The authors studied Nogo Receptor 1 (NgR1). Why? (I'd never heard of it before.)
Nogo Receptor 1 was originally identified as a mediator of myelin-dependent restriction of recovery from injury . In healthy brain, NgR1 was shown to be essential in closing the critical period for ocular dominance plasticity by single unit electrophysiology in anesthetized mice after monocular deprivation.
Which I gather means that earlier researchers found that the presence of this receptor "restricted" recovery from brain injury. Or maybe the other way around. And that if you cover an eye of an adult mouse, the open eye doesn't become dominant unless you disable these receptors. (I cheated and looked up the paper they referenced--I couldn't figure out what the Akbik et al were trying to say.)
So they tried to turn these receptors off and see what happened with dendritic spines. Normally small spines (tiny growths on the nerves) come and go all the time: only some of them go all the way and turn into synapses. UPDATE for clarification: Memories and learning are built in the brain using synapses. In adults the rate is smaller than in adolescents. So they used some mutant mice without the receptor (I think--their prose is hard to read!) and then appear to have also tried a chemical method of disabling the receptors:
Tamoxifen treatment leads to efficient ngr1 gene rearrangement and near total loss of mRNA and protein within 2 weeks. Mice with floxed ngr1 alleles with or without Actin-Cre-ERT2 transgene were allowed to develop with endogenous levels of NgR1. At P330, the mice received tamoxifen to delete NgR1 from the Cre subgroup. One month later, dendritic spine stability was assessed over 2 weeks. Even at this advanced age, deletion of NgR1 increases dendritic spine turnover to the level observed in adolescent mice
These are mice, hence the rather young "advanced age". "Floxed" means sandwiching a gene between two recombinant sequences, which makes it easy to remove.
They looked at the effects of different monitoring methods. (Apparently putting a tiny window in the skull stimulates spine development.) They looked at sensory deprivation followed by normal sensory experience, and so on.
The bottom line seems to be that without active NgR1 receptors, nerve dendrite spine generation in adult mice is like that in young mice.
Does that mean they learn like young mice? Well, maybe. It seems logical enough, and they tested some learning (using a rotarod), but that isn't very extensive. One thing they noticed was that memories of painful experiences seemed to diminish faster in NgR1-free mice.
Their conclusions include this little tidbit:
Here we show that NgR1 mutants have a decreased threshold for imprinting experience-dependent plasticity and accelerated learning in a motor training paradigm linked to cortical spine turnover. In the setting of rehabilitation, this suggests that antagonizing NgR1 decreases the threshold to reacquire motor skills via plasticity of neuronal connectivity
Or in English, it might be possible to recover more rapidly from nerve damage, maybe even spinal damage, if the doctor can suppress NgR1 activity for a while.
So should we all start taking suppressants before we start taking German?
Well... Apparently NgR1 slows memory loss. So without it... Come to think of it, adolescents aren't that good at remembering chores.
I'd decline to have them monkey with my NgR1.
In the matter of reforming things, as distinct from deforming them, there is one plain and simple principle; a principle which will probably be called a paradox. There exists in such a case a certain institution or law; let us say, for the sake of simplicity, a fence or gate erected across a road. The more modern type of reformer goes gaily up to it and says, "I don't see the use of this; let us clear it away." To which the more intelligent type of reformer will do well to answer: "If you don't see the use of it, I certainly won't let you clear it away. Go away and think. Then, when you can come back and tell me that you do see the use of it, I may allow you to destroy it."
This paradox rests on the most elementary common sense. The gate or fence did not grow there. It was not set up by somnambulists who built it in their sleep. It is highly improbable that it was put there by escaped lunatics who were for some reason loose in the street. Some person had some reason for thinking it would be a good thing for somebody. And until we know what the reason was, we really cannot judge whether the reason was reasonable. It is extremely probable that we have overlooked some whole aspect of the question . . . Chesterton