摘要:

AbstractCerebral energy metabolism was studied in brains of mice treated with the nicotinamide analog, 6‐aminonicotinamide (6‐AN), which is converted to a potent inhibitor of 6‐phosphogluconate dehydrogenasein viro.Six hours after administration of 6‐AN, the level of cerebral 6‐phosphogluconate was increased at least 170‐fold, whereas substrates for other NADP+‐dependent dehydrogenases either did not change or increased only slightly. Large increases in 6‐phosphogluconate were observed in the cerebral cortex, three layers of the cerebellum, and the dorsal column and anterior horn regions of the spinal cord after administration of 6‐AN. Thus, glucose was metabolized via the oxidative enrymes of the pentose phosphate pathway in a wide variety of neuronal structuresin vivo.Highest concentrations of 6‐phosphogluconate were observed in the cerebellar molecular layer.Energy use rates and glycolysis were studied by measuring the disappearance of the major energy reserves during periods of anoxic‐ischemia imposed on cerebral tissue of 6‐AN‐treated mice. Production of lactate and utilization of glycogen during anoxic‐ischemia were reduced in brain of 6‐AN‐treated mice, which is in accord with the suggestion that glycolysis is inhibited in cerebral tissue of 6‐AN‐treated animals. Levels and ratios of pyridine nucleotides in cerebral tissue were not altered by 6‐AN treatment. From changes in levels of ATP, phosphocreatine, glucose, and glycogen in brain during ischemia, the rate of energy use was calculated to be 21.7 mmol · kg wet tissue−1· min−1, which was not significantly different from that observed in normal adult mouse brain. Therefore, despite an apparent slowing of hexose utilization in cerebral tissue 6‐AN‐treated mice, normal cerebral energy use was maintain

ISSN:0022-3034    

DOI:10.1002/neu.480050502

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractComparative studies were undertaken on thein vivoandin vitroincorporation of [14C] ethanolamine, [3H] methionine and [14C]S‐adenosyl‐methionine into phosphatidylethanolamine (PhE) and phosphatidylcholine (PhC) of rat liver and brain. It was observed that brain can synthesizede novoPhC from PhE via the transmethylation pathway, however synthesis rates were (1) markedly lower than those of liver and (2) decreased significantly with age. In the choline‐containing lipids more than 95% of the radioactivity was found in PhC. Studies on the localization of the radioactivity in PhC following the intracranial injection of [3H] methionine or [14C] ethanolamine revealed that both precursors are incorporated almost exclusively into the choline moiety of this phospholipid. There was significant labeling of PhC only when the precursors were administered intracranially and much less incorporation was observed with the systemic routes. Thus following the intravenous administration of [14C] ethanolamine, the specific radioactivities of liver PhE and PhC were up to 75 times as high as those of brain and 4 to 5 times as high in the organs of the 20‐day old as those of the adult. In contrast, when this precursor was administered intracranially the specific radioactivities of both phospholipids in liver were only twice as high as those of brain. Although the short‐and long‐term time‐course studies on thein vivoincorporation of [14C] ethanolamine and [3H] methionine into PhC of both organs could suggest a precursor‐product relationship between the biosynthesis of this phospholipid in liver and brain, this apparent relationship could also be due to the high turnover of PhE in liver, with half‐life of 2.87 hr, and its low turnover in brain, with half‐life of 10.7 days. The present findings on the low rate of formation of PhC from PhE in brain coupled with the fact that this conversion declines sharply with age, especially when the isotopes are administered systemically, could explain the observation of previous investigators that the brain cannot synthesize its own choline and thus it must derive its choline from exogenous sources such as lipid‐choline. It was concluded that the brain can synthesize its own choline; however it remains also dependent on liver and dietary choline which are probably transported into the

ISSN:0022-3034    

DOI:10.1002/neu.480050503

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractConduction velocity within the through‐conducting nerve net of the sea anemoneCalamactis praelongusis altered as a result of the passage of one or more impulses. Facilitation of conduction velocity occurs when the second evoked impulse follows the first by less than 2 sec. The facilitating effect increases with decreasing interval between shocks until impulses are less than 0.5 sec apart and then it declines. Antifacilitation occurs when the nerve net is shocked at frequencies between one per 2 sec and one per 20 sec. It is seen also after the first two or three responses when shocks are applied at higher frequencies. Facilitation and antifacilitation increase with spread of excitation. Although the relationship of velocity changes to the behavior ofCalamactishas not yet been determined, facilitation of conduction velocity in the net may produce greater synchronization of muscle contractio

ISSN:0022-3034    

DOI:10.1002/neu.480050504

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractAsexual reproduction (fissioning) in planarians is controlled by group size; increased group size suppresses fissioning, isolation releases it. This effect is mediated through the brain; social stimulation from cohorts causes the brain to inhibit the segmental plexus fissioning system from initiating the events of fissioning. Experiments were conducted to elucidate (1) the stimulus cue conveying information regarding cohort number and (2) the switching characteristics of the control system. The results of these show that the social stimulus responsible for the effect involves neither vision nor discharge of pheromonal substances into the habitat; the sensory event apparently involves direct contact and chemoreceptive, as well as tactile, modalities. The switching characteristics (graduated response, long release time, short reinstatement time) found for the brain inhibitory system agree with those expected from the mathematical model derived for a simple neurohormonal control system in which it is postulated that social stimulation causes neurosecretory cells of the brain to release a fissioning inhibitory hormone (FIH) that inhibits the segmental plexus fissioning (SPF) system from initiating fissioning.

ISSN:0022-3034    

DOI:10.1002/neu.480050505

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

摘要:

AbstractAsexual reproduction (fissioning) in the planarianDugesia dorotocephalais socially controlled through a cephalic mechanism; isolation releases fissioning, grouping inhibits it; decapitation releases it even in grouped subjects. Experiments were performed to confirm previous indications that direct contact is involved in the sensing of cohorts; the partial release of fissioning in grouped planarians by introduction of a chemically inert lubricant (0.1% purified agar) into the habitat water further confirms the necessity of intimate contact between the sensors and bodily surfaces of the sensed cohorts. Further experiments, correlating electron microscopic observations with the release of fissioning by various selected surgical ablations, reveal the pertinent sensors to be clumps of neural cilia concentrated in the cephalic margins. Comparable structures occur in the chemoreceptors of catfish, lamprey, and honey bee as well as in the olfactory epithelium of mammals.

ISSN:0022-3034    

DOI:10.1002/neu.480050506

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

ISSN:0022-3034    

DOI:10.1002/neu.480050507

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

ISSN:0022-3034    

DOI:10.1002/neu.480050508

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY

ISSN:0022-3034    

DOI:10.1002/neu.480050501

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1974

数据来源: WILEY