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Some antidepressant drugs work by encouraging the growth of new brain cells. Scientists are unsure why exercise triggers the growth of grey matter, but it may be linked to increased blood flow or higher levels of hormones that are released while exercising. Exercise might also reduce stress, which inhibits new brain cells through a hormone called cortisol. The Cambridge researchers joined forces with colleagues at the US National Institute on Ageing in Maryland to investigate the effect of running.

They studied two groups of mice, one of which had unlimited access to a running wheel throughout. The other mice formed a control group. In a brief training session, the mice were put in front of a computer screen that displayed two identical squares side by side. If they nudged the one on the left with their nose they received a sugar pellet reward. If they nudged the one on the right, they got nothing.

After training the mice went on to do the memory test. The more they nudged the correct square, the better they scored.

At the start of the test, the squares were 30cm apart, but got closer and closer together until they were almost touching. This part of the experiment was designed to test how good the mice were at separating two very similar memories.

A Cellular View

The human equivalent could be remembering what a person had for dinner yesterday and the day before, or where they parked on different trips to the supermarket. The running mice clocked up an average of 15 miles 24km a day. But the ability to learn and remember, along with other mental and emotional processes, can be influenced by the effects of lifestyle and environment on the synapses. Studies suggest that neurons that are adversely affected by factors such as stress, lack of stimulation, or neurotoxins may be hampered in their ability to form new patterns of connectivity and may lose synaptic connections.

In psychiatry, the emphasis is generally on problems and benefits that come from the functioning of the brain's synapses and chemicals, whereas treatment for lesions of the brain such as those associated with stroke or brain injury is done by neurologists. This is a very challenging but important problem. New tools are on the way that may one day help scientists develop a deeper understanding of synaptic function.

How the synapse functionsNeurons send and receive messages using their single axon—a tubular filament that conducts electrical signals away from the cell—and dendrites—projections with a tree-like structure that receive signals from other cells across a synapse.

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What is memory? The present state of the engram | BMC Biology | Full Text

When one cell communicates with another, it sends a wave of electrical activity down its axon to one of a cluster of presynaptic terminals—branches at the end of the axon that are positioned close to a neighboring cell's dendrites. In most cell communication, once a signal reaches the presynaptic terminal, the nerve impulse is transformed into a message composed of one or more neurotransmitters. These neurotransmitters are then released into a gap called the synaptic cleft, where they relay their message by binding with receptors on the post-synaptic membrane of the neighboring cell.

It is generally agreed that learning occurs when the acquisition of new information causes synaptic changes, but scientists are not yet certain precisely how these changes come about. Several theories have been proposed.


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  • In one, called the Hebbian theory, it is thought that any two cells or systems of cells that are repeatedly activated at the same time will tend to become "associated," so that activity in one makes it more likely the other will become active. Repeated co-activation of connected cells is thought to make physical changes in the brain—such as the development of new synapses between neurons or more receptors in the post-synaptic membrane—that lead to a lasting memory.

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    Another theory ascribes learning to the strengthening of existing synapses. It is thought that the developing brain overproduces synapses early in life. Subsequently experience, by activating certain nerve cells repeatedly and ignoring others, determines which synapses become mature and stable and which ones wither away in a process of synaptic pruning.

    Over time, this process leaves us with only highly functional synapses. Learning and memory are thought to result when repeated stimulation of sets of neurons causes the communication across synapses to be strengthened, a condition called long-term potentiation. Keeping synapses healthyMaintaining brain cells and synapses in good condition is critical, since mental performance is totally reliant on the health of the brain's complex network of trillions of synapses.

    Deterioration or loss of synapses can result in changes in mood and cognition, and in alterations of brain functioning such as those associated with neurological disorders or aging.

    Associative memory cells: Formation, function and perspective

    Stress is a major cause of synapse dysfunction.. Research shows that prolonged exposure to stress can interfere with the function of neurotransmitters. Consistent with this view, we found that inhibition of glycolysis using 2DG was associated with increased activity of AMPK, an evolutionarily conserved protein kinase that enforces quiescence to limit energy demands in response to energy stress 9. Conversely, high glycolytic flux was accompanied by upregulation of transcription factors that regulate terminal effector differentiation, such as Blimp-1, and increased expression of components of the effector machinery, including Prf1 and Gzmb.

    Our results are consistent with a model whereby elevated glucose metabolism is used by the cell to sustain a global program of effector differentiation that is antagonistic to the molecular circuit regulating memory differentiation. Whether glucose metabolism directly or indirectly regulates distinct transcriptional factors of Teff versus memory T cell lineages needs further investigation. In the current study, we also addressed the metabolic qualities associated with increased effectiveness of adoptively transferred antitumor T cells.

    Current methods used to produce T cells for adoptive immunotherapy have the pitfall of driving cells toward terminal differentiation and senescence 52 , We found that inhibition of glycolysis limited the detrimental influence of ex vivo expansion on T cell differentiation, resulting in the generation of antitumor cells with improved fitness. T cells primed in the presence of 2DG accumulated at higher numbers in tumor deposits and displayed increased proliferative potential and effector function, as measured by enhanced tumor destruction.

    Mice and tumor lines. We crossed pmel-1 with Ly5. In vitro activation of T cells. T cells were incubated with 2DG Sigma-Aldrich or vehicle culture media at indicated doses in the main text and figure legends. Adoptive cell transfer, infection, recall response, and tumor experiments. Recall response experiments were performed 30 days after primary infection with gpVV by rechallenging mice with 10 8 pfu ad-gp Tumor experiments were performed using 10 6 activated pmel-1 Thy Cell proliferation assay.

    Dilution of Cell proliferation dye was then evaluated by flow cytometry. Antibodies, flow cytometry, and cell sorting.

    Noninvasive treatment improves memory and reduces amyloid plaques in mice

    Mouse antibody specific for anti-CD69 H1. Samples were analyzed with FlowJo software TreeStar. In experiments evaluating the acute response to glucose supplementation, we used media with 0 mM glucose and add 25 mM glucose at the indicated time point through the injection port. Gene expression was calculated relative to Actb. Retroviral vector construction and virus production. Platinum Eco cell lines Cell Biolabs were used for gamma retroviral production by transfection with DNA plasmids through the use of Lipofectamine Invitrogen , and virus was collected 48 hours after transfection.

    Immunoblot analysis. Western blot analysis was performed using standard protocols. A , dilution was used for all antibodies. Cell fractionation and protein analysis. Cytosolic and nuclear fractionation to study the subcellular distribution of Foxo1 were performed as described previously Enumeration of adoptively transferred cells.

    We euthanized mice at the indicated time points after infection. Splenocytes were enumerated by trypan blue exclusion. The frequency of transferred T cells was determined by measuring CD8 and Thy Glucose uptake assays. Cells were pelleted, washed in PBS, and then lysed in water. Lysate 3H content was then measured via liquid scintillation counting. A log-rank test was used for analysis of survival curves. For all analyses, a P value less than 0.

    Long Term Potentiation and Memory Formation, Animation

    Study approval. The authors thank N. Acquavella, D. Clever, E. Tran, and M. Rao for critical review of the manuscript; A. Mixon, S. Farid, and G. Wiegand of the Flow Cytometry Unit for help with cell sorting; and D. Goldstein and M. Malik for catalyzing interactions with Metabolon. We sincerely thank Steven A.