You are hereAsk the Neuroscientist
Ask the Neuroscientist
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. The following links provide additional information on this topic:
www.nimh.nih.gov/about/director/2012/the-long-paths-to-breakthroughs.shtml
www.nimh.nih.gov/science-news/2010/imaging-reveals-abnormal-brain-growth-in-toddlers-with-fragile-x.shtml
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. The following links provide additional information on this topic:
www.nimh.nih.gov/about/director/2012/the-long-paths-to-breakthroughs.shtml
www.nimh.nih.gov/science-news/2010/imaging-reveals-abnormal-brain-growth-in-toddlers-with-fragile-x.shtml
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.