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Your brain has the innate ability to physically change itself when faced with new, challenging experiences. This ability is called neuroplasticity. Your brain's billions of neurons —its cellular building blocks—interact with each other in complex ways. Signals travel from one neuron to another down intricate neural pathways whose structures determine your thoughts, impulses, emotions, insights, and more. As our brains age through childhood, these neural pathways change: less-used pathways are pruned away while pathways that you use regularly grow stronger. Each task relies on a different neural pathway.

Neuroplasticity is your brain's ability to create neural pathways and reshape existing ones—even as an adult. Your brain makes these small changes naturally throughout your lifetime. But when neuroplasticity's potential is thoughtfully and methodically explored, this physical reorganization can make your brain faster and more efficient at performing all manner of tasks—no matter how large or small they may be.

The nervous system controls behavior, and we have all witnessed the changes in behavior of children as they learn to talk and walk, and later on to ride a bicycle and to read and write. These changes occur because of the plastic properties of the brain: new contacts are formed, the properties of existing synapses and neurons change, and lately we have evidence that new neurons are born and added to the circuitry. Much of this learning occurs according to a pre-programmed, but still requires the appropriate experience: human children can learn to speak any first language, but their learning is much faster if they hear that language spoken to them and used around them during the first two years of life.

Similarly, bees are pre-programmed to learn where the hive is when the leave it the first time in the morning, and to learn where each flower patch is as they leave it to go on to another. Each of the different forms of learning and memory result from some change in the nervous system, and the study of the those changes is one of the most active areas of neuroscience today.

A Rich Body of Neuroplasticity Research

Neuroplasticity suggests that anyone can improve their brain, no matter what their age or background. A growing body of research adds more credence to this concept every day.

Recently, Dr. Susanne Jaeggi from the University of Michigan found that young adults improved fluid intelligence performance after training with a working memory task called dual n-back (Jaeggi, et al., 2008). Fluid intelligence is the type of dynamic problem-solving that you use when encountering new challenges—it's what most people mean by "intelligence".

A study of over 2,000 elderly adults in 2002 suggests that even older brains have plenty of room to improve and learn. (Ball, et al., 2002). After 10 hours of training over the course of six weeks, elderly participants gained skills that transferred to real-world abilities —they experienced fewer declines in their ability to perform basic daily activities.

And finally, Lumos Labs collaborated with Stanford and San Francisco State University researchers to publish a groundbreaking study showing that healthy adults benefit from web-based cognitive training (Hardy et al., 2011). Participants in this peer-reviewed controlled trial saw 20% improvements in visual attention and 10% improvements in working memory. The body of evidence for neuroplasticity and brain training is constantly growing. For a full picture of HCP research on these topics, see the Research Behind Lumosity.

How You Can Harness Your Brain's Abilities

You, too, could achieve amazing improvements. But not every experience can rewire your brain for the better: in order to fully harness the power of neuroplasticity, you need to challenge your brain with training that's novel, adaptive, and complete. This complex formula explains why some popular games such as Sudoku and crosswords don't increase intelligence—the more you play these games, the more you retrace overlearned pathways in your brain. You need carefully calibrated challenges to really strengthen and stretch your brain.

Novelty Forces Your Brain to Change

Novel challenges present unexpected obstacles, forcing your brain to work in new ways. When your brain encounters these new challenges, it must remodel its existing circuitry and find new pathways for information processing. That's because the brain assigns special neural pathways or each type of task. Just as you use different muscle groups for running and swimming, so you use different neural circuitry for reading and watching a movie. Familiar tasks simply reactivate existing circuitry—which can keep your brain active, but won't change or improve it in fundamental ways.

Adaptivity Keeps Your Brain Challenged

You have a unique set of cognitive strengths and weaknesses. A task that's easy for someone else may be a challenge to you, and vice versa. In order to improve, you need tasks appropriate for your brain's ever-changing ability levels. As your brain becomes stronger, it's able to handle tougher challenges. This response to challenges is a key part of neural growth, and you need challenges that adapt quickly enough to push you.

A Complete Program Makes Sure You're Improving in Every Way

Your brain is a complex machine with parts that work together. That's why it's important to get complete training that addresses multiple core brain functions—even the simplest tasks draw upon more than one cognitive ability. Imagine doing an action movement. You need to process information quickly to understand how the plot evolves. You need to pay sharp attention or you'll miss key details and movements. You need to store and manipulate information in your working memory throughout the movie to understand how all of it ties together. Even the simplest tasks require a sophisticated choreography of neural activity. That's why it's important to get balanced training that exercises a wide variety of skills—and improves abilities you need to successfully navigate your daily life.

Brain Training Has the Potential to Change Lives

Neuroplasticity can have wide-ranging applications if properly and carefully explored. Researchers have used brain training to rehabilitate patients with brain trauma, chemofog, Mild Cognitive Impairment, and more. But healthy people have also used brain training to sharpen their daily lives and ward off cognitive decline. You, too, can harness the power of neuroplasticity to remember more, think faster, and achieve your full potential in every aspect of life. The benefits may well be endless.

Homosynaptic depression and behavioral habituation. All of us are familiar with the experience of entering a room and being aware of a new odor, and then losing our awareness of it by a few minutes later. Similarly, we are aware of the feel of our clothes when we put them on, but again lose awareness of that as time passes. This decay of awareness is called HABITUATION, and without it we couldn't discriminate between the new and the old: all stimuli would appear fresh and novel and demand our attention. The neural mechanisms of habituation have been identified as the weakening of particular synapses in the path from sensory input to the CNS. This is called SYNAPTIC DEPRESSION, and it is usually found at the synapses made by sensory neurons onto interneurons. Synaptic depression usually results from a decrease in the amount of transmitter released by the presynaptic terminal. This may be because the repeated activation of the synapse has depleted the supply of transmitter available to be released, or because the mechanism for releasing transmitter has gradually become less effective. Repeated activation of a presynaptic input leads to a reduction in the response. On the first trial, the postsynaptic cell fires an action potential. Subsequently, it fails to fires and the EPSP drops in amplitude to a low level.

Classical Conditioning

At the last turn of the century, Ivan Pavlov in Russia defined a form of learning in which a neutral stimulus comes to take on the meaning of a natural stimulus by being paired with the natural stimulus. In his experiments, Pavlov found that a dog would salivate when presented with the odor of meat. He called the odor the UNCONDITIONED STIMULUS, or US, and the salivation was the UNCONDITIONED RESPONSE, or UR. If he presented the sound of a bell just before he presented the meat odor, and repeated that pairing a few times, he found that the dog would now salivate in response to the sound of the bell by itself. He called the sound of the bell a CONDITIONED STIMULUS (CS), and the salivation in response to the bell is the CONDITIONED RESPONSE (CR). This pattern of learning is called either Pavlovian conditioning or classical conditioning, and it is a major example of ASSOCIATIVE LEARNING, in which the association of one stimulus with another causes the new stimulus to take on the meaning of the old stimulus. Learning to read or to talk is an example of this: the forms on the page come to represent the meaning of the sounds of words.

Hebbian Learning In the late 1940s, Donald Hebb described a way in which a network of neurons could lead to classical conditioning. Imagine that a neuron has two sets of inputs, one from the olfactory system that is excited by the smell of meat, and one from the auditory system that is excited by the sound of a bell. Imagine that the first synaptic connection is quite strong, so that whenever the olfactory neuron becomes active it excites the postsynaptic cell to fire. Imagine that the postsynaptic cell then triggers a salivation response. The second connection is normally very weak, so that the sound of a bell causes only a small EPSP to occur in the salivation neuron. When the two stimuli are paired, however, so that the input from the bell neuron comes at about the same time as the salivation neuron fires in response to the olfactory neuron, then Hebb imagined that the strength of the bell neuron synapse would increase. This increase would only occur when the bell neuron's input coincided (or nearly coincided) with the salivation neuron's response: the pre- and postsynaptic neurons have to be active together for the strength of the synapse between them to increase. Several repetitions of this would strengthen the synapse to the point where the bell neuron alone was able to fire the salivation neuron, so that now the dog would salivate at the sound of the bell.

Long-term Potentiation (LTP)

For many years Hebbian learning and Hebbian synapses were merely theoretical, but in the early 1970s a phenomenon was discovered which suggested that it might actually occur. This was LONG-TERM POTENTIATION. LTP occurs in response to stimulating a synaptic input to a neuron at high frequency for a short-period of time. This causes the later responses to single inputs from that synapse to produce a significantly larger response than before. The potentiation of the normal response lasts for hours.

NMDA Receptors

LTP occurs primarily at central synapses where the transmitter is the amino acid glutamate. Glutamate acts at several different types of receptor molecules in the postsynaptic membrane; two of the most important are AMPA receptors and NMDA receptors.

AMPA receptors cause + ions like Na+ to enter the cell when the receptor has been activated by glutamate. NMDA receptors do the same thing, but the flow of ions is controlled by the postsynaptic cell's membrane potential. At normal rest potential, the NMDA receptors have only weak effects. When the cell is depolarized, however, much more + current comes into the cell in response to the same amount of glutamate, so that the glutamate creates a larger EPSP than before. This voltage-dependence occurs because a Mg++ ion normally blocks the channel in the NMDA receptor that permits + ions to enter the cell. When the cell is depolarized, however, the Mg++ ion is pushed out of the channel, and Ca++ and Na+ can both enter.

The Ca++ can act as a second messenger and produce other changes in the postsynaptic cell that elevate its response. NMDA receptors contribute to LTP because the high-frequency inputs strongly depolarize the cell by repeatedly activating the cell's AMPA receptors. This depolarization dislodges the Mg++ ion from the NMDA receptor channels, and allows them to have a much larger effect than previously. The Ca++ acts as a 2nd messenger and creates additional changes that allow the cell's increased responsiveness to persist. NMDA receptors are also useful for producing associative learning (classical or Pavlovian conditioning). Imagine that the normal (food odor) input to a salivation neuron activated AMPA receptors, whereas the conditioned input, a bell sound, activates NMDA receptors. If the bell sound comes at about the time of the food odor, the AMPA receptors will depolarize the cell and enable the input through the NMDA receptors to be more effective. When repeated, this will eventually allow the bell input to activate the salivation neuron by itself.

As you can see, the NMDA receptors provide a mechanism for Hebbian synapses and thereby for classical conditioning and associative learning. The cell body and dendrites (proximal) show a retraction in cell size and breakdown in the mature architecture (Golgi Body, RER) which utilizes the vesicular-transport system (Chromotolysis Reaction). The neuron now reverts to immature phenotype and produces structural proteins (actin and tubulin) to promote extension of its processes.

Apoptosis: the breakdown of chromosomes due to cytoskeletal collapse resulting from increase proteolysis mainly due to the enzyme caspase 3. Largely responsible to cell death occurring during development and after various brain disesases or aging.

FACTORS INVOLVED IN NEUROPLASTICITY

Neurotrophic Factor: The general class of a wide range of moleculaes which can increase cell survival, stimulate neurite outgrowth or branching

    a. Survival: A molecule (protein) which blocks apoptosis and increases the survival of a selective group of neurons. Neurotrophic factors have specific receptors (BDNF acts on TrkB, NGF acts on TrkA) which act on the phosphorylation of a tyrosine-directed kinase (increase phosphorylation). Removal of this factor will induce apoptosis.
    b. Neurite Extension: A molecule (protein, neurotransmitter) which promotes elongation by stimulating microtubule assembly or stabilizing microtubules/MAP associations. MAP are Microtubule Associated Protein which bind to polymers of tubulin (microtubles) when un-phosphorylated.
    c. Branching Factors: Molecules which promote the entry of Ca++ and local breakdown of cytoskeleton. When the Ca++ increase is localized to a spine (microfilaments, endoplasmic reticulum) there is an increase in spine size. Glutamate (Excitatiry Amino Acids), Hallucinogens, caffeine.
    d. Cajal's Chemotactic theory 1892, soluble, diffusible factor which directs the migration of neurons or the growth of processes. Morphogens have chemical gradients in brain which sets up differential genetic expression. Presence of source (fibers, blood vessels, Ventricles) and sink (transporter proteins).
    e. Ionic gradients produces by neuronal activity and glial sequestration of K+.
    f. Attachment Factos: Laminin, N-CAM, glial surface, Paul Weiss hypothesis (1934) of Contact Guidance.

CHEMICALLY INDUCED LESIONS AND SPROUTING

    A. Get sprouting after chemical damage, for example 6-OHDOPA, 5,7-DHT, MPTP (Parkinson's syndrome), methamphetamine, MDMA, fenfluramine (redux).
    B. Hormonal changes: Estrous Cycle, Hibernation, Pregnancy reduces brain cortical volume (15%)
    C. Time-associated: Seasonal changes, diurnal changes

SPROUTING CAN BE ASSOCIATED LEARING

    A. Plasticity is associated learning in aplysia and rats, increase in sprouts and synapses.
    B. Enriched Environment
    C. Spines and Calcium Channels

WHAT IS CELLULAR BASIS OF PLASTICITY?

Neuronal Instability: A model of plasticity that proposes that neurons fluctuate between mature and immature phenotypes, the role of trophic factors is to stabilize the neuron in a mature phenotype. Change in the cytoskeleton, induced by alterations in phosphorylation.

Growth Factors:

    A. Proteins Acting on Receptors: NGF, BDNF act on Trk receptors that are kinase enzymes. Immediate action of neurotrophic factors is to increase kinase activity, ligand and receptor are internalized and transported back to the cell body (NGF). Induce alterations in genes that are read.
    B. Protein Acting By Diffusion: S100b is an extension factor, stabilizes the cytoskeleton by inhibiting the phosphorylation of the MAP (microtubule associated proteins).

Trophic Role of Neurotransmitters

    a. NGF and S100b are produced and released by astrocytes. NGF is released adrenergic-b receptor and S100b is released by 5-HT1A receptor. Neurotransmitters are involved in regulating the availability of trophic and extension factors.
    b. Receptors, modulating the kinase enzymes, can directly modify the growth of neurons. For example, 5-HT at 10-9 M acts on the astrocytes to release S100b and on the neurons activates Gi, which inhibits cAMP production, and decrease PKA. On the other hand, 5-HT at 10-6 M acts on the 5-HT2A receptor to increase glycogenolysis by astrocytes and on the neurons activates a Gs which stimulates phospholipase-C and increase PI-3 and NAG, which in turn increase Ca++ and leads to increased PKC.
    c. When 5-HT levels are reduced to near 0, there is a dramatic loss of dendrites and synapses in the brain, decreased learning and induction of depression. These changes are reversible. Thus, neurotransmitters are not only involved in mediating the electrical connection between neurons, they are also involved in the plasticity of the neurons.

Brain Development and Neuroplasticity

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