Brain & Behavior: Nerve Cells and Nerve Impulses

Unfortunately I haven’t had nearly enough time for blogging these days. I want to continue sharing my journey and my knowledge. My end goal is a career in behavioral neuroscience, here’s a bit of what I’m learning along the way! =)

  1.  Carefully describe the differences between graded potentials and action potentials. Include how both are initiated:

 An excitatory (glutamate) or inhibitory (GABA) neurotransmitter can cause depolarization or hyperpolarization within a neuron. When a graded potential does not reach the threshold of excitation the charge will defuse on its own and return to resting potential (only axons have a threshold of excitation and action potential). If depolarization reaches the threshold of excitation an action potential is triggered. When an action potential is triggered in an axon and depolarization goes from around -70 mV (70 less positive that the outside of the cell) to -55 mV, voltage-gated Na+ and K+ channels open causing Na+ to rush in (at resting potential there will be more sodium on the outside of the cell and potassium on the inside of the cell creating an electrical gradient or polarization).  The voltage-gated sodium channels snap shut before the voltage-gated potassium channels, and potassium is also exiting via the leak channels. Meanwhile the sodium-potassium pump is working to remove sodium and bring in potassium causing hyperpolarization (during the refractory period). During the refractory period the sodium channels are closed and unable to open (sodium channels have 3 positions). After the refractory period, is the relative refractory period. During the refractory period, hyperpolarization occurs for a short amount of time before returning to resting potential (-70 mV) –thus even during the relative refractory period hyperpolarization makes it more difficult to reach the threshold of excitation (stronger stimulation is needed to trigger a reaction). This refractory period is what stops the positive charge from returning back down the axon where it came from.

  • Describe the forces acting on sodium ions (Na+) before and during an action potential. Briefly discuss why lidocaine (or any local anesthetic) disrupts pain signals

Sodium ions are acted on by 3 forces; First, the inside of the cell is negatively charged which attracts the positively charged sodium ions; Secondly, along with the electrical gradient, the concentration gradient also pushes the ions toward the cell; Lastly, the sodium-potassium pump actively pumps sodium ions out to maintain this resting potential. Local anesthetic, such as lidocaine, inhibits action potentials by removing sodium ions. Without depolarization an action potential will not be reached and the pain signal wont travel. 

  • Discuss what we mean by the statement that “potassium (K+) ions are at equilibrium when neurons are at rest”. What forces are at equilibrium?

When the neuron is at rest, there is more potassium inside of the cell than outside. Potassium ions are relatively happy inside because of the negative charge within the cell; however, when too many potassium ions build up, the concentration gradient pushes some of the ions out and they easily reach equilibrium. So essentially the electrical gradient and concentration gradient almost balance things out. 

  • Discuss how action potentials “propagate” along an axon. Why is this more rapid with myelinated axons?

After the initial triggering of the action potential, it is reproduced with equal velocity and amplitude down the axon (unlike a graded potential that is “graded” by the stimulus). When the threshold of excitation is reached, the sodium and potassium voltage-gated channels open. The most notable change is the Na+ rushing in as the K+ is nearly in balance already. At the peak of the action potential the sodium gates close and remain closed during the refractory period (a few milliseconds). The potassium ions are still free to leave the axon until milliseconds later, at which point the voltage dependent K+ channels close (they can still leak out slowly through other channels). The positive change/depolarization causes the axon to reach the threshold of excitation, section by section. The refractory period prevents the electrical charge from flowing back in the direction it came from. 

    Propagation is much faster in myelinated axons—or axons covered in a myelin sheath. A myelin sheath is a layer of fats and proteins that causes saltatory conduction. Essentially the action potential jumps from the initiation point to the next node of Ranvier and then from node to node after that, increasing the speed at which the action potential travels. The action potential is not reproduced under the myelin sheath due to lack of sodium channels.

  • Discuss the different roles glial cells play in normal cell functioning? Are their diseases that affect glia? Describe one.

Radial glial cells are interesting because they are responsible for placement/migration of young neurons and they can transform or disappear into oligodendrocytes and astrocytes. 

Microglia are a type of neuroglia that work as a part of the immune system. They act as scavengers removing unwanted and harmful cells (plaques, or dead/damaged cells). They proliferate after brain trauma. They also remove unnecessary synapses which is associated with memory function.

Oligodendrocytes and Schwann cells serve the same function, myelinating axons, in two different placesOligodendrocytes are associated with production of myelin sheaths in the brain and spinal cord and they supply nutrients. Schwann cells act in the same manner in the periphery of the body. 

Astrocytes are my favorite glial cell—yes, I have a favorite! Astrocytes are shaped like little stars that protect the neuron, synchronize synapses allowing messages to be sent in waves and potentially add to the intensity of the signal by causing its neighbor to release chemicals as well! They also bring nutrients to certain areas by dilating the blood vessels.

Glial cells are vital the health of the nervous system and work to prevent neurodegeneration. Unfortunately, there are several diseases that affect and harm glia. Autism, Alzheimer’s disease, multiple sclerosis, Parkinson’s, glioblastoma, and some psychiatric conditions disturb glial function. Glioblastoma, for instance is a type of cancer with an extremely high fatality rate; It can occur in the spinal cord or brain in the astrocytes. While the cancerous tumor can be removed, glioblastoma spreads to healthy brain tissue making it impossible to remove all. Radiation and chemotherapy are usually recommended after the tumor is removed, but because of the blood=brain barrier and extreme protective measures our bodies take to protect our brains, it is also difficult to purge them of disease. 

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Kalat, J. W. (2019). Biological psychology (13th ed). Boston, MA:Cengage

3 thoughts on “Brain & Behavior: Nerve Cells and Nerve Impulses

    1. That is really interesting, I’ve never heard of that. How long have you been taking it and is it working well? Seems to be a relatively new treatment prompted by data from systematic review and meta-analysis of clinical trials.

      Liked by 1 person

      1. Yeah, there’s not a lot to support it, but I’ve got quite bad psychomotor retardation and we’re kind of low on options and grasping at straws. I haven’t been on it that long, but it seems to help a bit. The next little experiment might be D-cycloserine, which acts at NMDA receptors. There’ve only been a handful of studies, but worth a shot.

        Like

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