Q: How does active learning and play impact brain plasticity?
A: This is a really important, key question. Educational researchers will answer that they observe inductively that play creates a state of motivation and concentration that increases learning without students having to think about the learning. Psychologists will refer to theories about intrinsic motivation, self-directed learning, flow and other ideas to describe behaviors that arise during both learning and play that promote learning. There’s literature on all of these. Neuroscientists have identified a circuit in the brain that recognizes when an experience is unexpected and positive that is called the reward circuit. This circuit is involved whenever we solve a puzzle, enjoy a treat, or experience any pleasurable activity. Animals will do work to activate this circuit. While this has to do with reward and motivation to get reward, learning can occur within any circuit in the brain.
In my mind the underlying reason play promotes learning comes from the observation that in rodents, play-like behaviors increase the number of NMDA receptors at synapses. At the level of individual neurons connected by synapses, learning occurs when synapses are strengthened. This occurs if multiple inputs to a single synapse are activated simultaneously or ‘associated’. NMDA receptors detect the elevated incoming activity and signal other molecules to build a stronger synapse or eventually more synapses as a result. Mice with abnormally high levels of NMDA receptors are really smart. So any activity that increases NMDA receptors (like play) will not only make that activity more memorable, but will also prime the circuit to be ready to learn other things more readily as well. Because the same sets of molecules that subserve synaptic activity, learning and memory are present in rodent brains and brains of higher mammals and humans, these same mechanisms should be active in our brains as well.
This is a really short explanation of a complex topic. If you want to understand synapses better, see the ‘movies’ which are really cartoons at brainu.org/movies. For circuits, play with the Virtual Neurons simulation at brainu.org/virtual-neurons. Once you’ve build a circuit, be sure to click ‘Zoom In’ and then ‘Learn’.
In my mind the underlying reason play promotes learning comes from the observation that in rodents, play-like behaviors increase the number of NMDA receptors at synapses. At the level of individual neurons connected by synapses, learning occurs when synapses are strengthened. This occurs if multiple inputs to a single synapse are activated simultaneously or ‘associated’. NMDA receptors detect the elevated incoming activity and signal other molecules to build a stronger synapse or eventually more synapses as a result. Mice with abnormally high levels of NMDA receptors are really smart. So any activity that increases NMDA receptors (like play) will not only make that activity more memorable, but will also prime the circuit to be ready to learn other things more readily as well. Because the same sets of molecules that subserve synaptic activity, learning and memory are present in rodent brains and brains of higher mammals and humans, these same mechanisms should be active in our brains as well.
This is a really short explanation of a complex topic. If you want to understand synapses better, see the ‘movies’ which are really cartoons at brainu.org/movies. For circuits, play with the Virtual Neurons simulation at brainu.org/virtual-neurons. Once you’ve build a circuit, be sure to click ‘Zoom In’ and then ‘Learn’.
Q: If your brain is always growing new dendrites and making new neural networks, does that mean your brain is getting bigger?
A: Yes. While new connections do mean that the brain grows bigger, fortunately, these changes are on a microscopic scale. A new dendritic spine see lesson, which can have multiple synapses on it, is only ~1 micron in length (0.000001 meters). For comparison, a human hair is about 75 microns wide.
To get a better handle on this, calculate the volume of a cylindrical spine with a diameter of 0.2 microns. At that volume, how many spines are there in a cubic micron? Since we haven't figured in the volume of dendrites, axons, cell bodies, and glia, this number is just an approximation but the dimensional issue should become clear. See Cruise through Hippocampal Neuropil: Brain Cells Visualized for more information. An Intimate Look at Your Brain features the Cruise video with comments from neurobiologist Kristin Harris.
For some fascinating comparisons and numbers about the brain, visit the Neuroscience for Kids Facts page.
To get a better handle on this, calculate the volume of a cylindrical spine with a diameter of 0.2 microns. At that volume, how many spines are there in a cubic micron? Since we haven't figured in the volume of dendrites, axons, cell bodies, and glia, this number is just an approximation but the dimensional issue should become clear. See Cruise through Hippocampal Neuropil: Brain Cells Visualized for more information. An Intimate Look at Your Brain features the Cruise video with comments from neurobiologist Kristin Harris.
For some fascinating comparisons and numbers about the brain, visit the Neuroscience for Kids Facts page.
Q: Does the brain ever get too big for the skull?
A: No, although when you consider what the brain contains, it is easy to see why you'd ask this question. It is estimated that there are 86 billion neurons packed into your amazing 3-pound brain.
One way the brain manages this bulk is by folding the brain matter into gyri (plural of gyrus) and sulci (plural of sulcus). The brain is floating in a sack of Cerebral Spinal Fluid (CSF) inside the meninges and there is some spatial flexibility in how tightly the gyri are packed together.
When talking about what happens in the brain as we learn, we tend to talk about all the new connections (synapses) we're generating. But while we are making new synapses as we learn, our brains are also pruning away unused synapses. This refinement – or streamlining – means that some dendritic spines are retracted. So any overall size change is minimal.
As individuals develop expertise in a field, we have been able to measure macroscopic size differences in parts of the brain. One case in point has to do with cab drivers in London, England. These individuals learn the thousands of roads and routes in the London area and this massive memorization task has been shown to dramatically increase the size of their hippocampi.
For more information on this research, check out this 2-minute clip from the PBS show The Brain with David Eagleman and these articles about the research:
Wellcome Trust. Changes in London taxi drivers' brains driven by acquiring 'the Knowledge' ScienceDaily, 22 December 2011.
Navigation-related structural change in the hippocampi of taxi drivers Eleanor A. Maguire, et. al. Proceedings of the National Academy of Sciences of the United States of America, vol. 97 no. 8.
One way the brain manages this bulk is by folding the brain matter into gyri (plural of gyrus) and sulci (plural of sulcus). The brain is floating in a sack of Cerebral Spinal Fluid (CSF) inside the meninges and there is some spatial flexibility in how tightly the gyri are packed together.
When talking about what happens in the brain as we learn, we tend to talk about all the new connections (synapses) we're generating. But while we are making new synapses as we learn, our brains are also pruning away unused synapses. This refinement – or streamlining – means that some dendritic spines are retracted. So any overall size change is minimal.
As individuals develop expertise in a field, we have been able to measure macroscopic size differences in parts of the brain. One case in point has to do with cab drivers in London, England. These individuals learn the thousands of roads and routes in the London area and this massive memorization task has been shown to dramatically increase the size of their hippocampi.
For more information on this research, check out this 2-minute clip from the PBS show The Brain with David Eagleman and these articles about the research:
Wellcome Trust. Changes in London taxi drivers' brains driven by acquiring 'the Knowledge' ScienceDaily, 22 December 2011.
Navigation-related structural change in the hippocampi of taxi drivers Eleanor A. Maguire, et. al. Proceedings of the National Academy of Sciences of the United States of America, vol. 97 no. 8.
Q:What is the difference between brain neurons and "normal" neurons? And could give a little bit of information on neural migration?
A: All neurons work the same way. Dendrites bring in information as small electrical signals. The neuronal cell body adds up all those signals and decides when the information should be passed on. Then a large electrical signal called the action potential moves down the neuron's axon. When the action potential arrives at the axon terminal, chemicals called neurotransmitters are spit out so the next neuron's dendrites can get the signal by tasting the neurotransmitter. This is what I would call normal.
The vast majority of neurons in your body are inside the brain and spinal cord which together make up the Central Nervous System (CNS). Motor neurons that innervate muscles live mostly inside the CNS; only their axons leave the brain or spinal cord and go to the muscles. Sensory neurons live just outside the CNS and have an axonal branch that brings information from the sense organs (eyes, inner ear, nose, taste buds, and nerve endings in muscle and skin) into the CNS. But other neurons that help control the organs inside your body, including your gut, have their cell bodies close to these organs, so they also live outside the CNS.
During very early development, the nervous system begins as a long thin tube of cells. The tube is filled with fluid. One end will become the brain; the other end will become the tail end of the spinal cord. New neurons are born by cell division along the inside edge of the tube. They then migrate away from where they are born or move to where they need to be as the brain and spinal cord grow into their final shapes and sizes. More cell division occurs at the brain end of the tube, which is why the brain is so much bigger than the spinal cord.
The vast majority of neurons in your body are inside the brain and spinal cord which together make up the Central Nervous System (CNS). Motor neurons that innervate muscles live mostly inside the CNS; only their axons leave the brain or spinal cord and go to the muscles. Sensory neurons live just outside the CNS and have an axonal branch that brings information from the sense organs (eyes, inner ear, nose, taste buds, and nerve endings in muscle and skin) into the CNS. But other neurons that help control the organs inside your body, including your gut, have their cell bodies close to these organs, so they also live outside the CNS.
During very early development, the nervous system begins as a long thin tube of cells. The tube is filled with fluid. One end will become the brain; the other end will become the tail end of the spinal cord. New neurons are born by cell division along the inside edge of the tube. They then migrate away from where they are born or move to where they need to be as the brain and spinal cord grow into their final shapes and sizes. More cell division occurs at the brain end of the tube, which is why the brain is so much bigger than the spinal cord.
Q:Which muscles and hormones move or secrete from neuromuscular and neuroglandular junctions, and which don't?
A: A muscle is made up of a lot of parallel muscle fibers. Each muscle fiber contracts when the neuron that connects to that muscle fiber sends it a chemical signal. The place where this occurs is called the neuromuscular junction. The neuromuscular junction is a special synapse between the end of a neuron's axon, called the nerve terminal, and a muscle fiber. For a description of how synapses work in general, this animation: The Synapse animation; there are several different formats available on our Movies page.
This same kind of communication goes on at the neuromuscular junction, only the receiving cell is a muscle fiber and it ends up contracting. You can simulate that in the Virtual Neurons program when you made the muscle contract. In this simulation, the motor neuron can only make the muscle contract if it is connected at the neuromuscular junction. Connecting to other parts of the muscle do not result in contraction because the specialized receptors that taste the released chemical neurotransmitter only live at the neuromuscular junction. Remember there are lots of motor neurons that run in parallel to all the muscle fibers of a single muscle that work together simultaneously to get the full muscle to contract. When the muscle does not receive signals from the motor neurons, then the muscle relaxes.
If the cell receiving synaptic input from a neuron is a gland cell, say a pituitary cell or adrenal gland cell, then when the incoming neuron sends a signal by releasing chemical neurotransmitter, the gland cell tastes that chemical and in turn releases its own hormone into the blood stream. The place where the incoming neuron makes a synapse on the gland cell is called the neuroglandular junction. This is also a specialized synapse that occurs on all glands.
So both terms, neuromuscular junction and neuroglandular junction, refer to the specialized synapses on muscle fibers and gland cells, respectively.
This same kind of communication goes on at the neuromuscular junction, only the receiving cell is a muscle fiber and it ends up contracting. You can simulate that in the Virtual Neurons program when you made the muscle contract. In this simulation, the motor neuron can only make the muscle contract if it is connected at the neuromuscular junction. Connecting to other parts of the muscle do not result in contraction because the specialized receptors that taste the released chemical neurotransmitter only live at the neuromuscular junction. Remember there are lots of motor neurons that run in parallel to all the muscle fibers of a single muscle that work together simultaneously to get the full muscle to contract. When the muscle does not receive signals from the motor neurons, then the muscle relaxes.
If the cell receiving synaptic input from a neuron is a gland cell, say a pituitary cell or adrenal gland cell, then when the incoming neuron sends a signal by releasing chemical neurotransmitter, the gland cell tastes that chemical and in turn releases its own hormone into the blood stream. The place where the incoming neuron makes a synapse on the gland cell is called the neuroglandular junction. This is also a specialized synapse that occurs on all glands.
So both terms, neuromuscular junction and neuroglandular junction, refer to the specialized synapses on muscle fibers and gland cells, respectively.
Q: I thought the video of the process of information traveling was great. However, what causes it to slow down or fall off? Is that too much information at once? What does this look like with a student who is mentally impaired or a student with lack of background knowledge? Does this process grow and become stronger with consistency and constantly introducing new information?
A: Great questions!
Once begun at the cell body, the action potential travels without failure to the ends of the axon. It travels at a constant speed that depends upon the diameter of the axon and upon whether the axon has myelin covering it. See faculty.washington.edu/chudler/cv.html for speeds and more details.
When an action potential moves down an axon, the portion of the axon it just left becomes resistant (scientists call this refractory) to firing another action potential for about 2 ms. This prevents the action potential from going back in the wrong direction.
So when an action potential reaches the nerve terminal at the end of the axon, it stops because it can't go further forward and it can't go backwards. The information carried by the action potential gets translated into a chemical signal that crosses the gap between neurons. The receiving neuron tastes the chemicals and starts new small electrical potentials in its dendrites. This is called synaptic transmission. See the animation The Synapse at brainu.org/movies.
This process of electrical-to-chemical-to-electrical communication occurs in all animal and human brains. The electrical signal is reliable, once started. The chemical signal can be variable and gets stronger with practice or weaker with disuse. This is the cellular basis for learning and memory. With learning, synapses strengthen and grow and new synapses form. See the animation Synapses Change at brainu.org/movies.
Mental retardation can have multiple causes, from trauma at birth to genetic. In Fragile X syndrome, the abnormal gene causes changes in dendritic spine shape that causes synapses to malfunction, limiting communication between neurons and causing developmental brain abnormalities.
Once begun at the cell body, the action potential travels without failure to the ends of the axon. It travels at a constant speed that depends upon the diameter of the axon and upon whether the axon has myelin covering it. See faculty.washington.edu/chudler/cv.html for speeds and more details.
When an action potential moves down an axon, the portion of the axon it just left becomes resistant (scientists call this refractory) to firing another action potential for about 2 ms. This prevents the action potential from going back in the wrong direction.
So when an action potential reaches the nerve terminal at the end of the axon, it stops because it can't go further forward and it can't go backwards. The information carried by the action potential gets translated into a chemical signal that crosses the gap between neurons. The receiving neuron tastes the chemicals and starts new small electrical potentials in its dendrites. This is called synaptic transmission. See the animation The Synapse at brainu.org/movies.
This process of electrical-to-chemical-to-electrical communication occurs in all animal and human brains. The electrical signal is reliable, once started. The chemical signal can be variable and gets stronger with practice or weaker with disuse. This is the cellular basis for learning and memory. With learning, synapses strengthen and grow and new synapses form. See the animation Synapses Change at brainu.org/movies.
Mental retardation can have multiple causes, from trauma at birth to genetic. In Fragile X syndrome, the abnormal gene causes changes in dendritic spine shape that causes synapses to malfunction, limiting communication between neurons and causing developmental brain abnormalities.
Q: If my brain is sending a signal to the quads to contract followed by a signal to relax (when walking, for example), is it a different neuron that brings the "relax" message down to the muscle?
A: Within the central nervous system where lots of different neurons can all synapse on one particular post-synaptic neuron, the mixes of excites and inhibits determine the overall balance (summed signal at the soma) of whether the post-synaptic cell decides to fire or not. When we throw down the bead neurons, the circuits we build model what goes on in the CNS (brain and spinal cord) where lots of neurons interact.
At the neuromuscular junction, only excitatory neurons reach the muscles themselves, so the muscle gets a signal that says contract. Otherwise, the muscle just relaxes. We have opposing muscles on opposite sides of joints that get excited alternately. So sending an excite signal to the quads makes them contract and lifts (extends) the lower leg at the knee. During this time, no signal goes to the hamstrings (back of the leg), so they don't contract but get stretched by the lower leg extension. When we decide to bend at the knee, no signal goes thru the neurons innervating the quad (so it now relaxes) and a signal goes through the motor neuron to the hamstrings causing them to contract, which in turn stretches the quads.
Fine control of these basic motions resides at the spinal cord level where inhibitory and excitatory synapses onto the motor neurons themselves fine tune how fast and frequently they send messages to the various muscles. So in reality, a muscle always gets a little stimulation to keep it a little bit taught. We call that muscle tone. No muscle is completely flaccid. When it's time to move the appropriate limb about a joint, all the agonist muscles that work together towards that motion contract in appropriately timed synchronous order.
At the neuromuscular junction, only excitatory neurons reach the muscles themselves, so the muscle gets a signal that says contract. Otherwise, the muscle just relaxes. We have opposing muscles on opposite sides of joints that get excited alternately. So sending an excite signal to the quads makes them contract and lifts (extends) the lower leg at the knee. During this time, no signal goes to the hamstrings (back of the leg), so they don't contract but get stretched by the lower leg extension. When we decide to bend at the knee, no signal goes thru the neurons innervating the quad (so it now relaxes) and a signal goes through the motor neuron to the hamstrings causing them to contract, which in turn stretches the quads.
Fine control of these basic motions resides at the spinal cord level where inhibitory and excitatory synapses onto the motor neurons themselves fine tune how fast and frequently they send messages to the various muscles. So in reality, a muscle always gets a little stimulation to keep it a little bit taught. We call that muscle tone. No muscle is completely flaccid. When it's time to move the appropriate limb about a joint, all the agonist muscles that work together towards that motion contract in appropriately timed synchronous order.