Chemical coding of the hypothalamic neurones in metabolic control. I. Acetylcholine-sensitive neurones and glycogen synthesis in liver.
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Acetylcholine↗
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Metabolic regulations of the rhythmic activity in pacemaker neurons. II. Metabolically induced conversions of beating to bursting pacemaker activity in isolated Aplysia neurons.
In pacemaker neurons of the sea hare Aplysia californica, isolated from their synaptic, ephaptic and humoral inputs, conversion of the regular beating to a bursting discharge pattern can be induced by certain cell metabolites. Administration of the phosphofructokinase (PFK) activator fructose-6-phosphate (F-6-P), or its nonmetabolizable analogue 1-deoxy-F-6-P, induced bursting discharges in R3, R5, R6 and R11 neurons, with spike doublets and triplets appearing transiently in the time pattern. With another PFK activitor, adenosine-5-monophosphate, only double spikes have been noted in R7, R8 and R14 neurons. Burst activity was induced also in the presence of the fructose-1,6-diphosphatase activators, citrate and 3-phosphoglycerate, in R9, R10 and R12 neurons. Cyclic 3',5'-AMP, which also activates the PFK (beside other effects on cellular metabolism), induced bursting discharges in all R3-R14 neurons. In contrast, the inhibitors of the PFK, citrate and ATP, decreased the spike activity of the bursting L3 and L6 neurons, even changing L3 neurons to the regular beating type. Among a variety of cell metabolites tested only pyruvate was able to induce a burst-like tendency in R9 neurons. The characteristic bursting patterns which appeared in the presence of the described metabolic effectors could not be duplicated by low Ca2+ and/or high K+ media nor by artificial shifts in membrane potential triggered by depolarizing and hyperpolarizing currents.
Adenosine Monophosphate↗
Pathobiology of cortical neurons in metabolic and unclassified amentias.
Visualization of the neuron in its entirety through the use of the rapid Golgi method has permitted detection of several pathobiological features of neurons that are intimately associated with profound mental retardation in infants and children. In cases of unclassified mental retardation, dendrites and particularly dendritic spines exhibit severe developmental abnormalities. Dendritic spines, the postsynaptic components of axospinodendritic synapses, may be absent or abnormally long and thin in retardates. Evidence is presented that some cases of progressive neurobehavioral deterioration in infancy and early childhood may be due to progressive degeneration of dendritic spine systems (dendritic spine "dysgenesis"). Golgi and electron microscopic studies of neurons in human and feline ganglioside storage diseases indicate that ganglioside accumulation in cortical neurons initiates several complex alterations in neuronal geometry and morphology. Small and medium pyramidal cells form massive structural compartments (meganeurites) that frequently give rise to secondary neurites and other embryonic growth processes. Meganeurites may possess spines and spine-synapses. Other cells such as large pyramidal neurons may exhibit many somatic spines, whereas intrinsic cells of the cortex (and caudate) are unaffected morphologically by ganglioside accumulation. It is suggested that neuronal geometry distortion and aberrant synaptogenesis are important factors in the onset of neuronal dysfunction in ganglioside storage disorders. These studies also point to an important role of gangliosides in neurite formation in immature mammalian cortical neurons. Perisomatic processes and somatic spines are normal morphological components of the cell body of Purkinje cells through the 28th fetal week of human gestation. By 36 weeks the Purkinje cell somas exhibit a smooth surface contour. Prominent polydendritic processes, perisomatic protuberances, and somatic spines are detectable by Golgi methods applied to Purkinje cells in Menkes' disease and Down's syndrome long after these somatic components should normally disappear. Thus Purkinje cell soma membrane differentiation is a particularly sensitive process that can provide information on mechanisms of site-specific membrane regulation.
Brain Diseases, Metabolic↗
[The metabolically disordered neuron].
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Adenosine Triphosphate↗
Cerebral energy consumption and provision: the predominance of neuronal oxidative metabolic processes.
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Adenosine Triphosphate↗
A comparison of gama-aminobutyric acid metabolism in neurones versus glial cells using intact isolated retinae.
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Aminobutyrates↗
Hyperammonaemia, plasma aminoacid imbalance, and blood-brain aminoacid transport: a unified theory of portal-systemic encephalopathy.
It is proposed that hyperammonaemia in liver cirrhosis or after portacaval shunt contributes to plasma neutral aminoacid imbalance and to increased activity of the blood-brain neutral amino-acid transport system. Plasma neutral aminoacid concentrations are deranged, partly, but not completely, because ammonia stimulates glucagon secretion; a high rate of gluconeogenesis and hyperinsulinaemia follow. Brain uptake of neutral aminoacids rises because ammonia stimulates brain-glutamine synthesis, which results in rapid exchange of brain glutamine for plasma neutral aminoacids. Hyperammonaemia therefore contributes to encephalopathy indirectly, by raising the brain concentration of neutral aminoacids which after neurotransmitter metabolism, rather than directly, by toxic effects on neuronal metabolism.
Amino Acids, Branched-Chain↗
[Phospholipid distribution and metabolism in the neurons and neuroglia].
Ratio and intensity of metabolism of phospholipid separate fractions were studied in neurons and neuroglia, isolated from brain cortex by differential ultracentrifugation in density gradient of sucrose and Ficoll with the rate of enriching up to 90% and 80%, respectively. Neurons were characterized by the higher ratio of monophosphoinositides and lysophosphatidyl cholines as compared with neuroglia. Content of phosphatide acids and sphingomyelins was higher in neuroglia. The most specific radioactivity was observed in phosphatide acids both in neurons and neuroglia if 2(-14)C-acetate was administered. Neurons were shown to have higher metabolism of the separate fractions of phospholipids.
Animals↗
[Comparative study of dehydrogenase and diaphorase activity in spinal ganglion neurons in vivo and during their cultivation in vitro].
Enzymatic activity was investigated in spinal ganglia of 10-day-old chick embryo and in 10-day-old cultures of these ganglia (the method of "flying glasses"). Histochemical preparations were photometrically treated with the one-wave plug-method in the device MCFB-1 (LOMO) with the diameter of the probe 8 mkm. As the result of the investigations on optic density, a definite conclusion was made about relative activity of 15 enzymes and a general scheme of neuronal metabolism was graphically presented under the conditions of cultivation, enzymatic activity of krebs cycle was demonstrated to decrease, while that of diaphorase and lactate dehydrogenase to increase. The data on topography of enzymatic distribution in neurons, satellites, lemmoncytes and fibroblasts were also presented.
Animals↗
Structural alterations in normal and axotomized facial nucleus neurons after treatment with morphine.
Chronic morphine administration induced ultrastructural alterations in neurons of the facial nucleus and increased the incidence of cell death after axotomy. These findings may correlate with the significant depression of neuronal metabolism known to occur after opiate treatment.
Animals↗
[Cytochemical characteristics of the neurons of the external geniculate body in the rabbit brain in a period of visual function recovery after deprivation].
To study the properties of the external geniculate body, both neuron protein concentration and content were measured cytophotometrically in the cytoplasm of the above neurons taken from nomal animals and animals transported to normal conditions of illumination only after 2.5 months of visual deprivation, where they were put just after birth. The normalization of protein concentration and content has been observed in the neuron cytoplasm and in the surrounding structures. The magnitude of changes observed was related to the size of the neurons. It is supposed that some portion of neurons may exist in the external geniculate body having different degrees of dependence upon the visual impulsation. Mechanisms of possible rearrangement of the neuron metabolism in the geniculate body during the restoring period are discussed.
Animals↗
Polioencephalomalacia in the dog.
Disturbance of cerebral blood flow from causes such as meningitis, thromboembolic disease and atherosclerosis was considered an important factor in the pathogenesis of polioencephalomalacia in 25 dogs. In dogs with polioencephalomalacia of undetermined cause, the distribution of lesions in neocortex and paleocortex suggested a change of neuronal metabolism secondary to cerebral anoxia/ischemia. Five dogs with canine distemper infection had bilateral necrosis of the hippocampus and pyriform cortex. Convulsions, central visual impairment and hemiparesis were the most prominent neurologic signs.
Animals↗
Metabolic control of respiratory neuronal activity and the accompanying changes in breathing movements of the rabbit. III. Phase shifts in respiratory neurons induced by inflation and collapse of the lung, hyperventilation, or metabolic modifiers.
Phase shifts between inspiratory-related and expiratory-related discharge patterns can be reversibly induced in respiratory neurons following volume changes of the lung, hypocapnic apnea as a result of hyperventilation, or superfusion with certain metabolic modifiers. Phase-spanning expiratory-inspiratory or inspiratory-expiratory discharges are frequently induced in those neurons which are activated either by pulmonary stretch receptors or collapse afferents. The same is true for regulatory effectors which activate key steps of the neuronal metabolism such as ADP, 3-phosphoglycerate, L-glutamine, fructose-6-phosphate and fructose-1,6-diphosphate. In contrast, inhibitory vagal inputs or superfusion with citrate, an inhibitory metabolic modifier, revert preexisting expiratory-inspiratory discharges into a phase-coupled inspiratory pattern. It is postulated that the respiratory neuronal networks represents a time-optimal control system which strives to adjust to a new equilibrium value in a minimum of time, following a given mechanical or chemical perturbation. Following the hypothesis advanced by Cohen (1974) that the phase-spanning units modulate the activity of the in-phase neurons, it is suggested that the additional recruitment of expiratory-inspiratory and inspiratory-expiratory units provides a measure of the quality of time-optimal control and hence a performance index of the system.
Animals↗
Effect of papaverine on cerebral electrogenesis.
A double-blind, placebo-controlled study was conducted in 20 elderly patients with dementia associated with diffuse cerebrovascular disease to determine the effects of papaverine on the electrical activity of the brain. Frequency spectrum analysis of electroencephalograms showed the mean electrical content of the delta-theta band (0 to 7.5 Hz) was decreased significantly and content of the alpha band (7.6 to 12.5 Hz) was increased significantly from baseline. The changes in electroencephalographic activity observed in this study suggest that papaverine favorably affects neuronal metabolism, possibly through improved perfusion of the tissue, although the exact mechanism of action remains unknown.
Aged↗
[Morphologic and histochemical responses of the body to introduction of C1. botulinum toxin. V. Response of locus coeruleus cells of the brain to introduction of the toxin of C1. botulinum type B].
After the per os administration of 1Dlm/ml of botulin, type B. there were observed at the period of development of the limb paralysis and myasthenia morphological changes in the locus coeruleus cells expressed in the development of a more pronounced than normal perinuclear clarification and some nuclear basophilia. Histochemical study of succinic dehydrogenase, acid phosphatase, cholinesterase, and catecholamines pointed to the intensified neuron metabolism of the locus coeruleus; this could serve as an indication of enhanced energopacemaker function of this nucleus in hypoxia which occurred.
Acid Phosphatase↗
Neuronal accumulation and metabolism of 3H-1-norepinephrine in rat portal vein: evidence in relation to possible uneven alpha receptor distribution.
The rate of accumulation and metabolism of 3H-1-norepinephrine in the neuronal plexus of rat portal vein produces a small transmitter concentration gradient across the longitudinal smooth muscle layer which cannot account for the prejunctional supersensitivity observed and suggests localization of the alpha-adrenergic receptors adjacent to the nerve plexus.
Animals↗
Does visual deprivation in adult animals affect macromolecular metabolism in visual neurons?
Two-wave-length visible cytospectrophotometry of gallocyanin-stained sections has shown that 30-day-long visual deprivation in adult rats results in an augmentation of RNA content per cell in the neurons of all cell layers in visual cortex. Light stimulation which in normally reared rats brought about an accumulation of RNA in visual cortex neurons gave rise in light-deprived animals to a disappearance of the deprivation-induced increase of neuronal RNA content. In retina ganglion neurons, RNA content per cell was not changed after the visual deprivation as well as after the illumination of the deprived rats although in normal animals this stimulation evoked an increase of RNA content in the retina neurons. The conclusion is made about marked alterations in macromolecular metabolism induced by a long-term hypoactivity in central and peripheral visual neurons of adult animals.
Animals↗
Microelectrophoretic application of metabolic modifiers of the phosphofructokinase-hexosediphosphatase-system onto various types of bulbar respiratory neurons.
Three metabolic modifiers of the PFK-HDPase system were applied to bulbar respiratory neurons and, for comparison, also to unspecific cells. F-6-P did not alter the spike density of the majority of the respiratory and about half of the unspecific neurons. When responding, IE units were activated and unspecific cells were inhibited. Citrate did not alter the spike density of about half of all neurons tested. When responding, excitation prevailed in IE and E units, while unspecific cells were inhibited. AMP did not alter the spike density of the majority of the respiratory and about half of the unspecific cells. When responding, I neurons were activated, inhibition preponderated in IE units and both effects occurred in unspecific cells. The large number of zero effects suggests that the activity of only part of the cells is governed by the PFK-HDPase system.
Adenosine Monophosphate↗