There are a number of ways to do in vivo examinations of the brains of living organisms. One technique is called time-lapse two-photon laser microcopy. Such technology is not good enough to clearly inspect individual synapses, which are very small. But such microscopy is good enough to show what are called dendritic spines.
A dendritic spine is a tiny protrusion from one of the dendrites of a neuron. The diagram below shows a neuron in the top half of the diagram. Some dendritic spines are shown in the bottom half of the visual. The bottom half of the visual is a closeup of the red-circled part in the top of the diagram.
An individual neuron in the brain may have about a thousand such dendritic spines. The total number of dendritic spines in the brain has been estimated at 100 trillion, which is about a thousand times greater than the number of neurons in the brain. The total number of synapses in the brain has also been estimated at 100 trillion. A large fraction of synapses are connected to dendritic spines. So by studying how long dendritic spines last, we can tell a good deal about how long synapses last.
It has been hoped that some relation could be drawn between learning and the formation of new dendritic spines. But scientists try to insinuate a connection between LTP and learning, and a paper says that "Sorra and Harris measuring three-dimensional reconstructed spines from serial section EM pictures, could not find any significant effect of LTP on morphological properties of spines."
No doubt the first scientists who examined dendritic spines were hoping to see some nice regularity and order, perhaps something that might be some kind of coding system by which dendritic spines might store information. But dendritic spines show no such regularity. Unlike positions in a DNA molecule (which must be one of only four nucleotide base pair types), dendritic spines can be any of many sizes, shapes or lengths. A length of dendrite and its spines (like the length shown in the bottom half of the visual above) seem to bear no resemblance to encoded information. The vast majority of new dendritic spines do not last longer than a few months.
Some unconvincing science papers have attempted to suggest a link between learning and dendritic spines. The latest is a paper promoted by a freely fantasizing Ohio State University press release that has the fictional title "Dendritic spines: The key to understanding how memories are linked in time." Everything the press release states in the quote below is flight-of-fancy stuff without any solid basis in fact:
"The study shows that memories are stored in dendritic compartments: When one memory forms, the affected dendrites are primed to capture new information arriving within the next few hours, linking memories formed close in time.
'If you think of a neuron as a computer, dendrites are like tiny computers inside it, each performing its own calculations,' said lead author Megha Sehgal, assistant professor of psychology at The Ohio State University. 'This discovery shows that our brains can link information arriving close in time to the same dendritic location, expanding our understanding of how memories are organized.' "
Sehgal can believe this wild speculation if she wants, but her statement above has no more basis in fact than a claim that the moon is mostly made of green cheese. The paper that Sehgal is promoting is an example of very low-quality science research.
The paper is the paper "Compartmentalized dendritic plasticity
in the mouse retrosplenial cortex links contextual memories formed close in time" which you can read here. It is another comedy-of-errors rodent study so badly designed that we should call it a mouse farce. The study hinges upon the totally unreliable "freezing behavior" technique of trying to measure fear recall in rodents. That method is utterly unreliable, for reasons I discuss at length in my post here. We have the graph below in the paper. You can tell from the number of dots corresponding to each bar that the study group size used was the way-too-small study group size of only 10 mice per study group.
Every time you see a graph like this, you can be sure the paper is not a credible scientific effort. Trying to judge "freezing behavior" is not a reliable way of measuring recall in rodents. And when a study claims that freezing behavior was produced in rodents after optogenetic stimulation (as this paper does), trying to claim that this was "memory activation," then we have the most unreliable way in which alleged "freezing behavior" can be used, because the very act of doing such optogenetic stimulation can itself produce "freezing behavior," even if no memory is recalled. Referring to immobility in rodents, a paper states, "It is possible to induce freezing by activating a variety of brain areas and projections, including the hippocampus (Liu et al., 2012), lateral, basal and central amygdala (Ciocchi et al., 2010; Johansen et al., 2010; Gore et al., 2015a), periaqueductal gray (Tovote et al., 2016), motor and primary sensory cortices (Kass et al., 2013), prefrontal projections (Rajasethupathy et al., 2015) and retrosplenial cortex (Cowansage et al., 2014)."
Another reason why the paper "Compartmentalized dendritic plasticity in the mouse retrosplenial cortex links contextual memories formed close in time" is a very bad example of low-quality research is its way too-small study group sizes, consisting of study group sizes such as only 4 mice or 9 mice or 10 mice or 12 mice. We have in this paper with 17 authors yet another farce of a study in which the number of authors is greater than the average study group size -- a situation we can very roughly describe using the scornful term "one mouse per scientist" research. No experimental neuroscience paper involving rodents should be taken seriously if it uses fewer than 15 or 20 subjects per study group; and typically the study group size needed for good statistical power in neuroscience experimental studies is much larger than 20 subjects per study group.
When experimental scientists have done their job properly, they produce in their papers something called a sample size calculation, in which they calculate the number of subjects needed to produce a result with a good statistical power such as 80%. When bungling experimental scientists fail to do their job properly, they will make no mention of doing such a calculation, or they will have a statement like this statement we find in the above paper: "No statistical methods were used to predetermine sample sizes but our sample sizes are similar to those reported in previous publications." A statement like this is similar to someone saying, "I didn't pay my taxes the last five years, but my friends also failed to pay their taxes." It is a very big ongoing disgrace in experimental neuroscience that experimenters are typically failing to use adequate study group sizes. So you do nothing to show that your study used an adequate study group sizes by claiming that similar studies used the study group size you used.
It seems that the paper has failed to even specify the sex of each of the mice that were used (which is quite a failure in a paper relying on freezing behavior judgments, as a tendency to "freeze" when afraid can differ very much between male and female rodents). The paper claims that "the investigator who collected and analyzed the data including behavior, imaging and staining was blinded to the mouse genotypes and treatment conditions." But the paper fails to give a detailed description of any blinding protocol followed, which should cause us to doubt that effective blinding occurred. A well-designed study of this type would have had a full description of a blinding protocol, to reassure us that the data gathering and analysis was not just a "see what ever you want to see" affair.
Contrary to the groundless tall tale that Sehgal has told, neither dendrites nor dendritic spines bear the slightest resemblance to any type of calculation device or computing device; and neither dendrites nor dendritic spines bear the slightest resemblance to memory storage devices. No one has ever found a number, token or symbol in a dendrite or dendritic spine, nor has anyone ever found the slightest speck of software in a dendrite or a dendritic spine. Dendritic spines no more resemble calculation devices or computing devices or memory storage devices than do the pimples on the face of a teenager with a bad case of acne. And each dendritic spine is about as short-lived as each such pimple.
The 2015 paper "Impermanence of dendritic spines in live adult CA1 hippocampus" states the following, describing a 100% turnover of dendritic spines within about six weeks:
"Mathematical modeling revealed that the data best matched kinetic models with a single population of spines of mean lifetime ~1–2 weeks. This implies ~100% turnover in ~2–3 times this interval, a near full erasure of the synaptic connectivity pattern."
The paper here states, "It has been shown that in the hippocampus in vivo, within a month the rate of spine turnover approaches 100% (Attardo et al., 2015; Pfeiffer et al., 2018)." The 2020 paper here states, "Only a tiny fraction of new spines (0.04% of total spines) survive the first few weeks in synaptic circuits and are stably maintained later in life." The author here is telling us that only 1 in 2500 dendritic spines survive more than a few weeks.
The same studies that show such short lifetimes for dendritic spines show that while they exist, dendritic spines very rarely maintain the same size and shape. During their short lifetimes, dendritic spines tend to change very much in size and shape. One paper says that even among a more stable subset of dendritic spines, "The majority of those (~80%) underwent a fluctuation in head size and neck length of more than 10% (~40% even of more than 30%) within 3 to 4 days." Units (dendritic spines) so short-lived and unstable cannot be any basis for storing memories that can last so reliably for decades.
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