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Studied by 9 people
week 2
How neurons communicate with eachother, why they fire and hat it takes
Resting Membrane Potential
LO 4.1 Describe how the membrane potential is recorded.
To record a neuron's membrane potential, one electrode must be placed inside the neuron and another in the extracellular fluid. The intracellular electrode, called a microelectrode, has an extremely fine tip to avoid damaging the membrane. When both electrodes are in the extracellular fluid, the voltage difference is zero. However, inserting the intracellular electrode into a resting neuron reveals a steady membrane potential of approximately -70 mV, meaning the inside of the neuron is 70 mV less than the outside. This resting potential indicates that the neuron is polarized.
LO 4.2 Describe the resting membrane potential and its ionic basis, and describe the three factors that influence the distribution of Na+ and K+ ions across the neural membrane.
The resting membrane potential of a neuron is approximately -70 mV, meaning the inside is more negative than the outside. This is maintained by the unequal distribution of sodium (Na⁺) and potassium (K⁺) ions. More Na⁺ ions are outside the neuron, while more K⁺ ions are inside.
Three factors influence this ion distribution:
Electrostatic Pressure – The negatively charged interior attracts positively charged Na⁺ ions.
Concentration Gradient – Ions naturally move from high to low concentration, pushing Na⁺ into the cell and K⁺ out.
Selective Permeability and Sodium-Potassium Pumps – Na⁺ channels are closed, preventing Na⁺ from rushing in, while K⁺ channels remain slightly open, allowing some K⁺ to exit. However, the sodium-potassium pump actively transports three Na⁺ out and two K⁺ in, maintaining the resting potential.
Hodgkin and Huxley discovered these ion exchanges, explaining how the neuron remains stable despite ion leakage.
Understanding the resting membrane potential is important in psychology because it is fundamental to how neurons function, which underlies all thoughts, emotions, and behaviors. Here’s why it matters:
Neural Communication – The resting membrane potential sets the stage for action potentials, which allow neurons to transmit signals. This is essential for all cognitive processes, including perception, memory, and decision-making.
Mental Health and Disorders – Many psychological disorders, such as depression, anxiety, and schizophrenia, are linked to disruptions in neural signaling. For example, imbalances in sodium and potassium ion channels can affect neurotransmitter release and brain function.
Effects of Psychotropic Drugs – Medications like antidepressants and antipsychotics influence ion channels and neural excitability, altering mood and behavior. Understanding the ionic basis of neural activity helps explain how these drugs work.
Neuroplasticity and Learning – Changes in resting membrane potential play a role in synaptic plasticity, which is essential for learning and memory. This has implications for therapy and rehabilitation in psychological treatment.
Generation, Conduction, and Integration of Postsynaptic Potentials
LO 4.3 Describe the types of postsynaptic potentials and how they are conducted.
When a neuron receives input from another cell, it generates postsynaptic potentials (PSPs), which are temporary changes in the membrane potential. PSPs occur when neurotransmitters bind to receptors on the neuron’s membrane, leading to either:
1. Excitatory Postsynaptic Potentials (EPSPs) – These depolarize the neuron (e.g., from -70mV to -67mV), increasing the likelihood of firing an action potential.
2. Inhibitory Postsynaptic Potentials (IPSPs) – These hyperpolarize the neuron (e.g., from -70mV to -72mV), decreasing the likelihood of firing.
PSPs are graded potentials, meaning their strength depends on the signal intensity. They are transmitted rapidly and decrementally, losing strength as they spread through the neuron. Most PSPs fade out within a few millimeters from their origin.
LO 4.4 Describe how postsynaptic potentials summate and how action potentials are generated.
The firing of a neuron is determined by the summation of postsynaptic potentials (PSPs), which occur when neurotransmitters bind to receptors on the postsynaptic membrane, causing disturbances in the resting membrane potential. These disturbances can be either excitatory (EPSPs) or inhibitory (IPSPs), and they are graded potentials, meaning their size depends on the strength of the stimulus.
EPSPs (Excitatory Postsynaptic Potentials): When neurotransmitters bind to receptors, they may cause depolarization of the neuron (making the inside of the neuron less negative). This increases the likelihood that the neuron will reach the threshold of excitation and fire an action potential. An example of an excitatory neurotransmitter is glutamate.
IPSPs (Inhibitory Postsynaptic Potentials): On the other hand, when neurotransmitters bind to certain receptors, they can cause hyperpolarization (making the inside of the neuron more negative). This makes it less likely that the neuron will fire an action potential. An example of an inhibitory neurotransmitter is GABA.
When these PSPs are generated, they travel passively and decrementally toward the axon. This means the signal weakens as it moves away from the synapse, and thus, the farther the PSP is from the axon, the less impact it has on whether the neuron fires.
Action Potential Generation:
For an action potential to occur, the sum of EPSPs and IPSPs must reach a certain level of depolarization at the axon initial segment. This depolarization must reach a critical threshold, typically around -65 mV, at which point an action potential is triggered. Once this threshold is reached, the neuron undergoes an all-or-nothing response, meaning the action potential is of a fixed size and duration, typically lasting around 1 millisecond.
Unlike PSPs, action potentials are not graded; they either occur fully or do not occur at all. Once triggered, an action potential travels down the axon without decrement, maintaining its full strength until it reaches the axon terminal, where it triggers the release of neurotransmitters.
Types of Summation:
The process by which PSPs determine whether an action potential is fired involves two types of summation:
Spatial Summation: This occurs when multiple PSPs from different synapses on the neuron’s dendrites and cell body are activated simultaneously. When these signals arrive at the axon hillock (or initial segment), they can combine, creating a larger depolarization (or hyperpolarization). For example, if multiple excitatory synapses activate at the same time, their EPSPs will add up to push the membrane potential closer to the threshold.
Simultaneous EPSPs can create a larger excitatory effect.
Simultaneous IPSPs can create a larger inhibitory effect.
Simultaneous EPSPs and IPSPs can cancel each other out if their effects are equal and opposite.
Temporal Summation: This occurs when multiple PSPs are generated in quick succession at the same synapse. Since PSPs last for a short time, if a neuron is repeatedly stimulated before the previous PSP has dissipated, these signals can add together, leading to a greater depolarization or hyperpolarization. For example, a subthreshold excitatory stimulus may not cause the neuron to fire on its own, but if it is applied repeatedly in rapid succession, it may push the membrane potential to the threshold and trigger an action potential.
Influence of Synapse Location:
It was once believed that synapses located closer to the axon had a stronger influence on whether the neuron fired, due to the decremental nature of PSPs. However, it has been shown that some neurons have mechanisms that can amplify signals from synapses located farther away from the axon, such as on the dendrites. This amplification allows signals from distant parts of the neuron to have a greater influence on firing.
All-or-None Nature of Action Potentials:
The firing of a neuron can be likened to pulling a trigger on a gun: it is a gradual process that reaches a critical point, at which the neuron fires an action potential or does not. Once the action potential is triggered, its magnitude is constant and does not vary depending on the strength of the stimulus. In the same way that pulling the trigger harder does not change the velocity of the bullet, increasing the intensity of a stimulus will not change the size or speed of the resulting action potential. The neuron is either "fired" or not, resulting in an all-or-none event.
Overall, the net effect of all incoming signals—both excitatory and inhibitory—determines whether the neuron will fire, with the summation of PSPs occurring both spatially and temporally to influence this decision.
1. What's a Neuron's Resting State?
Okay, so first things first—imagine your brain cells are like little electric wires, and they’re usually chilling at what we call a "resting membrane potential." It’s like the default setting. Think of it as the neuron just hanging out, not doing much. But when things get exciting, or when it receives input, that resting state gets disturbed. That’s when the neuron gets a signal from other neurons telling it to do something—like firing or staying quiet.
2. What Happens When the Neuron Gets a Signal?
So, let's say a neuron gets a signal. The signal comes from something called a postsynaptic potential (PSP). Now, imagine this: each signal is like a ripple in the water. When a neuron gets a signal, it either gets excited (like someone turning the heat up on a stove) or it gets a little more chilled out (like the AC kicking in). These signals are graded, meaning they can be strong or weak, depending on how intense the incoming signal is.
There are two types of these signals:
Excitatory Signals (EPSPs): These signals get the neuron excited, making it more likely to fire. Think of it like adding fuel to a fire. The stronger the signal, the more likely the neuron will "fire" and send its message.
Inhibitory Signals (IPSPs): These signals chill out the neuron, making it less likely to fire. It’s like putting water on that fire to cool it down.
3. How Do Neurons Decide to Fire?
Here’s the twist: neurons don’t just randomly fire every time they get a signal. Instead, they listen to a bunch of signals at once. Imagine you're at a party, and you hear a bunch of different conversations happening around you. Some people are cheering you on, others are telling you to relax. You have to decide if you’re going to jump into the conversation or not.
Neurons do something similar. They get signals from thousands of other neurons at the same time. Some signals are trying to fire it up (EPSPs), and some are trying to cool it down (IPSPs). The neuron will "add up" all these signals and decide whether it’s time to go for it and fire an action potential, or just stay quiet.
4. What Happens When the Neuron Reaches the Threshold?
Now, here's where things get juicy. If the neuron gets enough excitatory signals (like it’s really fired up) and reaches a certain level of excitement—let's call it the threshold—BOOM, the neuron fires an action potential. This is like pulling the trigger of a gun: once the threshold is hit, the neuron fires, and it does so with the same strength every time. It's an all-or-nothing response. Either the neuron fires, or it doesn’t. There’s no halfway.
When the neuron fires, it sends out a huge wave of electrical charge that travels down the neuron, sending a signal to the next neuron. It's like a domino effect!
5. How Do These Signals Travel?
Here’s a fun fact: when these signals travel down the neuron, they don’t just keep getting stronger. They decrease a little as they go. Imagine a ripple in a pond—the closer the ripple is to the point where it started, the bigger it is. But as it moves farther out, it gets weaker. Same with these signals—they fade the further they travel from their starting point. That’s called decremental transmission.
6. How Does a Neuron Decide to Fire (Again)?
Neurons have a way of summing things up. Think about a pile of snowflakes falling on a mountain. Each snowflake doesn’t have much of an impact on its own, but as more and more fall, they build up and make a big difference. Summation is how neurons combine all the little signals they get.
There are two ways they do this:
Spatial Summation: This happens when signals from different parts of the neuron come together at the same time. If you get enough of those signals in the right place, they’ll make the neuron fire.
Temporal Summation: This happens when the same synapse gets activated multiple times in quick succession. Imagine if someone keeps knocking on your door faster and faster. Even if each knock isn’t super loud, after a while, they can build up and get your attention. If the neuron gets too many signals in a short period, it fires!
7. Does Location Matter for Firing?
So, some people once thought that signals close to the neuron’s axon (the part that sends messages out) were the most important for firing the neuron. But guess what? It turns out that some neurons have ways of making signals from farther away more powerful—kind of like amplifying a distant sound to make it clear and loud.
8. All-or-Nothing!
Finally, just like a gun trigger, when a neuron fires, it’s all or nothing. The action potential either happens completely, or not at all. If you’re pulling the trigger on a gun, squeezing harder doesn’t make the bullet go faster. Similarly, if you stimulate a neuron more intensely, it doesn’t make the action potential bigger or faster. It’s either full-on, or nothing happens!
Conduction of Action Potentials
LO 4.5 Explain the ionic basis of an action potential.
The ionic basis of an action potential involves a series of events where the neuron’s membrane potential changes in response to specific ion movements. At rest, the neuron’s membrane is relatively impermeable to Na+ ions, and the small number that enter are pumped out, maintaining a resting potential of around -70 mV.
When a large excitatory postsynaptic potential (EPSP) depolarizes the axon to the threshold, voltage-gated sodium channels open, causing a rapid influx of Na+ ions, which flips the membrane potential from -70 mV to +50 mV. This is the rising phase of the action potential (AP).
The influx of Na+ triggers the opening of voltage-gated potassium channels, allowing K+ ions to flow out, driven by both their high internal concentration and the positive charge inside the cell. As Na+ channels close after about 1 millisecond, the repolarization phase begins due to the continued outflow of K+.
Once repolarization is complete, the K+ channels gradually close, resulting in a hyperpolarization phase, where the neuron briefly becomes more negative than its resting potential due to the excess outflow of K+.
Although the AP involves small movements of ions near the membrane, the concentrations of ions inside and outside the neuron remain mostly unchanged. The sodium-potassium pumps play a minor role in restoring the resting potential after the AP.
In summary, the action potential is driven by the influx of Na+ and the efflux of K+, with specific channels opening and closing at precise times, causing the membrane potential to change in a rapid, coordinated sequence.
potasum leaves to make room for sodium when ecistopry resonce happens, after, it gets more chill then when it started and then return to normal
LO 4.6 Explain how the refractory period is responsible for two important characteristics of neural activity.
The refractory period refers to the brief time after an action potential (AP) during which a neuron cannot fire again. It’s broken down into two phases:
Absolute refractory period (1-2 milliseconds): After an AP, it’s impossible for the neuron to fire again, no matter how strong the stimulus is.
Relative refractory period: It’s possible to fire the neuron again, but it requires a stronger-than-usual stimulus.
These refractory periods serve two key purposes:
Unidirectional AP travel: The refractory period ensures that action potentials move in one direction along the axon. After an AP travels down part of the axon, that part becomes refractory and cannot fire again, preventing the signal from reversing direction.
Rate of neural firing: The intensity of stimulation affects how often a neuron can fire. With high-intensity stimulation, neurons fire more frequently, up to about 1,000 times per second. Lower-intensity stimulation results in less frequent firing, as the neuron needs to wait for both the absolute and relative refractory periods to end before firing again.
LO 4.7 Describe how action potentials are conducted along axons—both myelinated and unmyelinated.
Axonal Conduction of Action Potentials: Myelinated vs. Unmyelinated Axons
Some axons are wrapped in a magical blanket called myelin. It's like giving your rollercoaster some special turbo boosts, allowing it to jump from one station to another without stopping – this is saltatory conduction.
Action potentials (APs) travel along axons in different ways depending on whether the axon is myelinated or unmyelinated.
How APs Travel:
Non-decremental conduction: Unlike postsynaptic potentials (PSPs), APs do not weaken as they move down the axon. They remain strong, ensuring the signal is transmitted without loss.
Slower than PSPs: APs travel more slowly due to the involvement of voltage-gated sodium channels.
The Process:
An AP travels along the axon as a graded potential (which is weaker as it moves). When the graded potential reaches the next sodium channel, if it’s large enough, the sodium channel opens, letting Na+ ions into the axon and triggering another AP.
This process of AP regeneration happens at each sodium channel along the axon, with the AP being "recreated" again and again.
Analogy: Imagine a row of mouse traps. When one trap is triggered, the vibration travels down the row, triggering each trap in turn. The same happens with APs in axons. The signal moves like a vibration from one sodium channel to the next, ensuring the AP travels without weakening.
Types of Conduction:
Antidromic conduction: If a stimulus is applied to the middle of an axon, an AP can travel back towards the cell body.
Orthodromic conduction: The AP typically travels in one direction from the axon terminal toward the cell body.
Conduction in Myelinated Axons
Myelin: Axons of many neurons are covered in myelin, a fatty tissue that acts as insulation, with small gaps called nodes of Ranvier between the myelin segments.
Saltatory conduction: In myelinated axons, the AP "jumps" from one node to the next, speeding up the conduction of the AP. The signal travels quickly, with a slight delay at each node as the AP is regenerated, but overall, it’s faster than in unmyelinated axons.
Speed of Conduction:
Large, myelinated axons: These conduct APs very quickly, up to 60 meters per second (around 134 miles per hour). These are usually motor neurons, which control muscles.
Small, unmyelinated axons: These conduct APs much more slowly, around 1 meter per second.
Axons Without APs:
Many neurons in the brain don’t have long axons or even axons at all. These neurons generally conduct signals through graded potentials instead of full APs.
Myelination and Axonal Conduction:
In myelinated axons, sodium channels are concentrated at the nodes of Ranvier. This allows the electrical signal to travel in a graded manner between the nodes, making conduction faster.
Summary:
APs in myelinated axons jump from node to node (saltatory conduction), speeding up the process.
Axons without myelin transmit APs more slowly and require regeneration at every point along the axon.
The conduction speed depends on the axon’s size and whether it’s myelinated.
LO 4.8 Explain the shortcomings of the Hodgkin-Huxley model when applied to neurons in the mammalian brain
The Hodgkin-Huxley model revolutionized our understanding of neural conduction when it was developed in the 1950s. It won the Nobel Prize in 1963 for explaining how neurons transmit signals through action potentials (APs). However, when we try to apply this model to neurons in the mammalian brain, there are several shortcomings.
### Shortcomings of the Hodgkin-Huxley Model
1. Based on Simple Neurons:
The Hodgkin-Huxley model was based on the study of squid motor neurons, which are large and simple. Squid neurons are much more accessible and easier to study than the smaller and more complex neurons in the mammalian brain. In the brain, neurons come in a vast variety, each with its own complex structures and functions, making the model less applicable to the diverse neural networks in mammals.
2. Doesn't Account for Neuron Complexity:
The mammalian brain contains hundreds of different types of neurons, and many of these neurons have characteristics not seen in simple motor neurons like those of the squid. The complexity and plasticity of mammalian brain neurons—such as their varied electrical properties and intricate communication patterns—aren't fully captured by the Hodgkin-Huxley model.
3. Doesn't Include Mechanical Factors:
Another limitation is that the Hodgkin-Huxley model focuses only on electrical impulses. Recent research shows that neural conduction may also involve mechanical processes, such as waves of expansion and contraction in the neural membrane, similar to ripples on a pond. This suggests that neural signaling may not be purely electrical and that mechanical forces also play a role. These aspects are not addressed by the original Hodgkin-Huxley framework.
### In Summary:
While the Hodgkin-Huxley model was groundbreaking, it is more suitable for explaining the behavior of simple motor neurons, like those in squid, rather than the complex and diverse neurons in the mammalian brain. The model doesn't fully capture the complexity of the brain's neurons or include the potential mechanical aspects of neural conduction, which means it should be applied cautiously when studying mammalian neurons.
Synaptic Transmission: From Electrical Signals to Chemical Signals
LO 4.9 Describe the structure of different types of synapses.
Types of Synapses
Axodendritic Synapse:
Structure: This synapse occurs when the terminal button of an axon forms a connection with the dendrite of another neuron.
Common Features: Many axodendritic synapses terminate on dendritic spines, which are small nodules located on dendrites.
Function: These synapses are crucial for typical synaptic transmission in the brain, contributing to communication between neurons.
Axosomatic Synapse:
Structure: In this arrangement, the terminal button of an axon synapses with the soma (cell body) of another neuron.
Function: Like axodendritic synapses, axosomatic synapses play a key role in neuron communication. However, synapses on the soma can have a more significant effect on the neuron's overall activity.
Tripartite Synapse:
Structure: This type of synapse involves three cells: two neurons and an astroglial cell (astrocyte).
Function: Astrocytes, a type of glial cell, are positioned at these synapses and communicate with both neurons. This tripartite model represents a more complex form of synaptic transmission, where both neurons and glial cells influence each other.
Dendrodendritic Synapse:
Structure: These synapses occur between the dendrites of two different neurons.
Special Feature: Dendrodendritic synapses can transmit signals in both directions, which is unusual since most synapses are typically unidirectional.
Function: These synapses are often found in certain brain circuits and contribute to complex signaling.
Axoaxonic Synapse:
Structure: In this arrangement, one axon synapses directly with another axon.
Function: Axoaxonic synapses are particularly important because they can mediate presynaptic facilitation and presynaptic inhibition. This means they can modify how much neurotransmitter is released from the axon terminal, allowing for selective control of specific synapses rather than influencing the entire presynaptic neuron.
Significance: This selectivity allows for fine-tuning of neural communication.
Axomyelenic Synapse:
Structure: This is a newly discovered type of synapse where an axon synapses with the myelin sheath of an oligodendrocyte (a glial cell).
Function: It represents a form of neuron-to-glial communication and suggests that glial cells play a more active role in neuronal signaling than previously understood.
Significance: This finding contributes to our understanding of how neurons and glial cells interact.
Types of Synaptic Arrangements
Directed Synapses:
Structure: In directed synapses, the site of neurotransmitter release (the terminal button) is located close to the site of neurotransmitter reception (the postsynaptic membrane).
Function: This is the most common type of synapse in the brain. The proximity of these sites ensures efficient signal transmission from the presynaptic neuron to the postsynaptic neuron.
Nondirected Synapses:
Structure: These synapses are characterized by neurotransmitter release from varicosities (swellings or bulges) along the length of the axon and its branches.
Function: The neurotransmitter released from these varicosities is widely dispersed to a broader area, affecting multiple target cells.
Appearance: Due to their characteristic appearance, these synapses are often referred to as string-of-beads synapses.
Significance: Nondirected synapses allow for more diffuse signaling, influencing a wider range of cells compared to directed synapses.
Summary
Synapses are crucial for neuron communication, and the structure of different synapses allows for diverse forms of neural signaling. The most common types are axodendritic (axon to dendrite) and axosomatic (axon to soma) synapses, but more complex forms such as dendrodendritic, axoaxonic, and axomyelenic synapses add further complexity and specialization to neural communication. Some synapses are directed, where neurotransmitter release and reception are in close proximity, while others are nondirected, allowing neurotransmitter spread over a wider area. These various synaptic types and arrangements enable the brain to manage the vast and intricate networks of communication that underlie neural function.
Imagine your brain is a super busy city, with neurons as the cars that drive around, delivering messages. These cars don’t just drive directly from point A to point B—they make stops at various intersections called synapses.
Axodendritic Synapse (Axon to Dendrite)
This is like a car stopping at a bus stop (the dendrite) where it hands off a message. So, the axon (the car) pulls up to a dendrite (the bus stop) and delivers its signal. Think of this as the classic, everyday stop in your brain city.
Axosomatic Synapse (Axon to Cell Body)
Here, instead of stopping at a bus stop, the car pulls up directly to the main office (the soma, or cell body). This is important because the main office is where all the big decisions are made about whether to send out the message or not.
Tripartite Synapse (Neuron + Glial Cell + Another Neuron)
Now things get fancy—imagine the car stops at a junction, but it doesn’t just drop off a message to one bus stop (neuron). There’s a third party involved—astrocytes, these are like the traffic controllers of your brain city. They help the signal get through smoothly, making sure everything runs without a hitch. So, you’ve got two neurons and one helper astrocyte all working together in a team.
Dendrodendritic Synapse (Dendrite to Dendrite)
Here’s a weird one: two cars (dendrites) are meeting at an intersection, but they can go both ways—no one is really in charge. It’s like a roundabout where cars are free to go in either direction.
Axoaxonic Synapse (Axon to Axon)
In this setup, one car pulls up next to another car—this is a VIP lane! One axon gets to control how much another axon sends out by helping or stopping it from passing a message. This is like one car telling the other to either speed up or slow down depending on what’s needed. It’s super selective and precise.
Axomyelenic Synapse (Axon to Myelin Sheath)
This is a new discovery! Imagine a car pulling up to a maintenance stop—the myelin sheath. This is the special coating that speeds up the signals, and now we know axons can talk to it directly! This is like a pit stop in the brain’s raceway.
Directed Synapses (Close Communication)
Now, back to the regular traffic. Directed synapses are like cars pulling up to a red light and directly handing off a message to a nearby bus stop. The signal’s pretty focused and direct, which is what most brain traffic looks like.
Nondirected Synapses (Spread Out Communication)
But sometimes, instead of a red light, the car (neuron) sprays out signals all over the place from little “beads” (varicosities) along the axon. These are the non-directed synapses. It’s like a car throwing messages out the window as it drives down the street, and the signals end up hitting all sorts of bus stops along the way. This is more of a spread-out, not-so-focused way of communicating.
LO 4.10 Describe how neurotransmitter molecules are synthesized and packaged in vesicles.
Neurotransmitter molecules are divided into two main types: large (neuropeptides) and small (small-molecule neurotransmitters).
Synthesis and Packaging of Small Molecule Neurotransmitters:
Small-molecule neurotransmitters are synthesized in the cytoplasm of the terminal button and packaged into synaptic vesicles by the Golgi complex of the button. These vesicles are stored near the presynaptic membrane until needed.Synthesis and Packaging of Neuropeptides:
Neuropeptides are short protein chains, synthesized in the cytoplasm of the cell body on ribosomes. After being synthesized, they are packaged into vesicles by the Golgi complex in the cell body and then transported to the terminal buttons along microtubules. Neuropeptide vesicles are larger than those containing small-molecule neurotransmitters and do not cluster as closely to the presynaptic membrane.Coexistence of Multiple Neurotransmitters:
Contrary to previous beliefs that each neuron releases only one neurotransmitter, many neurons release two neurotransmitters, a phenomenon called coexistence. These may include a neuropeptide in larger vesicles and a small-molecule neurotransmitter in smaller vesicles. Additionally, some neurons can release multiple small-molecule neurotransmitters.Neurotransmitter Changes Over Time:
Neurons can change the types of neurotransmitters they release throughout their lifespan, adding more complexity to neurotransmission.
In summary, small-molecule neurotransmitters are synthesized and packaged in the terminal button, while neuropeptides are made in the cell body and transported to the button. Some neurons can release multiple neurotransmitters, and their release patterns can change over time.
Imagine you're making a smoothie—small-molecule neurotransmitters are like your basic fruits, chopped up and thrown into a blender (the terminal button). They get packed into little containers (vesicles) by the kitchen staff (the Golgi complex) and wait in the fridge, ready to be served when needed.
But neuropeptides? Oh, they’re the fancy, protein-packed smoothies. They're made in the big kitchen (the cell body) by a team of chefs (ribosomes). They get packed into even bigger containers, and once ready, they get delivered to the serving area (terminal button) via a long delivery route (microtubules). These smoothies take longer, and they don’t just sit next to the fridge like the fruits—they're stored in a different area because they’re more high-maintenance.
And here’s the wild part—some neurons mix things up! Imagine you’re running a smoothie stand and you have both fruit and fancy smoothies in the same containers. That's coexistence—small and big neurotransmitters, hanging out together, waiting for their moment to shine. And over time, your stand may decide to switch up the smoothie flavors you make, adding even more flavor complexity.
So, in short: small neurotransmitters = quick & easy fruit smoothies, neuropeptides = fancy, protein-packed creations, and neurons can get a little crazy and mix it all up.
LO 4.11 Explain the process of neurotransmitter exocytosis.
When a neuron is stimulated by an action potential (AP), calcium ions (Ca2+) enter the presynaptic terminal through voltage-gated channels. This influx of calcium triggers synaptic vesicles containing neurotransmitters to fuse with the presynaptic membrane. As a result, neurotransmitters are released into the synaptic cleft in a process called exocytosis.
For small-molecule neurotransmitters, this release happens in pulses with each action potential. In contrast, neuropeptides are released gradually in response to higher levels of calcium, typically during prolonged neuron activity.
Not all vesicles fuse with the membrane. Some vesicles are released intact and carry larger molecules like proteins or RNA, which can influence gene expression and cell behavior over time.
Exocytosis—the process of neurotransmitter release
LO 4.12 Describe the differences between ionotropic and metabotropic receptors.
Neurotransmitters influence postsynaptic neurons by binding to specific receptors on the postsynaptic membrane. There are two main types of receptors: ionotropic and metabotropic.
Ionotropic Receptors: These are directly linked to ion channels. When a neurotransmitter binds to an ionotropic receptor, the ion channel opens or closes, creating an immediate change in the postsynaptic potential (either depolarization or hyperpolarization). This process is fast and localized, influencing neuron activity quickly.
Metabotropic Receptors: These are linked to G proteins and signal proteins, leading to slower, longer-lasting, and more diffuse effects. When a neurotransmitter binds, a subunit of the G protein separates and either activates nearby ion channels or triggers the production of second messengers, which can influence various cellular processes, including gene expression.
Autoreceptors are a special type of metabotropic receptor located on the presynaptic membrane. They bind to the neuron’s own neurotransmitters and regulate neurotransmitter release based on the levels in the synapse.
Small-molecule neurotransmitters tend to activate either ionotropic or metabotropic receptors for quick, brief signaling, while neuropeptides usually bind to metabotropic receptors, leading to slower, longer-lasting signals.
LO 4.13 Explain how neurotransmitters are removed from a synapse.
Neurotransmitters are removed from the synapse through two primary mechanisms: reuptake and enzymatic degradation.
Reuptake: This is the most common mechanism, where neurotransmitters are drawn back into the presynaptic neuron through transporter proteins. This process recycles neurotransmitters for future use, ensuring the synaptic message is terminated efficiently.
Enzymatic Degradation: In some cases, neurotransmitters are broken down in the synapse by enzymes. A notable example is acetylcholine, which is broken down by the enzyme acetylcholinesterase. This mechanism also terminates the neurotransmitter's action in the synapse.
After neurotransmitters are deactivated, either by reuptake or enzymatic breakdown, they or their breakdown products are recycled by being brought back into the presynaptic terminal. The vesicles used to transport the neurotransmitters are also recycled to form new vesicles.
LO 4.14 Describe the roles of glia and gap junctions in synaptic transmission.
Glia and Gap Junctions in Synaptic Transmission
Glial Cells: Once seen as merely supportive, glial cells, particularly astrocytes, play active roles in synaptic transmission. Astrocytes release chemical transmitters, contain neurotransmitter receptors, conduct signals, and influence the communication between neurons. They contribute to the regulation and coordination of neuronal activity. Given their widespread presence and complex interactions with neurons, they are now recognized as integral to brain function, moving beyond traditional neuron-to-neuron focus in neuroscience.
Gap Junctions: Gap junctions are protein channels that allow direct communication between adjacent cells. They are particularly important in glial cells, where they form networks that synchronize activities. Gap junctions also occur between inhibitory interneurons of the same type, helping to coordinate their functions in specific areas of the brain. This synchronization enables precise control over brain activity, promoting efficient neural communication and overall brain function.
Together, glial cells and gap junctions enhance synaptic transmission by enabling coordination within networks of cells, ensuring the smooth operation of complex brain functions.
Neurotransmitters
LO 4.15 Name the major classes of neurotransmitters.
LO 4.16 Identify the class, and discuss at least one function of each of the neurotransmitters discussed in this section.
Amino Acid Neurotransmitters
These neurotransmitters are the most prevalent in the central nervous system and are often involved in fast-acting synapses. The most well-known amino acid neurotransmitters are:Glutamate: The main excitatory neurotransmitter in the brain, responsible for enhancing synaptic transmission.
GABA (Gamma-Aminobutyric Acid): The primary inhibitory neurotransmitter, controlling neuronal excitability and preventing overexcitement of neurons.
Monoamine Neurotransmitters
These neurotransmitters are synthesized from amino acids and tend to have broader, more diffuse effects. They are subdivided into:Catecholamines (dopamine, norepinephrine, and epinephrine): These play a role in arousal, mood regulation, and the stress response.
Dopamine: Involved in reward, pleasure, and motor control.
Norepinephrine: Affects attention and alertness.
Epinephrine: Related to the fight-or-flight response.
Serotonin: Involved in mood regulation, sleep, and appetite control.
Acetylcholine
Acetylcholine is unique as it plays a role in both the peripheral nervous system (at neuromuscular junctions) and in the brain. It is involved in muscle movement, memory, and learning. Acetylcholine is broken down by the enzyme acetylcholinesterase.Unconventional Neurotransmitters
These neurotransmitters have unique mechanisms of action:Soluble Gas Neurotransmitters (e.g., nitric oxide, carbon monoxide): These diffuse across cell membranes and participate in retrograde signaling, regulating presynaptic activity.
Endocannabinoids: Similar to THC in marijuana, these molecules affect presynaptic neurons and modulate synaptic transmission.
Neuropeptides
Neuropeptides are larger molecules that are synthesized in the cell body and often function as both neurotransmitters and hormones. These include:Pituitary Peptides: Released by the pituitary gland and have various roles in regulating bodily functions.
Hypothalamic Peptides: Released by the hypothalamus and regulate various bodily functions.
Opioid Peptides: Similar in structure to opiates and involved in pain modulation and reward pathways.
Neurotransmitter Functions
Each class of neurotransmitter serves distinct physiological and behavioral functions. For example:
Glutamate: Responsible for most excitatory signaling in the brain, playing a key role in learning and memory.
GABA: Regulates neuronal excitability, important for maintaining balance in brain activity and preventing overactivation.
Dopamine: Involved in motivation, reward, and motor control, with disruptions leading to conditions like Parkinson's disease.
Serotonin: Affects mood, sleep, and appetite regulation, with imbalances linked to depression and anxiety disorders.
Acetylcholine: Vital for muscle control and cognitive functions like memory and learning.
Endocannabinoids: Modulate various physiological processes, including pain, appetite, and mood.
Pharmacology of Synaptic Transmission and Behavior
LO 4.17 Provide a general overview of how drugs influence synaptic transmission.
How Drugs Influence Synaptic Transmission
Drugs can influence synaptic transmission by modifying the typical processes that neurotransmitters undergo. The general process of neurotransmission follows these seven steps:
Synthesis of neurotransmitters
Storage in vesicles
Breakdown of neurotransmitters that leak from vesicles
Exocytosis (release into the synapse)
Inhibitory feedback via autoreceptors
Activation of postsynaptic receptors
Deactivation (through reuptake or enzymatic breakdown)
Drugs can interact with these steps in two primary ways:
Agonistic drugs: These drugs enhance neurotransmission by binding to postsynaptic receptors and activating them, mimicking the action of the natural neurotransmitter.
Antagonistic drugs (receptor blockers): These drugs bind to postsynaptic receptors without activating them. They block the neurotransmitter's ability to bind and activate the receptor, inhibiting neurotransmission.
Through these mechanisms, drugs can either enhance or block neurotransmitter effects, influencing brain function and behavior.
LO 4.18 Describe three examples of how drugs have been used to influence neurotransmission.
Resting Membrane Potential
The resting membrane potential (RMP) is the electrical charge difference across the membrane of a resting neuron. It typically ranges from -60 to -70 mV in most neurons. The ionic basis of RMP involves:
Sodium (Na⁺) and Potassium (K⁺) Ions: The RMP is primarily established by the sodium-potassium pump (Na⁺/K⁺ ATPase), which pumps 3 sodium ions out of the cell and 2 potassium ions into the cell. This creates a high concentration of Na⁺ outside the cell and a high concentration of K⁺ inside the cell.
Membrane Permeability: The membrane is more permeable to potassium ions than sodium ions, so potassium ions leak out of the neuron, making the inside of the cell more negative.
Equilibrium Potentials: Potassium’s equilibrium potential (K⁺) is around -90 mV, and sodium’s equilibrium potential (Na⁺) is around +60 mV. The combination of these forces establishes the resting potential.
Postsynaptic Potentials (PSPs): Generation, Conduction, Summation, and Integration
Generation of PSPs: Postsynaptic potentials occur when neurotransmitters bind to receptors on the postsynaptic membrane.
Excitatory Postsynaptic Potential (EPSP): If neurotransmitters (e.g., glutamate) open sodium channels, sodium ions flow into the postsynaptic neuron, depolarizing the membrane.
Inhibitory Postsynaptic Potential (IPSP): If neurotransmitters (e.g., GABA) open chloride (Cl⁻) or potassium (K⁺) channels, it results in hyperpolarization of the membrane, making it less likely to fire an action potential.
Conduction of PSPs: PSPs are local changes in membrane potential and do not travel down the axon. They decay over time and space but may be strong enough to trigger an action potential if they reach the axon hillock.
Summation of PSPs: PSPs can be summed in two ways:
Spatial Summation: Multiple PSPs from different locations on the postsynaptic membrane are added together.
Temporal Summation: PSPs from a single synapse are added together if they occur rapidly enough.
Integration of PSPs: The postsynaptic neuron integrates the various EPSPs and IPSPs it receives. If the sum of all postsynaptic potentials at the axon hillock reaches the threshold (typically around -55 mV), an action potential is initiated.
Generation and Conduction of Action Potentials
Ionic Basis:
Resting State: The neuron is at resting membrane potential, with high sodium outside and high potassium inside.
Depolarization: When a neuron reaches the threshold, voltage-gated sodium channels open, allowing Na⁺ to rush into the cell. This causes a rapid depolarization of the membrane (the inside becomes positive relative to the outside).
Repolarization: After a short delay, sodium channels close, and voltage-gated potassium channels open, allowing K⁺ to flow out of the cell, restoring the negative charge inside the cell.
Hyperpolarization: The membrane potential temporarily becomes more negative than the resting potential due to potassium overshoot.
Refractory Period: The neuron briefly becomes incapable of generating another action potential during the absolute refractory period and less likely during the relative refractory period.
Conduction: The action potential is propagated down the axon through saltatory conduction in myelinated neurons or continuous conduction in unmyelinated neurons. In myelinated axons, action potentials jump between nodes of Ranvier (where ion channels are concentrated).
Steps Involved in Synaptic Transmission
Action Potential Arrival: An action potential reaches the axon terminal.
Calcium Influx: The depolarization of the axon terminal opens voltage-gated calcium channels, allowing Ca²⁺ to enter the terminal.
Neurotransmitter Release: Calcium ions trigger the fusion of synaptic vesicles with the presynaptic membrane, releasing neurotransmitters into the synaptic cleft.
Receptor Binding: Neurotransmitters bind to receptors on the postsynaptic membrane, causing postsynaptic potentials (EPSPs or IPSPs).
Termination: The neurotransmitter is either degraded by enzymes (e.g., acetylcholinesterase breaking down acetylcholine), reuptaken into the presynaptic neuron, or diffuses away from the synapse.
Classes of Neurotransmitters and Their Roles
Amino Acids:
Glutamate: The primary excitatory neurotransmitter in the brain, involved in learning and memory.
GABA: The primary inhibitory neurotransmitter in the brain, involved in reducing neuronal excitability.
Amines:
Dopamine: Involved in reward, motivation, and motor control. Imbalances are linked to diseases like Parkinson’s and schizophrenia.
Serotonin: Regulates mood, sleep, and appetite. Its dysregulation is associated with depression and anxiety.
Norepinephrine: Involved in the fight or flight response, regulating arousal and attention.
Peptides:
Endorphins: Act as natural painkillers and are involved in pleasure and reward.
Substance P: Involved in the transmission of pain signals.
Acetylcholine: Involved in muscle activation, learning, and memory.
How Drugs Can Influence Synaptic Transmission
Blocking or Mimicking Neurotransmitters: Drugs can act as agonists (mimicking neurotransmitters) or antagonists (blocking neurotransmitter receptors). For example, morphine acts as an agonist at opioid receptors, mimicking the effects of endorphins.
Increasing or Decreasing Neurotransmitter Release: Some drugs increase neurotransmitter release (e.g., amphetamines increase the release of dopamine and norepinephrine), while others inhibit release (e.g., botulinum toxin inhibits acetylcholine release, causing muscle paralysis).
Inhibiting Neurotransmitter Reuptake: Drugs like SSRIs block the reuptake of serotonin, increasing its availability in the synapse and enhancing its effects.
Inhibiting Enzymatic Breakdown: Drugs like MAO inhibitors block the breakdown of neurotransmitters (such as dopamine and serotonin), thus prolonging their effects.
In summary, drugs can influence synaptic transmission by altering neurotransmitter availability, receptor binding, or the enzymes involved in neurotransmitter breakdown, all of which can enhance or inhibit neural signaling.
4o mini
Lecture--
Resting Membrane Potential Recording the Membrane Potential • The membrane potential is the difference in electrical charge between the INSIDE and OUTSIDE of the neuron • Measured using teeny tiny electrodes (microelectrodes) At rest (non-signalling) = -70mv
Resting Membrane Potential At rest (non-signalling) = -70mv The neuron is said to be ‘polarised’ in this state. 1. Concentration gradients (moving from high concentration to low) 2. Electrostatic pressure (Because opposite charges attract, the positively charged Na+ ions are attracted to the −70 mV charge inside resting neurons) 3. Sodium potassium pumps (active transport)
Think of a voting system within a company to decide whether to increase workers' salaries:
Imagine a group of executives in a meeting discussing whether to approve a salary increase. Each executive gives their input:
Some say YES (like EPSPs, which encourage firing an action potential),
Others say NO (like IPSPs, which discourage firing an action potential).
Now, just like in a real vote, each person's input counts. The decision to increase salaries depends on how many YES votes (EPSPs) there are in relation to the NO votes (IPSPs).
If enough YES votes (EPSPs) are cast, the decision is made to increase the workers' salaries – this is just like an action potential being triggered! The decision has been finalised, and the signal (salary increase) is sent out.
However, if there aren't enough YES votes (EPSPs), and the NO votes (IPSPs) outweigh them, then nothing happens—just like if an action potential doesn't fire. The salary increase is not approved.
This process works because the votes are summed up:
Spatial Summation: Different people (synapses) across the room may vote at the same time.
Temporal Summation: A person might vote multiple times over a short period - I know in reality this doesn't work for this analogy if everyone is only voting once... but bear with me!
If the total sum of the YES votes reaches the threshold (similar to reaching the threshold of excitation in neurons), then the decision is made - just like how the neuron fires an action potential when enough EPSPs outweigh the IPSPs.
So, PSPs "decide" whether an action potential will happen, and an action potential is the final result if enough excitation occurs.
The membrane potential is the difference in electrical charge between the INSIDE and OUTSIDE of the neuron; this is -70mv at rest and it maintained by concentration gradients, electrostatic pressure and the sodium potassium pump. 2. Post synaptic potentials (PSPs) are graded, decremental and instantaneous signals which are excitatory or inhibitory – and exert different influences on the membrane potential. The influence of these PSPs as to whether the neuron produce an Action Potentials (AP) depends on the spatial and temporal summation of these PSP. 3. Once the threshold of excitation is reached (-65mv), and AP is triggered – AP are non-graded (all or nothing events) that involve three phases with distinct ionic events within these. AP rely on voltage gated ion channels for their generation and conduction.
1. The steps involved in the synthesis, packing, transport and exocytosis of neurotransmitter molecules is slightly different for big and small neurotransmitters. 2. There are neurotransmitter specific receptors on the post synaptic membrane that have different functions (ionotropic, metabotropic), and auto receptors on the presynaptic membrane. Each of these types of receptors play a different role in the process of synaptic transmission. 3. Neurotransmitters don’t disappear – they are recycled! 4. There are five classes of neurotransmitters more generally, and drugs can influence any of the steps in synaptic transmission (more in textbook regarding this!)
