Relevant bibliographies by topics / Memory Methylene blue

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  1. Journal articles
  2. Dissertations / Theses

Academic literature on the topic 'Memory Methylene blue'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Memory Methylene blue"

1

Gonzalez-Lima, F. "Extinction Memory Improvement by the Metabolic Enhancer Methylene Blue." Learning & Memory 11, no. 5 (September 1, 2004): 633–40. http://dx.doi.org/10.1101/lm.82404.

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Rojas, Julio C., Aleksandra K. Bruchey, and F. Gonzalez-Lima. "Neurometabolic mechanisms for memory enhancement and neuroprotection of methylene blue." Progress in Neurobiology 96, no. 1 (January 2012): 32–45. http://dx.doi.org/10.1016/j.pneurobio.2011.10.007.

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3

Callaway, Narriman Lee, Penny D. Riha, Aleksandra K. Bruchey, Zeenat Munshi, and F. Gonzalez-Lima. "Methylene blue improves brain oxidative metabolism and memory retention in rats." Pharmacology Biochemistry and Behavior 77, no. 1 (January 2004): 175–81. http://dx.doi.org/10.1016/j.pbb.2003.10.007.

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Echevarria, David J., Erika M. Caramillo, and Francisco Gonzalez-Lima. "Methylene Blue Facilitates Memory Retention in Zebrafish in a Dose-Dependent Manner." Zebrafish 13, no. 6 (December 2016): 489–94. http://dx.doi.org/10.1089/zeb.2016.1282.

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Katzoff, Ayelet, Tziona Ben-Gedalya, Itay Hurwitz, Nimrod Miller, Yehoshua Z. Susswein, and Abraham J. Susswein. "Nitric Oxide Signals That Aplysia Have Attempted to Eat, a Necessary Component of Memory Formation After Learning That Food Is Inedible." Journal of Neurophysiology 96, no. 3 (September 2006): 1247–57. http://dx.doi.org/10.1152/jn.00056.2006.

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Inhibiting nitric oxide (NO) synthesis during learning that food is inedible in Aplysia blocks subsequent memory formation. To gain insight into the function of NO transmission during learning we tested whether blocking NO synthesis affects aspects of feeding that are expressed both in a nonlearning context and during learning. Inhibiting NO synthesis with L-NAME and blocking guanylyl cyclase with methylene blue decreased the efficacy of ad libitum feeding. D-NAME had no effect. L-NAME also decreased rejection responses frequency, but did not affect rejection amplitude. The effect of L-NAME was explained by a decreased signaling that efforts to swallow are not successful, leading to a decreased rejection rate, and a decreased ability to reposition and subsequently consume food in ad libitum feeding. Signaling that animals have made an effort to swallow is a critical component of learning that food is inedible. Stimulation of the lips with food alone did not produce memory, but stimulation combined with the NO donor SNAP did produce memory. Exogenous NO at a concentration causing memory also excited a key neuron responding to NO, the MCC. Block of the cGMP second-messenger cascade during training by methylene blue also blocked memory formation after learning. Our data indicate that memory arises from the contingency of three events during learning that food is inedible. One of the events is efforts to swallow, which are signaled by NO by cGMP.
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Li, Lei, Li Qin, Hai-long Lu, Ping-Jing Li, Yuan-Jian Song, and Rong-Li Yang. "Methylene blue improves streptozotocin-induced memory deficit by restoring mitochondrial function in rats." Brain Research 1657 (February 2017): 208–14. http://dx.doi.org/10.1016/j.brainres.2016.12.024.

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Riha, Penny D., Aleksandra K. Bruchey, David J. Echevarria, and F. Gonzalez-Lima. "Memory facilitation by methylene blue: Dose-dependent effect on behavior and brain oxygen consumption." European Journal of Pharmacology 511, no. 2-3 (March 2005): 151–58. http://dx.doi.org/10.1016/j.ejphar.2005.02.001.

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8

Al-Tahan, Farid J. "The effect of L-arginine and its antagonist L-NAME and Methylene blue on sensory and cognitive function in mice." Iraqi Journal of Veterinary Medicine 36, no. 1 (June 30, 2012): 99–106. http://dx.doi.org/10.30539/iraqijvm.v36i1.553.

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The present study was done to focus light on possible enhancement of the functional performance of male mice and female in neuronal behaviors by using L-arginine as a precursor of nitric oxide (NO). The results showed increase of latency period to reach the novel object in L-arginine treated groups and decrease in both L-NAME and methylene blue treated groups in both periods of treatment (15 and 30) days and were more prominent in male than in female mice as compared with control groups. Similar results were observed in passive avoidance latency period to enter the dark compartment. There was a reduction in latency period to reach the alternative arm of T-maze test in L-arginine treated groups and increase in both L-NAME and methylene blue treated groups in both periods of treatment (15 and 30) days in both genders. It could be concluded that L-arginine-NO pathway plays an important role in improving memory in male more than female mice.
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Bunge, Frank, Sander van den Driesche, and Michael J. Vellekoop. "Gas Supply through Agarose Walls in Cell Culturing Microchips." Advances in Science and Technology 100 (October 2016): 115–19. http://dx.doi.org/10.4028/www.scientific.net/ast.100.115.

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We present a novel structure to supply gases to microchambers in microfluidic chips. An exemplary application is the continuous feeding of oxygen and CO2 for on-chip cell cultivation of mammalian cells. In our device, the surrounding air diffuses into the culture medium inside the chip through a porous wall of agarose hydrogel resulting in an easy and robust design. One common method is the usage of gas permeable PDMS chips. However, liquid medium in which the cells grow is absorbed by PDMS causing unknown concentrations and memory effects. Another possibility is a complex setup where medium with already dissolved gas is pumped constantly through the chip. We designed and realized a silicon and borosilicate glass chip containing a gas permeable wall of agarose preventing leakage of medium. In order to precisely position the walls in the chip, we made use of surficial phaseguides (50nm high). The blue-bottle-experiment makes the effective dissipation of oxygen visible when the colorless leucomethylen-blue reacts to methylene-blue. Successful results were achieved when applying 0.5 g/l methylene blue, 10 g/l glucose and a pH of 12.6 set by a buffer solution. As a result a continuous color gradient through the chip was obtained, which reflects the oxygen gradient and confirms the oxygen diffusion.
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10

Callaway, Narriman Lee, Penny D. Riha, Kathryn M. Wrubel, David McCollum, and F. Gonzalez-Lima. "Methylene blue restores spatial memory retention impaired by an inhibitor of cytochrome oxidase in rats." Neuroscience Letters 332, no. 2 (October 2002): 83–86. http://dx.doi.org/10.1016/s0304-3940(02)00827-3.

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Dissertations / Theses on the topic "Memory Methylene blue"

1

Edlin, Shaun Michael. "Methylene blue, spatial memory and anterior thalamic lesions relevant to amnesic disorders." Thesis, University of Canterbury. Psychology, 2011. http://hdl.handle.net/10092/6521.

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While recent studies have focused on methylene blue’s interaction with amyloid plaques and neurofibrillary tangles in Alzheimer’s disease,!no studies have investigated the efficacy of methylene blue in animal-lesion models of regional pathology relevant to AD. The goal of this dissertation was to examine the effects of methylene blue on spatial memory in aged Wistar rats with lesions to the anterior thalamic nuclei (ATN), part of an extended episodic memory system that shows early pathology in AD and diencephalic amnesia. First, 12 ATN rats were compared to 14 aged shams (18 to 22 months old) to assess spatial memory acquisition in a standard water maze task (10 days). Rats in each group then received intraperitoneal injections of methylene blue (1 mg/kg) or placebo 1 hour after each daily trial for 10 days in which acquisition of a new platform position was examined, followed by a probe trial 5 days later. Anterior thalamic lesions impaired initial acquisition of the reference memory task. In the subsequent acquisition and probe trial, methylene blue treatment vs. placebo improved spatial learning in ATN rats, but there was no effect in sham rats. These results provide the first evidence that methylene blue may prevent the learning impairments observed in rats with lesions to the anterior thalamus and supports methylene blue as a potential therapeutic intervention for older humans with memory disorders associated with injury to the ATN and the extended episodic memory system.
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Wrubel, Kathryn Marigrace. "Memory improvement with the metabolic enhancer methylene blue." Thesis, 2006. http://hdl.handle.net/2152/2671.

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Riha, Penny Denise 1975. "Metabolic impairment of the posterior cingulate cortex and reversal by methylene blue: a novel model and treatment of early stage Alzheimer's disease." Thesis, 2007. http://hdl.handle.net/2152/3663.

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Alzheimer's disease (AD) is associated with decreased brain energy metabolism. Hypometabolism in the posterior cingulate cortex (PCC) occurs before the onset of memory deficits in subjects at genetic risk for AD who are not yet cognitively impaired. There is a specific inhibition in cytochrome oxidase (C.O.) in the PCC, an area involved in spatial navigation. Creating an animal model that exhibits the early pathophysiology of AD is important for developing and testing drugs that could reverse memory problems associated with such deficits. Methylene blue (MB) is a compound that improves C.O. activity and memory retention in rats. This dissertation had three specific aims: 1) to examine if isolated PCC hypometabolism causes spatial memory deficits in rats; 2) to find a dose of MB that improves memory without nonspecific behavioral effects; and 3) to prevent memory deficits from PCC hypometabolism with low dose MB. PCC hypometabolism was produced by focal administration of sodium azide, an inhibitor of C.O. activity. PCC hypometabolism resulted in impaired spatial memory in a hole board food-search task, increased oxidative damage, and neurotoxicity in the PCC. In addition, PCC hypometabolism resulted in reduced inter-regional correlations in brain activity. Our second set of studies examined the dose-response effects of MB. Our findings demonstrated that a low dose of MB: 1) enhanced memory in open field habituation and object recognition tasks; 2) did not affect general locomotor activity, exploration, motivation, or anxiety; and 3) increased brain oxygen consumption 24 hr after in vivo administration. Finally, our last study found that low dose MB prevented the deficits caused by PCC hypometabolism. MB did not prevent PCC inhibition or cell loss caused by sodium azide. Inter-regional correlations of brain metabolic activity suggested that rats treated with MB were using a different, but equally efficient, strategy for memory retrieval. This animal model of C.O. hypometabolism in the PCC can provide information to understand the mechanisms that regulate early pathological degeneration and reveal new therapeutic strategies aimed at reducing or preventing cognitive decline. Studies of low dose MB in humans are needed to examine its effects in AD patients.
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Bruchey, Aleksandra Krsmanović. "Metabolic mapping of rat brain activity associated with conditioned fear extinction and renewal, and improvement of extinction memory by the metabolic enhancer methylene blue." Thesis, 2006. http://hdl.handle.net/2152/2468.

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