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For all you AI and Singularity geeks out there, I found this article entitled "How to Build a Mind?" really interesting and intuitive. It is about a new theory that attempts to integrate recent findings from both neuroscience and deep learning. It explains how the hippocampus encodes recent episodic memories of life events, and then plays them back while we sleep in order to "train" the neocortex. This is very similar to the approach used by the folks at DeepMind to teach AlphaGo using a combination of supervised learning and reinforcement learning. In fact, Demis Hassabis, founder of DeepMind, was a co-author on the paper, along with neuroscientist Jay McClelland from Stanford - a former colleague and collaborator of mine during the earlier days of artificial neural networks while we were both at CMU, along with neural net pioneer Geoff Hinton, who is also now at Google. In fact, most of the smartest people I've ever worked with (literally, at least 10 people I can think of off the top of my head) now work at Google... Which reminds me, earlier today I watched a really good video (embedded below) by Demis about DeepMind, AlphaGo and the future of AI. Demis describes in very accessible detail (starting at 28:15) the way AlphaGo works, and how it was trained (by playing against itself millions of times) to beat Lee Se-Dol, one of the world's top human Go players. I predict that DeepMind's approach to the development of artificial general intelligence may actually work, and come to fruition in the next couple decades. That will really make things interesting. I usually shy away from offering investment advice, but for those of you who haven't but can afford to, I recommend investing at least a little of your retirement savings in Google as an insurance policy against technological unemployment. When and if a Google AI steals all the jobs, you'll be glad you did... --Dean https://www.youtube.com/watch?v=f71RwCksAmI
All, Here is an interesting article highlighting research that suggests silence (no not necessarily meditation, just quiet time) is good for the brain and cognition. Here are a couple passages I found most interesting: A 2013 study  on mice published in the journal Brain, Structure and Function used differed types of noise and silence and monitored the effect the sound and silence had on the brains of the mice. The silence was intended to be the control in the study but what they found was surprising. The scientists discovered that when the mice were exposed to two hours of silence per day they developed new cells in the hippocampus. The hippocampus is a region of the brain associated with memory, emotion and learning. The growth of new cells in the brain does not necessarily translate to tangible health benefits. However, in this instance, researcher Imke Kirste says that the cells appeared to become functioning neurons. “We saw that silence is really helping the new generated cells to differentiate into neurons, and integrate into the system.” In this sense silence can quite literally grow your brain. The 2013 study referenced is . Here is a quote from the abstract: We used the standard noise level in the animal facility as baseline and compared this condition to white noise, pup calls, and silence. In addition, as patterned auditory stimulus without ethological relevance to mice we used piano music by Mozart (KV 448). All stimuli were transposed to the frequency range of C57BL/6 and hearing was objectified with acoustic evoked potentials.... [A]fter 7 days, only silence remained associated with increased numbers of [hippocampal] cells. Compared to controls at this stage, exposure to silence had generated significantly increased numbers of [hippocampal] neurons. and again quoting from the popular press article: A study that was published in 2002 in Psychological Science (Vol. 13, No. 9) examined the effects that the relocation of Munich’s airport had on children’s health and cognition. Gary W. Evans, a professor of human ecology at Cornell University notes that children who are exposed to noise develop a stress response that causes them to ignore the noise. What is of interest is that these children not only ignored harmful stimuli they also ignored stimuli that they should be paying attention to such as speech. “This study is among the strongest, probably the most definitive proof that noise – even at levels that do not produce any hearing damage – causes stress and is harmful to humans,” Evans says. Apparently, silence may be golden when it comes to brain health. --Dean ----------  Brain Struct Funct. 2015 Mar;220(2):1221-8. doi: 10.1007/s00429-013-0679-3. Epub 2013 Dec 1. Is silence golden? Effects of auditory stimuli and their absence on adult hippocampal neurogenesis. Kirste I(1), Nicola Z, Kronenberg G, Walker TL, Liu RC, Kempermann G. Author information: (1)CRTD, DFG Research Center for Regenerative Therapies Dresden, Fetscherstraße 105, 01307, Dresden, Germany. We have previously hypothesized that the reason why physical activity increases precursor cell proliferation in adult neurogenesis is that movement serves as non-specific signal to evoke the alertness required to meet cognitive demands. Thereby a pool of immature neurons is generated that are potentially recruitable by subsequent cognitive stimuli. Along these lines, we here tested whether auditory stimuli might exert a similar non-specific effect on adult neurogenesis in mice. We used the standard noise level in the animal facility as baseline and compared this condition to white noise, pup calls, and silence. In addition, as patterned auditory stimulus without ethological relevance to mice we used piano music by Mozart (KV 448). All stimuli were transposed to the frequency range of C57BL/6 and hearing was objectified with acoustic evoked potentials. We found that except for white noise all stimuli, including silence, increased precursor cell proliferation (assessed 24 h after labeling with bromodeoxyuridine, BrdU). This could be explained by significant increases in BrdU-labeled Sox2-positive cells (type-1/2a). But after 7 days, only silence remained associated with increased numbers of BrdU-labeled cells. Compared to controls at this stage, exposure to silence had generated significantly increased numbers of BrdU/NeuN-labeled neurons. Our results indicate that the unnatural absence of auditory input as well as spectrotemporally rich albeit ethological irrelevant stimuli activate precursor cells-in the case of silence also leading to greater numbers of newborn immature neurons-whereas ambient and unstructured background auditory stimuli do not. PMCID: PMC4087081 PMID: 24292324
Dean Pomerleau posted a topic in CR Science & TheoryCR is known to improve spatial learning and memory in rodents on tasks like the Morris water maze. But it is a matter of some controversy as to whether this improvement is due to beneficial effects of CR on memory/cognition, or whether the lean CR rodents can just swim better . James Cain posted this new study  which speaks to this issue a bit. Researchers found that short-term CR in young rats resulted in beneficial changes in the microstructure of synapses in their hippocampus, part of the brain known to be important for spatial learning. So that is nice to see! --Dean ----------------  Hippocampus. 2015 Sep 19. doi: 10.1002/hipo.22533. [Epub ahead of print] Food restriction modifies ultrastructure of hippocampal synapses. Babits R1, Szőke B, Sótonyi P1, Rácz B1. Abstract Consumption of high-energy diets may compromise health and may also impair cognition; these impairments have been linked to tasks that require hippocampal function. Conversely, food restriction has been shown to improve certain aspects of hippocampal function, including spatial memory and memory persistence. These diet-dependent functional changes raise the possibility that the synaptic structure underlying hippocampal function is also affected. To examine how short-term food restriction (FR) alters the synaptic structure of the hippocampus, we used quantitative electron microscopy to analyze the organization of neuropil in the CA1 stratum radiatum of the hippocampus in young rats, consequent to reduced food. While four weeks of FR did not modify the density, size, or shape of postsynaptic spines, the synapses established by these spines were altered, displaying increased mean length, and more frequent perforations of postsynaptic densities. That the number of perforated synapses (believed to be an indicator of synaptic enhancement) increased, and that the CA1 spine population had on average significantly longer PSDs suggests that synaptic efficacy of axospinous synapses also increased in the CA1. Taken together, our ultrastructural data reveal previously unrecognized structural changes at hippocampal synapses as a function of food restriction, supporting a link between metabolic balance and synaptic plasticity. This article is protected by copyright. All rights reserved. © 2015 Wiley Periodicals, Inc. KEYWORDS: CA1; dietary restriction; electron microscopy; memory; synaptic plasticity PMID: 26386363 --------------  Physiol Behav. 2008 Feb 27;93(3):560-9. Epub 2007 Oct 30. Effects of chronic adult dietary restriction on spatial learning in the aged F344 x BN hybrid F1 rat. Fitting S(1), Booze RM, Gilbert CA, Mactutus CF. Author information: (1)Program in Behavioral Neuroscience, Department of Psychology, University of South Carolina, Columbia, SC 29208, USA. email@example.com <firstname.lastname@example.org> Dietary restriction (DR) has been shown to increase life span and reduce disease incidence across a variety of species. Recent research suggests that chronic adult DR may also alter age-related cognitive decline. The purpose of this study was twofold: (1) to examine the potential deficits in spatial learning ability in the aged F344 x BN hybrid F1 rat with specific attention to the contributory effects of motoric impairments and (2) to determine the influence of chronic adult DR on any such impairments. The Morris water maze (MWM) task was employed with a 1.8 m diameter tank, 10 cm2 escape platform, 28 degrees C water, and an automated collapsing central starting platform. Spatial learning impairments in the aged rats were evident on all dependent measures during training and the probe test. Motoric function, as reflected in measures of strength and locomotion demonstrated profound age-related performance impairments that were attenuated by chronic adult DR. The present data also replicate previous reports, indicating that DR attenuates the age-related impairments of performance in the MWM as indexed by the latency measure in acquisition, but critically was dissociated from any DR effect on measures of preference and, more critically, accuracy in the probe test. Collectively, the most parsimonious interpretation of DR effects on MWM performance would appear to be the preservation of motoric, and not cognitive, function. PMCID: PMC4041982 PMID: 18035382 -----------  J Gerontol A Biol Sci Med Sci. 2009 Aug; 64A(8): 850–859. Published online 2009 May 6. doi: 10.1093/gerona/glp060 Influence of Calorie Restriction on Measures of Age-Related Cognitive Decline: Role of Increased Physical Activity Christy S. Carter,corresponding author1,2,3 Christiaan Leeuwenburgh,1 Michael Daniels,4 and Thomas C. Foster3 Abstract Controversy exists as to whether lifelong 40% calorie restriction (CR) enhances, has no effect on, or disrupts cognitive function during aging. Here, we report the effects of CR versus ad-lib feeding on cognitive function in male Brown Norway × Fisher344 rats across a range of ages (8–38 months), using two tasks that are differentially sensitive to age-related cognitive decline: object recognition and Morris water maze (MWM). All ages performed equally in object recognition, whereas, as a group, CR rats were impaired. In contrast, there was an age-related impairment in the MWM that was attenuated by CR as measured by time in proximity with and latency to reach the platform. Distance to the platform, a more sensitive measure, was not affected by CR. Finally, CR resulted in an overall increase in physical activity, one of several behavioral confounders to consider in the interpretation of cognitive outcomes in both tasks. PMCID: PMC2709546