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Neuroscience & the Brain
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HenryDavidT
Jan 25, 2016, 4:30:45 PM1/25/16
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http://www.huffingtonpost.com/entry/brain-capacity-study_us_56a1a50be4b0404eb8f11d63?ir=Science§ion=us_science&utm_hp_ref=science
http://elifesciences.org/content/4/e10778
Introduction
Synapses between neurons control the flow of information in the brain and their strengths are regulated by experience. Synapses in the hippocampus are involved in the formation of new declarative memories.
Understanding how and why synaptic strengths undergo changes in the hippocampus is important for understanding how we remember facts about the world. A fundamental question is the degree of precision in the adjustment of synaptic strengths in view of the many sources of variability at synapses.
In this study we provide an upper bound on the variability of synaptic plasticity and quantify a lower bound on the amount of information that can be stored at a single synapse.
Excitatory synapses on dendritic spines of hippocampal pyramidal neurons have a wide range of sizes.
Anatomical measurements of the spine size, the area of the postsynaptic density (PSD), the number of AMPA receptors, the area of the presynaptic active zone and the number of docked vesicles in the presynaptic terminal are all highly correlated with each other and with physiological measurements of the release probability and the efficacy of the synapse (Harris and Stevens, 1989; Lisman and Harris, 1994; Harris and Sultan, 1995; Schikorski and Stevens, 1997; Murthy et al., 2001; Branco et al., 2008; Bourne et al., 2013).
Thus, each of these individual characteristics is a correlate of synaptic strength. The sizes and strengths of these synapses can increase or decrease according to the history of relative timing of presynaptic inputs and postsynaptic spikes (Bi and Poo, 1998).
If experience regulates synaptic strength then one might expect that synapses having the same pre- and postsynaptic histories would be adjusted to have the same strength.
But what would be the inherent variability, or conversely the precision, of this process? Due to the high failure rate and other sources of stochastic variability at synapses one might expect that the precision of changes in the strengths of these synapses in vivo to be low. The failure rate at synapses depends inversely on the strength, and therefore the size, of the synapse.
On this basis the strengths of weaker, and therefore smaller and less reliable synapses, would be expected to be less precisely controlled than the larger and stronger synapses, which have a lower failure rate.
An ideal experiment to test for the precision of the changes in synaptic strength would be to stimulate in vivo the axonal inputs to two well-separated spines on the same dendrite to insure that they have the same presynaptic and postsynaptic history of stimulation.
Nature has already done the experiment for us as pairs of spines on the same dendrite contacting the same axon satisfy this condition. Prior work suggests that such pairs of spines are more similar in size than those from the same axon on different dendrites (Sorra and Harris, 1993). Here we evaluated this axon-spine coupling in a complete nanoconnectomic three-dimensional reconstruction from serial electron microscopy (3DEM) (Harris et al., 2015) of hippocampal neuropil.
We determined the similarity of synapses among pairs of spines and set an upper bound on the variability and the time window over which pre- and postsynaptic histories would need to be averaged to achieve the observed precision.
http://elifesciences.org/content/4/e10778
Introduction
Synapses between neurons control the flow of information in the brain and their strengths are regulated by experience. Synapses in the hippocampus are involved in the formation of new declarative memories.
Understanding how and why synaptic strengths undergo changes in the hippocampus is important for understanding how we remember facts about the world. A fundamental question is the degree of precision in the adjustment of synaptic strengths in view of the many sources of variability at synapses.
In this study we provide an upper bound on the variability of synaptic plasticity and quantify a lower bound on the amount of information that can be stored at a single synapse.
Excitatory synapses on dendritic spines of hippocampal pyramidal neurons have a wide range of sizes.
Anatomical measurements of the spine size, the area of the postsynaptic density (PSD), the number of AMPA receptors, the area of the presynaptic active zone and the number of docked vesicles in the presynaptic terminal are all highly correlated with each other and with physiological measurements of the release probability and the efficacy of the synapse (Harris and Stevens, 1989; Lisman and Harris, 1994; Harris and Sultan, 1995; Schikorski and Stevens, 1997; Murthy et al., 2001; Branco et al., 2008; Bourne et al., 2013).
Thus, each of these individual characteristics is a correlate of synaptic strength. The sizes and strengths of these synapses can increase or decrease according to the history of relative timing of presynaptic inputs and postsynaptic spikes (Bi and Poo, 1998).
If experience regulates synaptic strength then one might expect that synapses having the same pre- and postsynaptic histories would be adjusted to have the same strength.
But what would be the inherent variability, or conversely the precision, of this process? Due to the high failure rate and other sources of stochastic variability at synapses one might expect that the precision of changes in the strengths of these synapses in vivo to be low. The failure rate at synapses depends inversely on the strength, and therefore the size, of the synapse.
On this basis the strengths of weaker, and therefore smaller and less reliable synapses, would be expected to be less precisely controlled than the larger and stronger synapses, which have a lower failure rate.
An ideal experiment to test for the precision of the changes in synaptic strength would be to stimulate in vivo the axonal inputs to two well-separated spines on the same dendrite to insure that they have the same presynaptic and postsynaptic history of stimulation.
Nature has already done the experiment for us as pairs of spines on the same dendrite contacting the same axon satisfy this condition. Prior work suggests that such pairs of spines are more similar in size than those from the same axon on different dendrites (Sorra and Harris, 1993). Here we evaluated this axon-spine coupling in a complete nanoconnectomic three-dimensional reconstruction from serial electron microscopy (3DEM) (Harris et al., 2015) of hippocampal neuropil.
We determined the similarity of synapses among pairs of spines and set an upper bound on the variability and the time window over which pre- and postsynaptic histories would need to be averaged to achieve the observed precision.
HenryDavidT
Jan 28, 2016, 1:00:42 PM1/28/16
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http://www.nature.com/nature/journal/vaop/ncurrent/full/nature16874.html
http://nymag.com/scienceofus/2016/01/huge-genetic-breakthrough-on-schizophrenia.html
According to these new findings, a genetic stamp that people with schizophrenia inherit causes a normal process of brain development called synaptic pruning to go haywire, something some scientists already had a hunch about by comparing schizophrenic brains against typical ones. Let's back up for a moment: In a baby's brain, an incredible number of neurons and synaptic connections form -- sometimes up to 40,000 per second. By toddlerhood, the brain has amassed more neurons and synapses than it needs, so the excess ones are eliminated; this process begins in early childhood and is completed by early adulthood.
In a typically developing brain, this pruning process helps speed up cognitive functioning. But the schizophrenic brain takes this too far, eliminating too many of those neurons and synapses. "Normally, pruning gets rid of excess connections we no longer need, streamlining our brain for optimal performance, but too much pruning can impair mental function," said Thomas Lehner, the director of the office of genomic research coordination at the National Institute of Mental Health, in a statement. "It could help explain schizophrenia's delayed age-of-onset symptoms in late adolescence/early adulthood and shrinkage of the brain's working tissue."
Research has found, for instance, that certain brain regions in people with schizophrenia contain fewer synaptic connections, as compared to the brains of people without schizophrenia. Now this new genetic discovery may help explain why. As Post writer Amy Ellis Nutt explains:
In patients with schizophrenia, a variation in a single position in the DNA sequence marks too many synapses for removal and that pruning goes out of control. The result is an abnormal loss of gray matter. The genes involved coat the neurons with "eat-me signals," said study co-author Beth Stevens, a neuroscientist at Children's Hospital and Broad. "They are tagging too many synapses. And they're gobbled up."
For their paper in Nature, the researchers analyzed the brains of 700 people who'd had schizophrenia and donated their brains to science when they died. They also examined data pulled from the Psychiatric Genomics Consortium, which included more than 65,000 people -- about 29,000 with schizophrenia and 36,000 without -- from 22 countries across the globe. The team of scientists also studied the brains of mice to pinpoint the C4 protein, which "tags a synapse for pruning by depositing a sister protein in it called C3," according to the NIH. "Again, the more C4 got switched on, the more synapses got eliminated."
http://nymag.com/scienceofus/2016/01/huge-genetic-breakthrough-on-schizophrenia.html
According to these new findings, a genetic stamp that people with schizophrenia inherit causes a normal process of brain development called synaptic pruning to go haywire, something some scientists already had a hunch about by comparing schizophrenic brains against typical ones. Let's back up for a moment: In a baby's brain, an incredible number of neurons and synaptic connections form -- sometimes up to 40,000 per second. By toddlerhood, the brain has amassed more neurons and synapses than it needs, so the excess ones are eliminated; this process begins in early childhood and is completed by early adulthood.
In a typically developing brain, this pruning process helps speed up cognitive functioning. But the schizophrenic brain takes this too far, eliminating too many of those neurons and synapses. "Normally, pruning gets rid of excess connections we no longer need, streamlining our brain for optimal performance, but too much pruning can impair mental function," said Thomas Lehner, the director of the office of genomic research coordination at the National Institute of Mental Health, in a statement. "It could help explain schizophrenia's delayed age-of-onset symptoms in late adolescence/early adulthood and shrinkage of the brain's working tissue."
Research has found, for instance, that certain brain regions in people with schizophrenia contain fewer synaptic connections, as compared to the brains of people without schizophrenia. Now this new genetic discovery may help explain why. As Post writer Amy Ellis Nutt explains:
In patients with schizophrenia, a variation in a single position in the DNA sequence marks too many synapses for removal and that pruning goes out of control. The result is an abnormal loss of gray matter. The genes involved coat the neurons with "eat-me signals," said study co-author Beth Stevens, a neuroscientist at Children's Hospital and Broad. "They are tagging too many synapses. And they're gobbled up."
For their paper in Nature, the researchers analyzed the brains of 700 people who'd had schizophrenia and donated their brains to science when they died. They also examined data pulled from the Psychiatric Genomics Consortium, which included more than 65,000 people -- about 29,000 with schizophrenia and 36,000 without -- from 22 countries across the globe. The team of scientists also studied the brains of mice to pinpoint the C4 protein, which "tags a synapse for pruning by depositing a sister protein in it called C3," according to the NIH. "Again, the more C4 got switched on, the more synapses got eliminated."
HenryDavidT
Jan 28, 2016, 10:20:07 PM1/28/16
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