Notes for Lesson 1

Please answer each question in about 275 words.

Use clear headings (1.1, 1.2, 1.3, etc.) and keep answers separate.

Follow my module/lecture materials as the main references (attached).

Questions:

1.1

What is the difference between afferent and efferent neurons? What are interneurons? Come up with your own example going from sensory to cognition to motor, naming the type of neurons along the way.

1.2

Which type of glia cells are found in the peripheral nervous system (PNS)? Which types are found in the central nervous system (CNS)? Which type(s) remove waste? Which type(s) myeline axons? Which type(s) help with structural support? Make your own chart or table organizing these types of cells.

1.3

1.4

What is the difference between the synapse and synaptic cleft? What kind of neurotransmitters bring the neuron closer to firing an action potential?

1.5

What is the difference in the distribution of sodium and potassium ions during the resting potential (i.e. which are more concentrated inside versus out)? How does the sodium-potassium pump maintain this difference?

1.6

State in your own words why sodium immediately rushes in to the cell as soon as the ion channels for sodium are open. Why might potassium and chloride not be as compelled to move into or out of the cell then their ion channels are open?

1.7

Describe the difference between a hyperpolarization and a depolarization. Based on the normal resting potential of -70mV, would a shift to -65 mv be a depolarization or a hyperpolarization? Also based on the normal resting potential of -70mV, would a shift to -75 mv be a depolarization or a hyperpolarization?

1.9

What is the difference between the synapse and synaptic cleft? What is the difference between the pre-synaptic neuron and the post-synaptic neuron?

1.10

What is the role of exocytosis in the pre-synaptic neuron? How does a graded potential differ from an action potential? What ion channel might open for an excitatory NT? What ion channel might open for an inhibitory NT?

1.11

What is the difference between a neurotransmitter and a hormone? If serotonin is metabotropic and Acetylcholine is ionotropic which will take longer to open the ion channel? Which will last longer? Finally, given what you have read which would open CL- and which would open Na+?

1.12

Will a serotonin antagonist produce an inhibitory or an excitatory effect? Why? You may need to refer to the previous lesson to find out if serotonin is excitatory or inhibitory.

Here’s there copy and paste Modules:

Modules

1.1 The Purpose of the Nervous System: To Transmit Information

The nervous system is responsible for conveying all kinds of information. It tells you what is going on outside yourself – i.e. sensory information. Sensory neurons are called afferent neurons and deliver information to the brain.

o For example: Feeling that its getting too hot, or seeing the fog roll in over the mountains.

It allows you to access memories and make decisions by transmitting information about the past and current conditions, i.e. information processing. These neurons are called interneurons.

o For example: Deciding to change the temperature or to stay home because you remember the difficult time you had driving in the last fog.

It passes on information to muscles so that you can move, i.e. motor. Motor neurons are called efferent neurons and deliver information from the brain to the muscles.

o For example: Moving your muscles to walk to thermostat or pulling the blankets back over yourself as you are staying in bed!

And so on from simply breathing to studying something as esoteric as Chaucers influence on Middle English consonant-vowel inflections we can thank the information conveyed by our nervous systems!

1.2 GLIA CELLS: Not all cells convey information

Glia cells are a sub-type of cell within the nervous system. These cells support the nervous system by doing thing like creating structure and transporting nutrients, but they typically do not transmit information. Below is a description of certain types of glia cells.

1.4 Some Important facts about Neurons

o There are over 85 billion neurons in the nervous system.

o Neurons do not touch one another in the nervous system.

o The space in between each neuron is called the Synaptic Cleft.

o The terminal button of Neuron 1, the space, and the receptor of Neuron 2 is called a Synapse.

o There may be over 1,000 trillion synapses.

o When the Neuron fires, it releases Neurotransmitters into the synaptic cleft.

1.5 The Resting Potential of a Neuron

The term “resting” potential is a misnomer in that the neuron isn’t actually resting. That is to say, when I am resting, I am on my sofa watching Netflix with some cookies and tea. In a neuron, it is more like a professional baseball player who is prepared for the pitcher to do his thing.

When we speak of a neuron’s potential, what we mean is the difference in electrical charge between the inside and the outside. The resting potential is this difference in charge when the neuron is not firing an action potential. At the resting potential, the neuron is about 70 millivolts more negative on the inside than the outside (-70 mV). Why? This difference is due to the difference in ions (particles with a postive or negative charge). Look over this graphic:

Here is a guide to the ions:

Abbreviation for Ion

Name of Ion

Charge Valence

Concentration at Resting Potential

A-

Anions / Protein

Negative

More inside Neuron

K+

Potassium

Positive

More inside Neuron

Na+

Sodium

Positive

More outside Neuron

Cl-

Chloride

Negative

More outside Neuron

Ca++ (not shown)

Calcium

Positive

More outside Neuron

Inside the resting neuron, these postive and negative charges add up to make the inside about 70 mV more negative. But everything is about to change because sodium really, really wants to get inside the neuron. Why? Find out in the next lesson!

But first, what keeps the resting potential going? One of the most well-studied ways is the sodium-potassium pump. This is an active transport system (a biological system that requires energy) that transports 2 potassium into the cell while transporting 3 sodium ions out. This system is constantly at work, so it is a mechanism that maintains the resting potential. Here is a video about the Na+ – K+ pump:

The receptors the receiving (postsynaptic) are along the dendrites. The postsynaptic neuron picks up the neurotransmitter, which may be Excitatory or Inhibitory.

Excitatory neurotransmitters bring the neuron closer to conveying an electric charge down the axon called an Action Potential.

Action potentials cause neurotransmitters to be released into the synaptic cleft.

But before that happens, there is the resting potential, which is described next.

1.6 Ions Move Against their Gradients

As I’ve said, Sodium wants to come in … it is poised and ready because of 2 forces moving Neuron away from the Resting Potential and toward an Action Potential: the Electrical Gradient and the Concentration Gradient.

o Electrical Gradient: Difference in the distribution of Charge between inside and outside (ignoring the type of ions producing that charge)

More negative inside than out – usually a difference of 70 millivolts

o Concentration Gradient: The distribution of Ions between inside and outside (ignoring the charge – focusing only on the kinds of ions)

Sodium more concentrated outside (Sodium is more positive than potassium)

Think about it this way: Nature seeks balance. So if there is more outside, it wants to come inside to make it even. In other words, ions move against their gradients as if they are attempting to make the charge and the concentration even across the membrane.

Speaking of the membrane, it is useful to think of it like skin covered in pores. These pores are often called “gates” or “channels” which are open at certain times to selective ions. In other words, the neuron is covered with a semi-permeable membrane. There are different ways to open the gates to open these gates. The two main ways are 1) through voltage or 2) through chemicals that can bind to a receptor (aka ligands). This makes for 2 important ion channels”

1) Voltage-gated ion channels: Open in response to the membrane reaching a certain voltage

2) Ligand-gated ion channels: Open in response to a specific chemical attaching to the neuron.

The two major ion players here are Sodium and Potassium. What happens when the gates for Sodium and Potassium open???

Electrical Gradient

Concentration Gradient

Sodium (Na+) Channels Open

Sodium moves in due to it being more negative inside the cell

Sodium moves in due to there being less Sodium inside the cell

Potassium (K+) Channels Open

Potassium moves in due to it being more negative inside the cell

Potassium moves out due to there being less Potassium outside the cell

So, when the gates open, sodium rushes in because both the electrical and concentration gradients compel it in the same direction. In contrast, potassium gradients compelling it to move in opposite directions. This is why sodium will enter the cell as soon as its ion channels open.

1.7

Action Potentials

An action potential is an electrical impulse that travels down the axon. In an action potential, the polarization is going to reverse and the charge is going to temporarily be more positive inside the neuron. Let’s consider 2 terms:

Hyperpolarization: Increased Polarization, i.e. an increased difference in charge between the inside and outside. For example, when the difference in charge goes to -90 (a 90 mV difference between the inside and the outside – further from 0 compared to the baseline of 70). A hyperpolarization moves the neuron away from reaching an action potential.

Depolarization: Reduction of polarization toward 0: For example, when the difference in charge goes to -50 (a 50 mV difference between the inside and the outside – closer to 0 compared to the baseline of 70). A depolarization moves the neuron toward from reaching an action potential.

For an action potential to take place, the threshold of excitation must be reached. This is the point when the voltage-gated sodium channels snap open. Because sodium rushes into the cell, this produces a sudden and massive depolarization. The depolarization is so big, the inside of the neuron becomes more postive – usually reaching about +30 mV. This begins at the axon hillock, and propagates all the way down the length of the axon. So, more specifically, the action potential then is this postive charge zipping down the length of the axon.

An action potential is interesting because it follows the allor nonelaw: The amplitude, velocity of an Action potential is always the same no matter how intense the initial stimulus was. So, it doesn’t matter if it is a kitten in the gutter or Pennywise the terrifying clown – the action potentials in your heart will not go any faster or slower down the axon! What changes? The frequency of producing action potential can change.

Following an Action Potential, there is a period where the neuron is not likely to produce another one. this is the refractory period. There are two stages to the refractory period: 1) Absolute refractory period: Can not fire an action potential, sodium is closed. Relative refractory period: unlikely to fire an action potential, potassium is open.

1.9

Synapses

There are about neurons. To do their job, each one of these has to be able to send signals to other neurons. This connection between 2 neurons is called a synapse. Each neuron can make connections with thousands of other neurons, making over in the cortex alone!

Understanding these Connections: Terms

Synaptic cleft: Gap between one neuron and the next. Also called the synaptic gap.

Pre-synaptic: 1st (sending) neuron

Post-Synaptic: 2nd (receiving) neuron

Synapse: includes pre-synaptic neuron, synaptic cleft, and post-synaptic neuron

When an action potential occurs in the pre-synaptic neuron, chemicals called neurotransmitters are released into the synaptic cleft to be picked up by the post-synaptic neuron.

1.10

Processes in the Synapse

2

In the Pre-Synaptic Neuron:

Neurotransmitters (NTs) are stored in vesicles: Little sacs or packets full of neurotransmitter!

When the action potential reaches the axon terminal, calcium gates open.

Calcium allows vesicles to bind to the inside of the axon membrane

This binding allows an opening into the synaptic cleft and the NT is excreted into the gap.

This is called exocytosis: releasing the NT into the synaptic cleft.

In the Post-Synaptic Neuron:

The neurotransmitters released by the pre-synaptic neuron are picked up by the dendrites of the post-synaptic neuron. more specifically, the dendrites are lined with receptors, and these receptors are specifically shaped for a particular neurotransmitter. We will review the different kinds of neurotransmitters in the next lesson – but you can understand some important principles here. Each receptor only fits with one kind of neurotransmitter, what is called lock and key. In other words, dopamine receptors won’t accept any neurotransmitter other than dopamine and likewise for glutamate and GABA, etc. It is kind of like these receptors are bouncers at a very exclusive club!

An important thing to remember is that whereas the action potential is an all-or-nothing process along the axon, the activity in the dendrites and soma are far from all-or-nothing. In the dendrites, shifts in the relative positive/negative valence follow what is called graded potentials. This means that there is a big effect at the receptor site that gets smaller and smaller the further away this potential travels from the receptor.

Neurotransmitters may be excitatory or inhibitory. Excitatory NTs open ion channels that depolarize the neuron and bring it closer to firing an action potential. This is called an excitatory post-synaptic potential or EPSP. In contrast, inhibitory NTs open ion channels that hyperpolarize the neuron and bring it further away from firing an action potential. This is called an inhibitory post-synaptic potential or IPSP.

To get the neuron to fire, the polarization has to shift to -55 mV at the axon hillock. Because the potentials in the dendrites are graded potentials, they have to add up in some way to reach this threshold. There are 2 ways these potentials may add up: temporal summation and spatial summation. Temporal summation happens at only one synapse on the post-synaptic cell. Here, EPSPs (or IPSPs) happen so close together on time they add up – cause a larger depolarization to travel further through the cell body. Spatial summation, in contrast, happens along several synapses on the post-synaptic cell. For spatial summation, EPSPs (or IPSPs) happen all along the cell at the same exact time.

Here is a summary of what is going on in the Post-synaptic membrane:

EPSP: Excitatory; causes depolarization and increases probability of action potential

IPSP: Inhibitory causes hyperpolarization and reduces the probability of an action potential

Temporal Summation: Postsynaptic neuron receives messages close together that will add together and have a cumulative effect

Spatial Summation: Postsynaptic neuron receives simultaneous information at many locations which has a cumulative effect.

Interesting fact – some neurons have a Spontaneous Firing Rate or production of action potentials without any synaptic input. They still have IPSPs and EPSPs – it is just that IPSPs decrease rate of firing action potentials and EPSPs increase this rate.

1.11 Neurotransmitters: Chemicals that Excite or Inhibit

The process of neural communication is electrochemical and neurotransmitters represent the chemical side of this (potentials are the electrical).

A neurotransmitter (NT) is a chemical substance released at the axon terminal of the pre-synaptic neuron after an action potential. After diffusing across the synapse cleft these chemicals cause an IPSP or EPSP bringing the synaptic neuron closer to or further away from firing an action potential of its own. NTs differ from hormones which are secreted by a gland (vs. neuron) and conveyed by blood to other organs whose activity it influences. Hormones coordinate long lasting changes in multiple parts of the body, whereas NTs only effect local synapses.

Neurotransmitters open gates for some ions as soon as they bind with receptor. When glutamate binds it opens sodium causing and EPSP, making it an excitatory NT. When GABA it opens chloride and causes an IPSP, making it an inhibitory NT. There are 2 ways NTs ca open ion channels:

Ionotropic Effects: NT Immediately opens gates for some ion polarization is immediately changed. Also, short lived no longer than 30 msecs Usually around 10 msecs. Acetylcholine and Nicotine Smokers know immediate.

o These effects are common in vision and muscle movements.

Metabotropic Effects are slower and longer lived. The effects can last hours but they usually last for minutes. Here is what happens:

o When the NT bind, it bends protein along the membrane

o The protein reacts with other molecules which increases the concentration of another substance (specifically cyclic AMP). This is called a “second messenger”

o This second messenger opens the ions channels

Here are 2 of the major NTs and the ion channels they open:

NTIonEffect

Glutamate

Na+

EPSP

Gamma-aminobutyric acid (GABA)

K+ leaves and Cl- enters

IPSP

And here are the major neurotransmitters we will study in this class:

NTBehavior Associated EPSP or IPSP?

Adrenaline (Epinephrine) *

Fight or Flight

Excitatory

Nordrenaline (Norepinephrine) *

Fight or Flight; Concentration

Mostly Excitatory

Dopamine*

Reward; Movement

Mostly Inhibitory

Serotonin

Mood; Impulse; Sleep

Inhibitory

GABA

Calm; Focus, Sleep

Inhibitory

Acetylcholine

Learning; Attention; Wakefulness

Excitatory

Glutamate

Memory

Excitatory

Endorphins

Euphoria; Pain Reduction

Inhibitory

Catecholamines an important class of neurotransmitters include the following:

Dopamine

Norepinepherine

Epinepherine

Where do Neurotransmitters come from?

Neurotransmitters are derived from food and are synthesized in the neuron itself.

Acetylcholine comes from Choline found in milk and cauliflower

Serotonin comes from Tryptophan which comes from turkey

Dopamine comes from Phenylalanine which comes from chicken or liver

1.12 Drugs and Behavior

There are 2 kinds of drugs: Antagonists and Agonists.

Antagonist: Block effects of NT

Agonist: Increase the effects of NT

Don’t be deceived! it can be confusing sometimes: What is it when a NT is inhibitory and the drug blocks the effect so that the result is excitatory. = Antagonist! In other words, antagonist does not equal inhibitory and vice versa.

How do drugs produce effects on NTs? The drug can:

Disrupt or facilitate synthesis of the NT

Cause the NT to leak from vesicles

Stop the NT’s breakdown into inactive chemicals

Increase the NT release

Block reuptake of the NT so it stays in synapse longer to continue effecting the post-synaptic neuron

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