Among the many proteins produced are neurotrophins , which stimulate the growth of the synapse and structural elements, stabilizing increased sensitivity to neurotransmitters. This molecular cascade is essential for memories to become long-lasting. The prevailing view is that declarative memories are encoded in the hippocampus, then transferred to the frontal lobes for long-term storage and consolidation.
Research suggests that, over time, the hippocampus becomes less important for retrieving older memories as the frontal cortex assumes that task. As researchers gain new insights into the molecular mechanisms underlying memory, pharmaceutical and technological advances may enable artificial manipulation of synaptic plasticity.
New treatments could be developed for synapse-related neurological disorders — such as eradication of harmful memories tied to post-traumatic stress disorder PTSD — or for boosting our ability to learn and remember. This article was adapted from the 8 th edition of Brain Facts by Alexis Wnuk. Deborah Halber Deborah Halber is a Boston-based author, science writer and journalist. Her work has appeared in The Atlantic, Time. See how discoveries in the lab have improved human health. Read More. Do you believe any of these common neuromyths?
Test your knowledge. For Educators Log in. This also works the other way round: as soon as the activity level exceeds an upper limit, the number of synaptic connections is reduced to prevent any overexcitation -- the neuron firing rate falls.
Similar forms of homeostasis frequently occur in nature, for example in the regulation of body temperature and blood sugar levels. However, Markus Butz stresses that this does not work without a certain minimal excitation of the neurons: "A neuron that no longer receives any stimuli loses even more synapses and will die off after some time. We must take this restriction into account if we want the results of our simulations to agree with observations.
When the retina is damaged, this percentage increases even further. Using computer simulations, the authors succeeded in reconstructing the reorganization of the neurons in a way that conforms to experimental results from the visual cortex of mice and monkeys with damaged retinas. The visual cortex is particularly suitable for demonstrating the new growth rule, because it has a property referred to as retinotopy: This means that points projected beside each other onto the retina are also arranged beside each other when they are projected onto the visual cortex, just like on a map.
If areas of the retina are damaged, the cells onto which the associated images are projected receive different inputs. These crosslinks are formed slowly from the edge of the damaged area towards the centre, in a process resembling the healing of a wound, until the original activity level is more or less restored. As early as , psychology professor Donald Olding Hebb discovered that connections between neurons that are frequently activated will become stronger.
Those that exchange little information will become weaker. Today, many scientists believe that this Hebbian principle plays a central role in learning and memory processes. While synaptic plasticity in involved primarily in short-term processes that take from a few milliseconds to several hours, structural plasticity extends over longer time scales, from several days to months.
Structural plasticity therefore plays a particularly important part during the early rehabilitation phase of patients affected by neurological diseases, which also lasts for weeks and months. The hippocampus is generally regarded as the organ where most memories are stored. Scientists long believed that the formation of memories in the brain was mainly due to the extremely large number of excitatory neurons.
However, it is now known that inhibitory interneurons, of which there are about ten times fewer, also make a significant contribution to our ability to remember things.
While excitatory nerve cells activate neighbouring cells, interneurons switch off the following cells, resulting in the separation of similar memories. Nerve cell activity reveals insights into how the strength of synaptic transmission can be modulated. First, how can the synapses of these granule cells activate interneurons, which in turn inhibit other granule cells? And second, how does this work during learning and memory formation?
The strengthening of synapses between cells can be achieved if they are all active simultaneously. This basically means that the granule cell must be active at the same time as the interneuron. By the seventh month of a pregnancy, the fetus starts to emit its own brain waves. New neurons and synapses are formed by the brain at an extremely high rate during this time.
During the first year of life, the number of synapses in the brain of an infant grows more than tenfold. By age 2 or 3, an infant has about 15, synapses per neuron. In the visual cortex of the brain the part responsible for vision , synapse production hits its peak at about 8 months of age.
In the prefrontal cortex, peak levels of synapses occur sometime during the first year of life. This part of the brain is used for a variety of complex behaviors, including planning and personality. During the second year of life, the number of synapses drops dramatically. Synaptic pruning happens very quickly between ages 2 and During this time, about 50 percent of the extra synapses are eliminated.
In the visual cortex, pruning continues until about 6 years of age. Synaptic pruning continues through adolescence, but not as fast as before.
The total number of synapses begins to stabilize. While researchers once thought the brain only pruned synapses until early adolescence, recent advancements have discovered a second pruning period during late adolescence. According to newer research, synaptic pruning actually continues into early adulthood and stops sometime in the late 20s. Research that looks at the relationship between synaptic pruning and schizophrenia is still in the early stages.
For example, when researchers looked at images of the brains of people with mental disorders, such as schizophrenia, they found that people with mental disorders had fewer synapses in the prefrontal region compared to the brains of people without mental disorders. Then, a large study analyzed post-mortem brain tissue and DNA from more than , people and found that people with schizophrenia have a specific gene variant that may be associated with an acceleration of the process of synaptic pruning.
More research is needed to confirm the hypothesis that abnormal synaptic pruning contributes to schizophrenia. While this is still a long way off, synaptic pruning may represent an interesting target for treatments for people with mental disorders.
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