Catecholaminergic contributions to the neuronal machinery of the olfactory bulb: aftoradiographic, immunohistochemical and evoked feild potential studies

aftographic exeperiments on the localization of radiolabelednoradrenaline, dopamine and dopa, as well as immunohistochemicalstudies on hydroxylase-like activity, are summarized and comparedin both rat and turtle olfactory bulbs. Evoked field potentialstudies on effects of dopamine are also discussed. The histochemicalstudies suggest that dopaminergic periglomerular neurons arethe most significant cellular component of the catecholaminergicsystem in the olfactory bulb of both species. Scattered fluorescentcell group was also present in the internal plexiform layerand superficial granule cell layer of the turtle olfactory bulb.Other fibres, not related to intrinsic bulbar neuronal cellbodies, were also labeled, mostly in the granule cell layerbut also in the external plexiform layer. These might belongto a centrifugal catecholaminergic system from brain stem neurons.In the in vitro turtle olfactory bulb, dopamine and apomorphinedepressed the amplitude of field potentials evoked by a singlevolley in the olfactory nerve or lateral olfactory tract, andreduced the depression and latency of reponses when paired volleywere delivered. It is suggested that catecholaminergic systemsplay a key role in modulating mitral cell activity through actionsin both superficial (glomerular) and deep (granule) layers.This may involve direct actions, or other, non-catecholaminergicinterneurons.     

Effects of the transciption inhibitory protein, TF1, on phage SP01 promoter complex formation and stability.

The uptake of a homologous single-stranded fragment by superhelical DNA produces a complex that contains a stable displacement loop. When the circular DNA was relaxed by the random action of pancreatic DNAase, complexes dissociated by a process which requires that the single-stranded arm of the D-loop be intact. We attribute the dissociation to branch migration, the exchange of like strands at a branch point. The kinetics of dissociation were biphasic. A fraction of the nicked complexes dissociated in a few seconds, the rest dissociated much more slowly. The fraction of molecules that dissociated slowly was directly related to the length of the third strand, and inversely related to temperature. Salt also inhibited dissociation. Under physiological conditions, 37 °C and 0.15 m-NaCl, more than half of complexes containing a third strand of 1000-nucleotide residues survived for at least one minute. These observations provide a guide to handling certain natural or synthetic branched derivatives of DNA. Analyzing our data by the method of Thompson et al. (1976), we have estimated that the time for the exchange of one nucleotide for another at a single-stranded branch is 12 microseconds; but the calculated value depends strongly upon the assumption that single-strand branch migration occurs by a random walk.     

CARBOHYDRATE AND ENERGY METABOLISM IN PERINATAL RAT BRAIN: RELATION TO SURVIVAL IN ANOXIA

The ability of rats of different ages to survive exposure to anoxia was correlated with rates of high energy phosphate consumption (metabolic rates) of the fore-brain. Fetal rats at term, delivered by hysterotomy following maternal decapitation, survived in nitrogen at 37°C twice as long as 1-day-old neo-nates, 5 times longer than 7-day-old rats, and 45 times longer than adults. During ischemia induced by decapitation, the cerebral concentrations of the labile energy reserves (ATP, ADP, P-creatine, glucose and glycogen) and of lactate were determined in fetuses, 1- and 7-day post-natal animals. From the changes, the cerebral energy use rates were calculated to be 1·57 mmol/kg/min in fetuses, 1·33 mmol/kg/min in 1-day-olds and 2·58 mmol/kg/min in 7-day-olds. Maximal rates of lactate accumulation during ischemia, as a measure of glycolytic capacity, were comparable in fetuses and neonates, but were about twice as great in 7-day-old rats. It is concluded that in post-natal animals survival in anoxia and cerebral energy consumption are inversely, and nearly quantitatively, related. However, the reduced cerebral energy requirement cannot entirely account for the greater anoxic resistance of fetuses.     

Ntau-methylhistidine excretion is a valid index of myofibrillar protein breakdown in the guineapig (Cavia porcellus).

The recovery of radioactivity in the urine of guineapigs following a bolus intravenous dose of chromatographically pure 14C-Ntau-methylhistidine was measured in order to test whether the excretion of Ntau-methylhistidine (Ntau-MH) is a valid index of myofibrillar protein breakdown in these animals. Four male and four female guineapigs were dosed and after 7 days, 91.65+/-2.82% and 3.58+/-0.91% of injected radioactivity was recovered in the excreta and tissues, respectively. The average total recovery of 95.2+/-3.0% was not significantly different from 100%. Male guineapigs excreted the radioactivity more slowly than females (70% of the dose excreted within 74 h vs 39 h, respectively) but cumulative excretion at 7 days was the same for each sex. Chromatographic analysis of the urine showed almost all of the radioactivity to be associated with a single peak corresponding to Ntau-MH, indicating a lack of significant metabolism. These data show that although the clearance of 14C-Ntau-MH is slower than in rats or humans the urinary excretion of Ntau-MH is a valid index for myofibrillar protein degradation in the guineapig.     

Increased Concentrations of 3-Hydroxykynurenine in Vitamin B6 Deficient Neonatal Rat Brain

Increased concentrations of the endogenous tryptophan metabolite 3-hydroxykynurenine (3-HK) were measured in the brains of vitamin B6 deficient neonatal rats. Mean concentrations of 3-HK in B6 deficient cerebellum, corpus striatum, frontal cortex, and pons/medulla ranged from 9.7 to 18.6 and 102 to 142 nmol/g of wet tissue at 14 and 18 days of age, respectively. 3-HK was not significantly increased in control neonatal or adult rat brain, vitamin B6 deficient rat brain at 7 days of age, or in brains from adult rats deprived of vitamin B6 for 58 days. The administration of daily intraperitoneal injections of vitamin B6 from the 14th to the 18th day of age decreased the concentration of 3-HK to control levels. 3-HK has been shown by other investigators to produce seizures when injected into the cerebral ventricles of adult rodents. Thus, our studies show the accumulation in brain of a putative endogenous convulsant as the result of a nutritional deficiency.