so chapter 48 isn't going to focus on a specific system we're going to time talk about neurons and synapses as well as signaling to get us prepared for chapter 49 which is about the nervous system so that picture you saw in the first slide was showing you a cone snail they are able to kill their prey using venom that disables neurons neurons are your nerve cells that are able to move information throughout your body two types of signals that neurons use for communication electrical signal signals which are a long distance and then chemical signals which are short distance the nervous system has to interpret those signals and it is able to do that using some complex paths and connections and this processing will take place either in simple clusters of neurons which are ganglia or more complex organization of neurons a brain okay this was studied a lot in this particular organism because you can see it has really really are sorry the squid because it's really really large axons so that made it a lot easier to be able to examine what happened okay Noren organization structures going to show us how is going to play a role in reflecting function in that information transfer in other words neurons have different shapes depending on the type of neuron that they are representing we have three overlapping stages in which nervous systems are able to process that information from their neurons we have sensory neurons which are the ones that are able to detect external stimuli internal conditions they move information along to the integration stage where inter neurons are able to integrate sensory input and motor output these are typically in the brain or again in your ganglia and then in the motor output we use a third type of neuron a motor neuron which move signals out of these processing centers and motor neurons when they transmit these signals are able to trigger muscular and/or gland activity so there's a picture at the top showing you the sensory neuron and how it overlaps with the inter neuron which overlaps with the motor neuron and then the pictures at the bottom are showing you the shapes of those different neurons you can see how the sensory neuron is cell body which contains its organelles its nucleus is in the middle while the inner neuron it's actually a part of the axons and then with the motor neuron it is right at the top along with its dendrites but that the majority of the axon is straight and able to connect with whatever its target is using the hillock and then the red that you see in the picture above we'll talk about that a little bit those are myelin sheaths and they help to improve conduction rates so nervous system again we're going to spend a lot more time on this in the next chapter animals have a pretty complex nervous system it consists of two parts central nervous system and peripheral nervous system the central nervous system is where the sensory input is integrated with the motor output your brain in your nerve port the peripheral nervous system are your nerves that extended to different parts of your body tend to be bundled together they're the ones that take the information to the CNS and take it out from the CNS so your eyes acting as a sensor in this particular case that information that it is sending is integrated in the central nervous system and then it is sent out at the central nervous system to be affected in this case muscle through the peripheral nervous system and then the information is sent in from the eye to the central nervous system via the peripheral nervous system neurons picture neurons have cell bodies dendrites and axons the cell body again has your organelles primarily along with nucleus and cytoplasm it's found pretty much in the CNS there are some they're found in ganglia and then they have two extensions or two extension like objects dendrites and axons dendrites are the ones that receive signals from other neurons the axon again is a much longer extension and it's going to transmit signals so dendrites receive them axons transmit them and it's cone-shaped base is known as the axon hillock okay supporting cells vertebrate neurons most invertebrate neurons require these they help to provide support for the neurons and help it do its job they are not involved in conducting impulses and there are large numbers of them present they outnumber mammalian brain neurons ten to fifty fold we have the glial cells your astrocytes and oligodendrocytes we'll talk about those a little bit more later and your Schwann cells the glial cells the astrocytes and oligodendrocytes the example it's the one on the left the Schwann cell is the one on the right and it's the purple one okay so there you can see all the glial that are surrounding your neurons neural circuits populations of neurons that are connected together by synapses that carry out specific functions after they have been activated we have large-scale brain networks when they're all circuits interconnect with other neuro circuits so individual towns coming together to make up a city simple circuits are present when a presynaptic neuron is able to stimulate a single postsynaptic neuron there are more complex types of neural circuits and we'll talk about each of those on the next slide sorry it's like coming up after that so there's your presynaptic cell to the top the signal is being sent down this axon to the postsynaptic cell where the dendrites are there and it sends it off to where it needs to go to we talked about how it could be electrical signals it can also be at the synapse where the presynaptic cell and the postsynaptic cell interact it could be a neurotransmitter a chemical signal that sends it off more complex circuits diverging circuits when one neuron synapses with multiple postsynaptic cells and we tend to see that with motor neurons in a converging neuro circuit you're taking in information from lots of different sources and converging it into one output and that's what we see with the brainstem and respiratory being able to breathe need to connect a lot of information together to make that process take place in a reverberating neural circuit neuron sends signals one to another in a linear pattern and then they send it send it right back the last one to the first one breathing would be an example of a reverberating neuro circuit because we don't ever want to stop breathing in a parallel after discharge circuit this involves both diverging and converging a neuron sends input to several their own chains of varying sizes so that would be the diverging and because they're different sizes they're going to converge on a single output neuron at different time intervals that would be the converging piece continuing firing after the output neuron has stimulated after after stimulation has been ceased it's called after discharge and blinking would be an example because we can blink at different rates of a parallel after discharge circuit okay so those are visible or sorry pictorial representations of those four types of more complex circuits sorry this next section is gonna be a lot of Khem ion pumps ion channels are able to determine neurons resting potential between the cells and the interstitial fluid there are ions that are not distributed equally they are attracted across the membrane to one another opposite charges attract and that is a source of potential energy and that difference in which we are going to call voltage is known as your membrane potential when a neuron is not sending any signals it is at its resting potential inside the cell it typically is between negative 60 and negative 80 millivolts and when there are changes in this membrane potential those are able to act as signals and will cause at times for the neuron to become activated to transmit and process information so how do we get this resting potential when you have a mammalian neuron that is at resting potential the potassium concentration is greatest inside the cell and the sodium concentration is the greatest outside of the cell a while back we talked about sodium potassium pumps and how they are able to use energy concentration gradients to move sodium out of this cell potassium into the cell and those gradients are sources of chemical potential energy when those ion channels open they are able to convert chemical potential into electrical potential there are because you have a selectively permeable membrane there are potassium channels and sodium channels and if you have opens potassium channels you're going to allow potassium to leave the cell and if the sodium channels aren't open that the sodium and the anions are going to stay in the cell and eyes remember your negatively charged ions so because you have allowed a lot of potassium ions to move out and you've kept the sodium and the anions and in this cell you have a negative charge that builds up and that becomes the prominent predominant source of membrane potential okay so there is your different concentrations we're going to focus mostly on potassium and sodium a lot of potassium in the cell a lot of sodium outside a cell again if you move potassium out you're losing positive charge and that's what causes that negative potential to develop at resting potential okay so there's your sodium potassium pump you can see how you have sodium ions moving out and you have potassium moving in and then when that pump is open it allows potassium to move out and it can allow some sodium to move in but we see a lot more potassium moving out than we see sodium moving in so basically look at this as two chambers the potassium chloride concentration the source of potassium ions is greater in the inner chamber and less in the outer chamber so it's going to move down its gradient to that outer chamber going from higher concentration to lower concentration until both electrical and chemical forces are at equilibrium that they're balanced and because the chloride stays in the inner chamber you've got that charge gram attraction for the two sides and when you reach equilibrium both the electrical and the chemical gradients have to be balanced we can actually measure or calculate this equilibrium potential for specific ions using what's known as the Nernst equation which is giving you that the potential or the voltage of that particular ion is equal to 62 millivolts times the log of its outside concentration divided by the inside concentration and so you take the log of that ratio for a potassium ion that equilibrium potential will be negative since you have more ions that have moved down while sodium having not left will have a positive potential and when you are at a resting neuron the currents of those two ions are equal and opposite one another so that resting potential because they're changing at the same rates is going to remain pretty constant so we've got here your potassium channel and you can see how the potassium is moving out and while sodium is not being able to move out there are some channels that are not voltage-gated sodium will move in we see that the membrane is going to have a positive cell potential for sodium action potentials are able to be generated by the signals that are conducted via these axons and they are able to take place because of these gated ion channels that will open and close in response to stimuli when the kept aciem channels that are gated open up potassium leaves and that makes the inside of your cell have a more negative potential and we refer to that as hyper polarization when the magnitude the size of that membrane potential increases is becoming more negative you can have some ion channel changes that will cause the membrane to be D polarized which would reduce the magnitude of that membrane potential making it become less negative so if you open up your sodium channels and you increase the sodium concentration inside the cell you're adding positive ions which are going to help to balance out the negative charge from the chloride and that would reduce your overall cell potential so sodium potassium changes can both influence hyperpolarization and depolarization graded potentials are polarization changes where the magnitude of your change will vary depending on your stimuli depending on how far they are away from your stimulus source you're going to lose that magnitude as it gets further away it's going to decay so these aren't the actual nerve signals but they have an effect on generating them regardless of the stimuli that has played a role if you are able to generate enough of a depolarization if you were able to reduce that negative cell potential to what we call its threshold about negative 55 millivolts and the million neurons that neuron is going to go through transmission and once that transmission occurs it doesn't matter how wrong that stimuli is even if it depolarized it more than that as long as it depolarized it up to that point you're going to have an action potential generated these action potentials are not one-off events they can occur in adjacent regions along that membrane they can't occur halfway they either happen or they don't and they are able to send signals rememory talked about how electrical signals are sent over long distances because some of the ion channels and your membrane are voltage-gated not all are once that membrane potential gets to a certain level one depolarization will lead to additional channels opening which can lead to additional depolarization so we see that positive feedback mechanism in place so how an action potential works when you're at a resting potential the reason the cell potential is not the same as potassium cell potential is because there is some there are some channels where sodium is able to passively move through into the membrane and so that causes your resting cell potential to be just under potassium once so the voltage-gated sodium and potassium channels are closed when you're at resting potential when you have some sort of stimuli come along that opens up the voltage-gated sodium channels and you increase your concentration of sodium ions inside of the cell in the member in the cytoplasm inside the cell membrane if that depolarization meets that threshold value you have an action potential occur there will be both a rising phase and a following phase with the rising phase once the threshold is crossed the depolarization will cause the most of the remaining voltage-gated sodium channels to open but it'll keep the potassium voltage-gated channels closed when that occurs because you're moving in lodz of sodium ions your membrane potential is going to become more positive in the falling phase the sodium channels that are both educated are block they are not able to allow sodium ions to come in anymore but the voltage-gated potassium channels open up and because potassium is gonna be moving towards its concentration gradient gradient it flows out so that's going to reduce your positive ions and it's going to cause that potential to become even more negative the undershoot period is we've got the voltage-gated sodium channels closed off but even though we have gone more negative sometimes they stay open a little longer than they need to and the that causes your membrane potential to be more negative than what we would expect once it reaches a certain point the potassium channels will be closed and the sodium channels will become unblocked but they won't allow sodium ions to move out and that resting potential will be restored there's a refractory period after an action potential where you cannot initiate a second action potential the sodium channels are going to be temporarily inactivated for a period of time so there's pictures of it starting down in the bottom left-hand corner there's your resting state where sodium is coming in potassium is not you have depolarization occur and you have more sodium you can see the charges Tatum showing up there you have more sodium coming in okay but you can't have potassium going out in the rising phase we see that we've got lots more sodium coming in so we're becoming even more positive and then in the following phase the sodium channels are blocked off sodium can't come in but now potassium can leave which is going to drop your potential and then the undershoot where you've gone on to far beyond that resting potential where your sodium channels are open but there are sorry they're not blocked anymore but they can't allow any more sodium to come in and potassium is still able to leave and then we eventually reestablish that resting potential going back to number one so where these action potentials are conducted is usually at the axon hillock the electrical current they polarized a region on the axon membrane they only travel towards the synaptic terminals from presynaptic to postsynaptic because the sodium channels have been inactivated behind them we talked a little bit about how you can't start that second one off I can't this is also done in part to keep that action potentials and going in reverse but we also said how it can move from one part of a membrane to another part so it can keep generating as it moves across that axon an action potential speed will increase with this diameter and wherever to Brett's are able to increase that diameter with that myelin sheath which is made by glia the oligodendrocytes in the central nervous system the Schwann cells in the peripheral nervous system these potentials get formed at nodes around the air their myelin sheath gaps where we can find those voltage-gated sodium channels and the action potentials will move in these mylady and axons in a process we call saw satori conduction ok so it allows them to keep moving and it increases that diameter which speeds up that process so that's when you have damage to your myelin sheets and you have more opportunities for the depolarization process to occur that you can start to run into some nerville nerville nervous system disorders okay so there's your Schwann cells and you can see there again where the gaps are that you're able to have those depolarization regions along your membrane neurons are able to communicate with cells at synapses the action potentials aren't going to be transferred necessarily between neurons and other cells but information will be in electrical synapses the current is transferred to help to promote additional action potentials from being generated at chemical synapses which is what we find for the majority of them and neurotransmitter will take information across and that neurotransmitter will help to activate channels it's taken across and synaptic vessels and the action potential will help to release it which diffuses it across the synaptic cleft and then it's received by the postsynaptic cell so there you see your ACTU action potential coming down the axon and this particular was a chemical signal the synaptic vessel has your neurotransmitter the cleft is between the presynaptic and the postsynaptic membranes as that synaptic vesicle fuses with the membrane is released it's able to bind to those ion channels and that's going to cause additional depolarization events to occur so that you can have more two action potentials you can also see calcium is going to play a role as well as that enters the voltage-gated channel for the presynaptic cell so direct synaptic transmission is going to be binding those transmitters we talked about to the ligand gated ion channels which will generate postsynaptic potentials and there's actually two ways you can have postsynaptic potentials you can have excitatory postsynaptic potentials epsps ones that will help to get your membrane more towards the resh hold and you can have in inventory postsynaptic potentials ipsps which will move you further away from threshold hyperpolarization so feedback after release once the transmitter has been diffused out of synaptic cleft and taken up by the cells it can be used to help to generate more of these postsynaptic potentials or it can be broken down by enzymes so there are synaptic terminals of presynaptic neurons and you've got a whole bunch of them that are at and right next to that postsynaptic neuron so sometimes you can have multiple postsynaptic potentials play a role at the same time a lot of neurons have multiple synapses on their dendrites and cell body one epi P or one ipsp is typically going to be too small to generate an action potential in a postsynaptic neuron but if they get it from multiple sources then those can be summed together and result in additional action potentials spatial summation is when you have two or more epsps occur in a single synapse so quickly that they are added together your postsynaptic neuron doesn't get to go to resting potential it happens so fast it's not able to return back in temporal summation you have it occurring at different synapses on the same postsynaptic neuron and in that case they would be added together so when you add these epsps through both spatial and temporal summation together they may trigger an action potential and then the same thing would work with ipsps to counter an epsps effect and so depending on what all is taking place at that postsynaptic membrane it will determine whether the axon hillock the neurons integrating center can reach that threshold and have another action potential so in letter A we've got the terminal branch of your presynaptic neuron and that it is having releasing its electrical or chemical signal on the postsynaptic neuron it did not generate enough of a potential change so therefore there was no threshold with the second particular example we have that first II one that first branch of the presynaptic neuron hitting it twice because it hit it twice it was able together to generate enough of potential to reach threshold enough of a depolarization event and the action potential continued and then the axon hillock was able to move it forward in letter C we have two different presynaptic neurons hitting the same postsynaptic membrane and together when they were some together spatial summation we have the action potential that was generated from the shopping and met in letter D we have e1 undergoing its potential and depolarizing this the membrane of the postsynaptic membrane then we have an eye so now we have that is hyperpolarizing the membrane and when you combine those two together you have not reached thresholds so there is no summation event and there is no action potential that occurs some synapses the neurotransmitter binds to receptors that are not part of ion channels meta petrovic when this takes place the ion is able to move through the channel via metabolic steps the neurotransmitter when it binds to it will set off a signal transduction pathway involving a second messenger and so although it is not going to necessarily generate an action potential they will take a little bit longer to get going but they also last longer so some examples of neurotransmitters there's five main groups we have a co co lines the biogenic amines the amino acids and our peptides and the gases and each of these individual neurotransmitters can have lots of different receptors so there are examples of them and we'll talk about each of them on the subsequent slides acetic ila coli is a common neurotransmitter in vertebrates and invertebrates it plays key roles and muscle simulation memory formation and learning vertebrates have both ligand gated and meta petrovic acetylcholine receptors amino acids are active both in your CNS and p NS the ones that and work in the CNS are glutamate this is going to play a role in your long-term memory GABA gamma-aminobutyric acid which is present at most of the inhibitory synapses in your brain and glycine which acts at inhibitory synapses in the CNS that exists outside of your brain biogenic amines at the nephron we talked a little bit about some of these earlier we did endocrine made from tyrosine infection heart norepinephrine is also made for tyrosine and similar to epinephrine is for going to be affecting your blood vessels primarily dopamine is coming from tyrosine it affects your boat movements and emotions serotonin which is from tryptophan and that's able to help relay messages in your brain and all of these are active both in your CNS and your pianist neuropeptides short chains of amino acids that are able to operate via those meta petrovic receptors they are made by cleaving larger protein precursors and orphan substance P are two examples of those they are sorry neurotransmitters that affect our pain perceptions and opiates bind to the same receptors as endorphins which is why they are able to be used as painkillers gases some neurons and vertebrates are able to release dissolved gases like nitric oxide and carbon monoxide these gases are not just made on a constant basis they're synthesized on demand they act as local regulators and your p NS they help with smooth muscle cells and they regulate hypothalamic hormone release in your brain