyelinating process was evaluated in organotypic cultures of embryonic nerve tissue. The amount of myelin of mouse spinal cord explants exposed to media supplemented with IGF-I beginning on the first day of explantation was recorded by light-microscopic examination and quantitation of the 2',3'-cyclic nucleotide 3'-phosphohydrolase (CNPase) activity. After 9 days in vitro (DIV), the cultures treated with medium supplemented with 0.1-1 microgram/ml IGF-I showed a greater amount of myelin and an increase over the controls in CNPase activity between 50 and 80% at 16 DIV and 100% at 21 DIV. Total demyelination with a concomitant reduction of about 80% in the CNPase activity resulted when anti-white matter antiserum and complement were added to the nutrient medium of fully myelinated cultures. This effect was partially reverted when IGF-I was included in the demyelinating medium. The higher inhibition, about 50%, was obtained with concentrations of IGF-I between 0.1 and 0.5 micrograms/ml. To study the effect of IGF-I on remyelination, well-myelinated cultures were completely demyelinated, maintained in that state for 2 or 15 DIV and after that allowed to remyelinate for 14 days. Cultures exposed to medium supplemented with 0.01-0.1 microgram/ml IGF-I showed a degree of remyelination similar to that of the normal nutrient medium-fed cultures.(ABSTRACT TRUNCATED AT 250 WORDS)
It was shown previously that addition of cyclic AMP (cAMP) to a synaptic membrane fraction incubated with [gamma-32P]ATP stimulated the phosphorylation of two proteins, designated proteins Ia and Ib, found only in nerve tissue. Addition of Ca2+ plus veratridine to synaptosomes preincubated with 32Pi stimulated the phosphorylation of two proteins with similar apparent molecular weights. Various techniques have now been used to determine whether the two proteins phosphorylated in synaptosomes in the presence of Ca2+ plus veratridine are the same as proteins Ia and Ib phosphorylated in synaptic membranes in the presence of cAMP. The proteins phosphorylated by the two procedures were extracted under similar conditions, had similar apparent molecular weights and charges, and were digested by collagenase at similar rates and to the same radioactive intermediates and end products. Furthermore, the two sets of proteins were digested by three other proteolytic enzymes to phosphopeptides with similar molecular weights. The results indicate that Ca2+ and cAMP are each capable of regulating the phosphorylation of proteins Ia and Ib.
The activity of lactate dehydrogenase (LDH), indophenol oxidase, aspartate aminotransferase (AsAT), alkaline phosphatase, acid phosphatase and aldolase at different stages of rat development was measured. We have also determined changes in the activity of these enzymes resulting from transplantation of embryonic nerve tissue (ENT) into the brain of adult animals. During development from the embryo to the adult animal, LDH and AsAT activities increased, while alkaline phosphatase activity diminished. After ENT transplantation, the most prominent changes were in the alkaline phosphatase activity whereas the activity of LDH, AsAT and acid phosphatase remained unchanged and similar to that in the brain cortex of intact adult animals. Changes in the enzyme activity resulting from ENT transplantation changed in a manner characteristic of the transplant. Local brain damage did not change the activity of the studied enzymes fifty days after surgery.
Effect of intracerebral allotransplantation of neocortex, hippocampus, septum, cerebellum, substantia nigra embryonic nerve tissue have been studied in white non-inbred, Wistar and Krushinski-Molodkina rats with phenotypically (portal destruction of hippocampus, gyrus serratus, corpus amygdaloideum and cerebral hypoxia) and genotypically conditioned by the low threshold of convulsive cerebral activity (TCCA). In focal cerebral affection transplants with monoergic neurones increase TCCA, while polyergic neurones of embryonic neocortex increase TCCA in diffuse cerebral affection. Phenotypically conditioned low TCCA increases in 4-6 days after transplantation and genotypically one--in 39-44 days because of the more complicated mechanisms of cerebral epileptization.
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To investigate different types of potential signalling mechanisms that regulate neuronal reactions to axotomizing injury, we compared the re-expression of the low-affinity neurotrophin receptor, p75NTR, and the down-regulation of choline acetyltransferase expression, after various combinations of axotomy, crush injury and blockade of axonal transport in adult hypoglossal motor neurons in the rat. We found that pure axotomy in the absence of crush injury down-regulated choline acetyltransferase, but did not induce p75NTR re-expression. Blockade of axonal transport with colchicine had an identical effect. In contrast, both a crush injury on its own, or a crush injury proximal to a complete axotomy, induced p75NTR re-expression and down-regulated expression of choline acetyltransferase. Blockade of axonal transport with colchicine or tight ligation proximal to a crush prevented the crush injury-induced re-expression of p75NTR. Infusion of vehicle, nerve growth factor or ciliary neurotrophic factor induced low levels of p75NTR re-expression that were not significantly different from each other and were substantially lower than crush-induced levels. These findings confirm previous suggestions that the loss of choline acetyltransferase expression is due to the interruption of a constitutive retrograde signal, and show that the re-expression of p75NTR by adult motor neurons after axotomy is triggered by the retrograde transport of a positive signal derived from axons that are regrowing through damaged or denervated peripheral nerve tissue. The precise source and nature of this signal are not yet clear.
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An analysis of the morphological and immunological aspects of xenotransplantation has shown that the xenotransplantation is a model for investigation of a wide range of problems of neurobiology: specific immune reactions in the brain and mechanisms of its immune privilege, conditions facilitating the take of transplants and mechanisms underlying autoimmune diseases of the CNS when the degenerative phase of the disease is accompanied by a cellular immune response. The use of xenotransplantations for studying potencies of the embryonic nerve tissues of man allowed to give grounds and to practically employ the method of treatment of parkinsonism. The first results of clinical use of the method obtained at the Institute of Experimental Medicine have shown its positive effects.
The effects of tissue explants and nerve homogenates on cholinesterase activity of muscle of the newt Triturus in organ culture were measured. Sensory ganglia, ganglia separated from muscle by a Millipore filter, spinal cord, liver, and nerve homogenates produced greater activity of muscle cholinesterase than occurred in untreated muscle cultured for the same period of time. Boiled ganglia, kidney, oviduct, and spleen were ineffective. This procedure serves as a convenient bioassay for a neurotrophic process and indicates that the trophic effect is mediated by a diffusible chemical substance produced by nerves.
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With the use of a mixed hemagglutination test (MHT), circulating antibodies against human peripheral nerve tissue (PNT) were found in 22 of 38 patients with Guillain-Barré syndrome (GBS) or chronic relapsing demyelinating inflammatory polyneuropathy (CR-DIP). The antibodies were found in only 1 of 34 patients with polyneuropathy of other origin, and in 3 of 32 patients without polyneuropathy. The presence of antibodies was related to response to intravenous gamma globulin treatment in CR-DIP patients. Antibodies against PNT may be pathogenic.