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Depolarisation of post synaptic neuron

Depolarisation of post synaptic neuron


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When the post synaptic neuron begins to depolarise as positive sodium ions move into it and it reaches threshold- does the inside of the neuron actually switch to being more positive than the outside?

I thought depolarisation meant that the inside became less negative but still remained more negative than the outside, hence having a voltage of -55mV. If the inside became more positive wouldn't the voltage be 55mV?


When the neuron reaches threshold, this is the trigger that leads to sodium channels opening and this creates a positive feedback process causing the neuron to become less negative and more positive, triggering more sodium channels to open until it is inevitable an action potential will be reached. During an action potential, the neuron cell becomes more positive compared to the outside for a very short period(ie, 1 millisecond or less).

Yes, depolarisation does mean the inside becomes less negative in this context. You would expect the inside of the neuron to be at +55mV (or perhaps more) during an action potential, as the depolarisation of the neuron grows closer to reaching the sodium equilibrium potential which is estimated to be around +58mV. However, during the phase leading up to an action potential, potassium channels also remain open. The diffusion of potassium ions can lead to the cell becoming more negative. In other words, it limits the voltage of an action potential to around +33mV instead of +55mV.

Sources:

(1)https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/a/depolarization-hyperpolarization-and-action-potentials

(2)https://opentextbc.ca/anatomyandphysiology/chapter/12-4-the-action-potential/


a decrease in the difference in voltage between the inside and outside of the neuron

Nerve Impulse Transmission within a Neuron: Action Potential

  • Signals are transmitted from neuron to neuron via an action potential, when the axon membrane rapidly depolarizes and repolarizes.
  • Once the sodium channels open, the neuron completely depolarizes to a membrane potential of about +40 mV.
  • Once the threshold potential is reached, the neuron completely depolarizes.
  • As soon as depolarization is complete, the cell "resets" its membrane voltage back to the resting potential.
  • The action potential is conducted down the axon as the axon membrane depolarizes, then repolarizes.

Electrical Events

  • Cardiac contraction is initiated in the excitable cells of the sinoatrial node by both spontaneous depolarization and sympathetic activity.
  • The SA node nerve cells are specialized in that they undergo spontaneous depolarization and generation of action potentials, without stimulation from the rest of the nervous system.
  • The SA node nerve impulses travel through the atria and cause muscle cell depolarization and contraction of the atria directly.
  • The AV node slows the neural impulse from the SA node by a slight amount, which causes a delay between depolarization of the atria and the ventricles.
  • The system of nerves that work together to set the heart rate and stimulate muscle cell depolarization within the heart.

Nerve Conduction and Electrocardiograms

  • This inrush of Na+ first neutralizes the inside membrane (called depolarization), and then makes it slightly positive.
  • The adjacent membrane depolarizes, affecting the membrane farther down, and so on.
  • Just as nerve impulses are transmitted by depolarization and repolarization of an adjacent membrane, the depolarization that causes muscle contraction can also stimulate adjacent muscle cells to depolarize (fire) and contract.
  • An electrocardiogram (ECG) is a record of the voltages created by the wave of depolarization (and subsequent repolarization) in the heart.
  • The P wave is generated by the depolarization and contraction of the atria as they pump blood into the ventricles.

Stages of the Action Potential

  • Neural impulses occur when a stimulus depolarizes a cell membrane, prompting an action potential which sends an "all or nothing" signal.
  • Depolarization: A stimulus starts the depolarization of the membrane.
  • The refractory phase takes place over a short period of time after the depolarization stage.
  • During the refractory phase this particular area of the nerve cell membrane cannot be depolarized.
  • A neuron must reach a certain threshold in order to begin the depolarization step of reaching the action potential.

Postsynaptic Potentials and Their Integration at the Synapse

  • At excitatory synapses, neurotransmitter binding depolarizes the postsynaptic membrane.
  • Since the electrochemical gradient of sodium is steeper than that of potassium, a net depolarization occurs.
  • If enough neurotransmitter binds, depolarization of the postsynaptic membrane can reach 0mV, which is higher than threshold of -30-50mV.
  • This figure depicts the mechanism of temporal summation in which multiple action potentials in the presynaptic cell cause a threshold depolarization in the postsynaptic cell.

Synaptic Transmission

  • When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated Na+ channels.
  • Na+ ions enter the cell, further depolarizing the presynaptic membrane.
  • This depolarization causes voltage-gated Ca2+ channels to open.
  • When the presynaptic membrane is depolarized, voltage-gated Ca2+ channels open and allow Ca2+ to enter the cell.
  • The neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels in the postsynaptic membrane, resulting in a localized depolarization or hyperpolarization of the postsynaptic neuron.

Mechanism and Contraction Events of Cardiac Muscle Fibers

  • The mechanism for CIRC is that receptors within the cardiomyocyte will bind to calcium ions when calcium ion channels open during depolarization, and will release more calcium ions into the cell.
  • Similarly to skeletal muscle, the influx of sodium ions causes an initial depolarization, however in cardiac muscle, the influx of calcium ions sustains the depolarization so that it lasts longer.
  • CICR creates a "plateau phase" in which the cell's charge stays slightly positive (depolarized) for longer before it becomes more negative as it repolarizes due to potassium ion influx.

Excitation–Contraction Coupling

  • This reduces the voltage difference between the inside and outside of the cell, which is called depolarization.
  • As ACh binds at the motor end plate, this depolarization is called an end-plate potential.
  • The depolarization then spreads along the sarcolemma and down the T tubules, creating an action potential.

Peripheral Motor Endings

  • These receptors open, allowing sodium ions to flow in and potassium ions to flow out of the muscle's cytosol, producing a local depolarization of the motor end plate known as an end-plate potential (EPP).
  • This depolarization spreads across the surface of the muscle fiber and continues the excitation-contraction coupling to contract the muscle.
  • The action potential spreads through the muscle fiber's network of T-tubules, depolarizing the inner portion of the muscle fiber.
  • The depolarization activates L-type voltage-dependent calcium channels (dihydropyridine receptors) in the T-tubule membrane, which are in close proximity to calcium-release channels (ryanodine receptors) in the adjacent sarcoplasmic reticulum.

Electrocardiogram and Correlation of ECG Waves with Systole

  • The ECG works by detecting and amplifying tiny electrical changes on the skin that occur during heart muscle depolarization.
  • The P wave indicates atrial depolarization, in which the atria contract (atrial systole).
  • The QRS complex refers to the combination of the Q, R, and S waves, and indicates ventricular depolarization and contraction (ventricular systole).
  • The T Wave indicates ventricular repolarization, in which the ventricles relax following depolarization and contraction.
  • The ST segment refers to the gap (normally flat or slightly upcurved line) between the S wave and the T wave, and represents the time between ventricular depolarization and repolarization.
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Depolarization

Nerve Impulse Transmission within a Neuron: Action Potential

  • Signals are transmitted from neuron to neuron via an action potential, when the axon membrane rapidly depolarizes and repolarizes.
  • Once the sodium channels open, the neuron completely depolarizes to a membrane potential of about +40 mV.
  • Once the threshold potential is reached, the neuron completely depolarizes.
  • As soon as depolarization is complete, the cell "resets" its membrane voltage back to the resting potential.
  • The action potential is conducted down the axon as the axon membrane depolarizes, then repolarizes.

Synaptic Transmission

  • When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated Na+ channels.
  • Na+ ions enter the cell, further depolarizing the presynaptic membrane.
  • This depolarization causes voltage-gated Ca2+ channels to open.
  • When the presynaptic membrane is depolarized, voltage-gated Ca2+ channels open and allow Ca2+ to enter the cell.
  • The neurotransmitter diffuses across the synaptic cleft and binds to ligand-gated ion channels in the postsynaptic membrane, resulting in a localized depolarization or hyperpolarization of the postsynaptic neuron.

Excitation–Contraction Coupling

  • This reduces the voltage difference between the inside and outside of the cell, which is called depolarization.
  • As ACh binds at the motor end plate, this depolarization is called an end-plate potential.
  • The depolarization then spreads along the sarcolemma and down the T tubules, creating an action potential.

Balance and Determining Equilibrium

  • The moving otolith layer, in turn, bends the sterocilia to cause some hair cells to depolarize as others hyperpolarize.
  • The exact tilt of the head is interpreted by the brain on the basis of the pattern of hair-cell depolarization .

Signal Summation

  • Sometimes, a single excitatory postsynaptic potential (EPSP) is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential.

Transduction and Perception

  • In the nervous system, a positive change of a neuron's electrical potential (also called the membrane potential), depolarizes the neuron.
  • If the magnitude of depolarization is sufficient (that is, if membrane potential reaches a threshold), the neuron will fire an action potential.

Synaptic Plasticity

  • However, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out and Ca2+ ions pass into the postsynaptic cell.
  • The next time glutamate is released from the presynaptic cell, it will bind to both NMDA and the newly-inserted AMPA receptors, thus depolarizing the membrane more efficiently.

Reception and Transduction

  • Binding of an acid or other sour-tasting molecule triggers a change in the ion channel which increases hydrogen ion (H+) concentrations in the taste neurons thus, depolarizing them.

Transduction of Light

  • Thus, unlike most other sensory neurons (which become depolarized by exposure to a stimulus), visual receptors become hyperpolarized and are driven away from the threshold .

Nerve Impulse Transmission within a Neuron: Resting Potential

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The Resting Membrane Potential is Critical

In the previous example, the resting membrane potential of that cell was -60 mV, so chloride moved into the cell. If the resting membrane potential was instead equal to chloride’s equilibrium potential of -65 mV, then chloride would be at equilibrium and move into and out of the cell, and there would be no net movement of the ion. Even though this would lead to no change in membrane potential, the opening of chloride channels continues to be inhibitory. Increased chloride conductance would make it more difficult for the cell to depolarize and to fire an action potential.

Animation 5.4. If the cell is at rest at chloride’s equilibrium potential, when a stimulus opens the chloride channels, there will be no net movement of chloride in either direction because chloride will be at equilibrium. Since there is no net movement, there will also be no change in membrane potential because there is an equal amount of ion flow into and out of the cell. The dotted, blue channels represent sodium channels the striped, green channels represent potassium channels the solid yellow channels represent chloride channels. ‘IPSP at Equilibrium’ by Casey Henley is licensed under a Creative Commons Attribution Non-Commercial Share-Alike (CC BY-NC-SA) 4.0 International License. View static image of animation.

If the resting membrane potential of the cell was more negative than chloride’s equilibrium potential, for example, at -70 mV, then chloride would leave the cell, in order to move the membrane potential toward -65 mV. This would result in a depolarization of the membrane potential. However, the overall effect is still inhibitory because once the cell reaches -65 mV, the driving forces acting on chloride would try to keep the cell at that membrane potential, making it more difficult for the cell to depolarize further and fire an action potential.

A good rule of thumb is to remember that opening of sodium channels is excitatory whereas opening of chloride channels is inhibitory.

Animation 5.5. If the cell is at rest at chloride’s equilibrium potential, when a stimulus opens the chloride channels, chloride will leave the cell, removing its negative charge. This causes a depolarization in the membrane potential, but it is still inhibitory since chloride movement will try to keep the cell near -65 mV. TThe dotted, blue channels represent sodium channels the striped, green channels represent potassium channels the solid yellow channels represent chloride channels.‘Inhibitory Depolarization’ by Casey Henley is licensed under a Creative Commons Attribution Non-Commercial Share-Alike (CC BY-NC-SA) 4.0 International License. View static image of animation.


Myasthenia Gravis

Nils Erik Gilhus , Jenny Lindroos , in Reference Module in Biomedical Sciences , 2021

8 Symptomatic drug treatment

Drugs that inhibit the acetylcholine esterase at the neuromuscular synapse will increase the amount of available acetylcholine at the postsynaptic membrane . This increase in available acetylcholine leads to an increase in muscle strength in MG. Acetylcholine esterase inhibitors do not influence the loss of AChR, the AChR function, or the synthesis of new AChR. Thus, such drugs do not influence the MG disease process. However, the increased time interval for acetylcholine to be present at the synapse means a better chance for binding to an intact AChR before the transmitter substance is inactivated. Acetylcholine esterase inhibitors have been used as symptomatic MG treatment since 1934 and represented the first effective drug treatment for the disease.

Pyridostigmine is the preferred first-line acetylcholine esterase inhibitor in MG ( Gilhus, 2016 Skeie et al., 2010 ). Optimal dose is determined through a gradual increase of dose during some days or a few weeks. Dose is a balance between clinical effect as reported by the patient and side-effects (see below). Optimal single dose is usually 60–120 mg, and optimal daily dose is usually 120–600 mg. For some sensitive patients, a much smaller dose is helpful. The patient can vary the dose from day to day based on variation in the need for muscle strength and endurance. The great majority of MG patients are capable of such self-medication. The pyridostigmine effect appears after around 30 min, and the half-life of the drug is 3–4 h. Many MG patients with only mild symptoms and no obvious muscle weakness by ordinary clinical testing continue to use pyridostigmine because they feel a positive effect. Pyridostigmine and other acetylcholine esterase inhibitors do not have any muscle-enhancing effect in healthy individuals and do not appear on doping lists.

Neostigmine is another acetylcholine esterase inhibitor. It has a much shorter half-life than pyridostigmine and is therefore less used. Ambenonium chloride similarly inhibits the acetylcholine esterase. No controlled studies have been undertaken of the drug, and no formal comparisons with pyridostigmine have been reported. Ambenonium is regarded as less effective, perhaps because of some variation in bioavailability. The drug is not generally available on the market in most countries. In patients who do not tolerate pyridostigmine, ambenonium chloride should be tried, especially if they have an allergic reaction to pyridostigmine.

Acetylcholine receptor inhibitors are usually less effective in MG with MuSK antibodies than for the other MG subgroups ( Evoli et al., 2018 ).

The side-effects of acetylcholine esterase inhibitors are due to cholinergic effects in the autonomic nervous system. The muscarinic AChR in this system is not attacked by the autoantibodies in MG, but the drugs inhibit the degradation of their acetylcholine. Stomach pain, diarrhea, increased salivation, nausea and accommodation disturbances are therefore common. Many patients experience muscle cramps and fasciculations. The side-effects are dose-dependent, and the optimal drug dose represents the best balance between effect and side-effects.


Neurotransmitters and Neurotransmission in the Developing and Adult Nervous System

Presynaptic Effects of Endocannabinoids

The presynaptic action of endocannabinoids was the first function to be described for these transmitters and is now appreciated as one of their canonical actions. Endocannabinoids can mediate two separate but similar presynaptic phenomena: depolarization-induced suppression of inhibition (DSI) or depolarization-induced suppression of excitation (DSE). In CA1 of hippocampus, low-frequency train stimulation of GABAergic terminals synapsing onto pyramidal cells produces an eIPSC of similar magnitude until a depolarization is applied to the pyramidal cell. With the application of depolarization, the magnitude of the eIPSC decreases rapidly. This effect requires an intracellular calcium increase in the pyramidal cell and indicates that endocannabinoids synthesis is calcium dependent. Determining that this process does not require synaptic vesicular release requires the use of botulinum toxin, which acts by preventing vesicular fusion to the presynaptic membrane. In the presence of botulinum toxin, DSI is still observed when recordings are conducted on CA1 pyramidal cells. In addition to the use of botulinum toxin, application of the presynaptic neurotransmitter (eg, GABA) has been used to demonstrate that the observed DSI is not simply an alteration in the postsynaptic cell that changes the sensitivity to the presynaptic neurotransmitter. For example, application of GABA produces a postsynaptic response of equal magnitude in CA1 pyramidal cells before and after depolarization (before and after DSI is elicited). This was the first conclusive set of experiments to demonstrate that endocannabinoids act retrogradely through their postsynaptic release and subsequent modulation of presynaptic neurotransmitter release.

Since the initial description of DSI, DSE has also been identified. With DSE, the presynaptic cell releases a neurotransmitter that elicits an EPSC on the postsynaptic cell (eg, glutamate). Then, when the postsynaptic cell is depolarized, a reduction in the amplitude of the EPSC is observed that is mediated by the CB1 receptor ( Fig. 3.26 ). CB1-dependent DSI and DSE has been described at a wide variety of synapses and modulate the release of numerous neurotransmitters, including GABA, glutamate, glycine, and ACh.

Figure 3.26 . Postsynaptic depolarization inhibits excitatory cell afferents. (A) Stimulus protocol with the holding potential of the postsynaptic cell (hp upper) and the stimulation timing (stim below). Parallel fiber (B) and climbing fiber (C) EPSC amplitudes are plotted over time for control responses with no preceding prepulse to 0 mV (open circles) and test responses following Purkinje cell depolarization closed circles). Average parallel fiber (B) and climbing fiber (C) EPSCs are shown at the right. Stimulus artifacts are blanked for clarity. Parallel fiber and climbing fiber responses are from two representative experiments. The duration of the depolarization to 0 mV was 50 ms for parallel fiber experiments and 1 s for climbing fiber responses. The test stimulus followed the depolarization by Δt = 5 s.

Reproduced with permission from A.C. Kreitzer, W.G. Regehr. Retrograde Inhibition of Presynaptic Calcium Influx by Endogenous Cannabinoids at Excitatory Synapses onto Purkinje Cells. Neuron 200129(3):717-27.

Activation of Gi/o signaling at presynaptic terminals is often associated with a suppression of the conductance mediated by the voltage-gated calcium channels, thereby decreasing the synaptic release of neurotransmitter. CB1 receptors are coupled to the Gi/o signaling pathways, since PTX abolishes CB1 effects. Mechanistically, CB1 activation has been found to suppress N- and P/Q-type calcium channel-mediated currents and reduce synaptic neurotransmitter release. Presynaptic CB1 activation has also been found to modulate different potassium channels, kinases, and other GPCRs.


How does excitatory postsynaptic potential (EPSP) in a typical neuron occur?

EPSP stands for excitatory postsynaptic potential. Excitatory postsynaptic potentials (EPSPs) are associated with a transmitter-induced increase in Na+ and K+ conductance of the synaptic membrane, resulting in net entry of positive charge carried by Na+ and membrane depolarization. During this potential, the postsynaptic membrane is depolarized temporarily.

An excitatory postsynaptic potential occurs when there is an unexpected flow of positive ions into the cell. It can also be caused when positive ions outflow reduces.

An excitatory postsynaptic potential causes depolarization most times because it has changed the membrane potential of the cell. When there are larger EPSPs, they caused more membrane depolarization. Therefore, they cause the postsynaptic cell to reach the threshold needed to fire an action potential. This usually causes a voltage change from 70 mV to -69.5 mV.

IPSPs, which is the opposite of Excitatory postsynaptic potentials, are caused when positive ions outflow increases or when negative ions outflow increases in the postsynaptic cells.

L. Agate

EPSP is known as Excitatory Postsynaptic Potential. This occurs when there is a change in the membrane voltage of the postsynaptic cell. You should first understand that EPSP is known to be a temporary depolarization of the postsynaptic membrane. This happens when the flow of the positively&minuscharged ions go to the postsynaptic cell when the ligand&minussensitive channels open.

Through EPSP, the potential of the neuron membrane also increases significantly. EPSP is depolarizing which means that it will make the inside of the cell become more positive. This will allow the membrane to become closer to the needed action potential. The response will depend on the type of channel that is coupled to the needed receptor.

T. Lopez

Let's see how far my knowledge stretches

The correct answer to this question is A voltage change from -70 mV to -69.5 mV. EPSP stands for excitatory postsynaptic potential. This is related to the field of neuroscience, and it is a postsynaptic potential.

During this potential, the postsynaptic membrane is temporarily depolarized. EPSPs are the opposite of IPSPs. IPSPs stands for inhibitory postsynaptic potentials. They are caused by the flow of negative particles in the cell.

They are also caused by positive particles that leave the cell. In the end, IPSPs are created by positive cell expansion. ESPSs are caused by the flow of particles known as EPSC or excitatory postsynaptic current.

D. Loukas

Calculating, Processing, Integrating, Differentiating are what intrigues me the most in a very beautiful way.

The opening of sodium channels causes an excitatory postsynaptic potential. When sodium channels are open, the electrochemical gradient drives sodium to come into the cell. When sodium gives its positive charge into the cell, its membrane potential becomes more positive or depolarized.

This depolarization raises the likelihood a neuron will be able to come to the action capability therefore, it is excitative. It happens in the postsynaptic cell, and it is a shift in potential: excitatory postsynaptic potential.

In neuroscience, an excitatory postsynaptic potential makes the postsynaptic neuron more prone to ignite an action potential. This brief depolarization of membrane potential, caused by the movement of positively charged particles into the postsynaptic cell, is an aftereffect of opening particle channels.

H. Barnes

An EPSP or Excitatory Postsynaptic Potential refers to the postsynaptic potential that causes the postsynaptic neuron to produce an action potential. An excitatory postsynaptic potential is usually caused by a sudden flow of positive ions into the cell. Another main cause of EPSPs is when there is a decrease in positive ions outflow.

Excitatory postsynaptic potentials are the direct opposite of the opposite of IPSPs or inhibitory postsynaptic potentials. IPSPs are caused when there is an increase in positive ions outflow or when there's an increase in the flow of negative ions out of the postsynaptic cells.

An excitatory postsynaptic potential usually causes depolarization because it has altered the membrane potential of the cell. When there are larger EPSPs, they, in turn, result in more membrane depolarization. As a result, they cause the postsynaptic cell to reach the threshold needed to fire an action potential. However, this usually causes a voltage change from 70 mV to -69.5 mV.

C.Dorothy

A voltage change from -70 mV to -69.5 mV
In neuroscience, an excitatory postsynaptic potential (EPSP) is a postsynaptic potential that makes the postsynaptic neuron more inclined to conflagrate an action potential. This brief depolarization of postsynaptic membrane potential, caused by the flow of positively charged particles into the postsynaptic cell, is an aftereffect of opening ligand-gated particle channels. These are the inverse of inhibitory postsynaptic potentials (IPSPs), which for the most part result from the flow of negative particles into the cell or positive particles out of the cell. EPSPs can likewise come about because of a reduction in active positive charges, while IPSPs are here and there caused by an expansion in positive charge outflow. The flow of particles that causes an EPSP is an excitatory postsynaptic current (EPSC).


EPSPs, as IPSPs, are review. At the point when different EPSPs happen on a solitary fix of the postsynaptic membrane, their consolidated impact is the total of the individual EPSPs. Bigger EPSPs result in more prominent membrane depolarization and along these lines improves the probability that the postsynaptic cell achieves the limit for terminating an activity potential.


Optogenetic Manipulation of Postsynaptic cAMP Using a Novel Transgenic Mouse Line Enables Synaptic Plasticity and Enhances Depolarization Following Tetanic Stimulation in the Hippocampal Dentate Gyrus

cAMP is a positive regulator tightly involved in certain types of synaptic plasticity and related memory functions. However, its spatiotemporal roles at the synaptic and neural circuit levels remain elusive. Using a combination of a cAMP optogenetics approach and voltage-sensitive dye (VSD) imaging with electrophysiological recording, we define a novel capacity of postsynaptic cAMP in enabling dentate gyrus long-term potentiation (LTP) and depolarization in acutely prepared murine hippocampal slices. To manipulate cAMP levels at medial perforant path to granule neuron (MPP-DG) synapses by light, we generated transgenic (Tg) mice expressing photoactivatable adenylyl cyclase (PAC) in DG granule neurons. Using these Tg(CMV-Camk2a-RFP/bPAC)3Koka mice, we recorded field excitatory postsynaptic potentials (fEPSPs) from MPP-DG synapses and found that photoactivation of PAC during tetanic stimulation enabled synaptic potentiation that persisted for at least 30 min. This form of LTP was induced without the need for GABA receptor blockade that is typically required for inducing DG plasticity. The paired-pulse ratio (PPR) remained unchanged, indicating the cAMP-dependent LTP was likely postsynaptic. By employing fast fluorescent voltage-sensitive dye (VSD: di-4-ANEPPS) and fluorescence imaging, we found that photoactivation of the PAC actuator enhanced the intensity and extent of dentate gyrus depolarization triggered following tetanic stimulation. These results demonstrate that the elevation of cAMP in granule neurons is capable of rapidly enhancing synaptic strength and neuronal depolarization. The powerful actions of cAMP are consistent with this second messenger having a critical role in the regulation of synaptic function.

Keywords: VSD imaging cAMP electrophysiology long-term potentiation optogenetics photoactivatable adenylyl cyclase (PAC) synaptic plasticity.

Copyright © 2020 Luyben, Rai, Li, Georgiou, Avila, Zhen, Collingridge, Tominaga and Okamoto.

Figures

Generation and characterization of photoactivatable…

Generation and characterization of photoactivatable adenylyl cyclase (PAC) expressing transgenic (Tg) mice. (A)…

Baseline transmission at medial perforant…

Baseline transmission at medial perforant path to granule dentate gyrus (MPP-DG) synapses of…

Long-term potentiation (LTP) enabled by…

Long-term potentiation (LTP) enabled by photoactivation of PAC. (A) Lower: Blue light (480…

Configuration for PAC photoactivation and…

Configuration for PAC photoactivation and voltage-sensitive dye (VSD) imaging. A schematic of the…

Spatial-temporal mapping of the PAC-induced…

Spatial-temporal mapping of the PAC-induced enhancement of DG depolarization. (A) Representative time-lapse images…


Brain Structure: Depolarization & Neurotransmitters

1) Negative charge inside of membrane (due to K ions) positive charge on outside (Na), more negative than positive.

2) Action potential causes the sodium channels to open and Na ions flow into inner membrane K+ ions flow out.

3) Sodium-potassium pump depolarize cell during refractory period 2:3 Na:K pumped into cell

  • Actions potential do not vary but the rate/ number of neuron stimulated will result in high-intensity stimulation
  • Axons covered by myelin sheath= insulation/ protective
  • Nodes of Ranvier: section of axon where myelin sheath are not present or absent. Impulses hope along these nodes to get better conductivity and speed.
  • Synapse: connection between neurons (axons and dendrites)
  • Neurotransmission occurs between axon and dendrites in synaptic cleft
  • Synthesis- chemicals have made within the neuron
  • Storage- these chemicals are stored within the synaptic vesicles
  • Release- chemicals move across the synaptic cleft from presynaptic neuron (axon) to post synaptic neuron (dendrites)
  • Binding: the vesicle bind to the receptor sites on the neurons. These chemicals will (a) depolarize the neuron by exciting it or (b) hyperpolarize the neuron and inhibit it.
  • Deactivation: shuts off, is depolarized
  • Exciting Chemicals: Glutamate, Acetylcholine, Norepinephrine, Dopamine
  • Inhibiting Chemicals: GABA, Serotonin, Dopamine
  • Acetylcholine -> (motor movement, sleep, dreaming, muscle) Alzheimer’s disease (lack of)
  • Botulism: blocked Ach, paralysis
  • Dopamine -> Parkinson’s disease (lack of) can be treated also treats schizophrenia (overload)/ delusions
  • Serotonin (5HT) -> sensitivity to it linked to depression (due to undersupply of it)
  • Endorphins -> reduce pain
  • Neuromodulators -> widespread effect
  • Drugs can mimic some neurotransmitters (block uptake, bind at stop TP)
  • Sensory Neurons: sent info the brain/ spine
  • Motor Neurons: send impulses from brain/ spine to muscles/ organs
  • Interneurons: connective neurons

CNS: brain/ spine PNS: everything else

  • Somatic Nervous system: voluntary movements (muscles, senses)
  • Autonomic Nervous system: controls glands, heart, etc.
  • Fight-or-Flight: Sympathetic:arousal to stress Parasympathetic:recovery from stress [HOMOEOSTATIS]

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How Neurons Communicate

All functions performed by the nervous system—from a simple motor reflex to more advanced functions like making a memory or a decision—require neurons to communicate with one another. While humans use words and body language to communicate, neurons use electrical and chemical signals. Just like a person in a committee, one neuron usually receives and synthesizes messages from multiple other neurons before “making the decision” to send the message on to other neurons.

Nerve Impulse Transmission within a Neuron

For the nervous system to function, neurons must be able to send and receive signals. These signals are possible because each neuron has a charged cellular membrane (a voltage difference between the inside and the outside), and the charge of this membrane can change in response to neurotransmitter molecules released from other neurons and environmental stimuli. To understand how neurons communicate, one must first understand the basis of the baseline or ‘resting’ membrane charge.

Neuronal Charged Membranes

The lipid bilayer membrane that surrounds a neuron is impermeable to charged molecules or ions. To enter or exit the neuron, ions must pass through special proteins called ion channels that span the membrane. Ion channels have different configurations: open, closed, and inactive, as illustrated in [link]. Some ion channels need to be activated in order to open and allow ions to pass into or out of the cell. These ion channels are sensitive to the environment and can change their shape accordingly. Ion channels that change their structure in response to voltage changes are called voltage-gated ion channels. Voltage-gated ion channels regulate the relative concentrations of different ions inside and outside the cell. The difference in total charge between the inside and outside of the cell is called the membrane potential.

This video discusses the basis of the resting membrane potential.

Resting Membrane Potential

A neuron at rest is negatively charged: the inside of a cell is approximately 70 millivolts more negative than the outside (−70 mV, note that this number varies by neuron type and by species). This voltage is called the resting membrane potential it is caused by differences in the concentrations of ions inside and outside the cell. If the membrane were equally permeable to all ions, each type of ion would flow across the membrane and the system would reach equilibrium. Because ions cannot simply cross the membrane at will, there are different concentrations of several ions inside and outside the cell, as shown in [link]. The difference in the number of positively charged potassium ions (K + ) inside and outside the cell dominates the resting membrane potential ([link]). When the membrane is at rest, K + ions accumulate inside the cell due to a net movement with the concentration gradient. The negative resting membrane potential is created and maintained by increasing the concentration of cations outside the cell (in the extracellular fluid) relative to inside the cell (in the cytoplasm). The negative charge within the cell is created by the cell membrane being more permeable to potassium ion movement than sodium ion movement. In neurons, potassium ions are maintained at high concentrations within the cell while sodium ions are maintained at high concentrations outside of the cell. The cell possesses potassium and sodium leakage channels that allow the two cations to diffuse down their concentration gradient. However, the neurons have far more potassium leakage channels than sodium leakage channels. Therefore, potassium diffuses out of the cell at a much faster rate than sodium leaks in. Because more cations are leaving the cell than are entering, this causes the interior of the cell to be negatively charged relative to the outside of the cell. The actions of the sodium potassium pump help to maintain the resting potential, once established. Recall that sodium potassium pumps brings two K + ions into the cell while removing three Na + ions per ATP consumed. As more cations are expelled from the cell than taken in, the inside of the cell remains negatively charged relative to the extracellular fluid. It should be noted that chloride ions (Cl – ) tend to accumulate outside of the cell because they are repelled by negatively-charged proteins within the cytoplasm.

The resting membrane potential is a result of different concentrations inside and outside the cell.
Ion Concentration Inside and Outside Neurons
Ion Extracellular concentration (mM) Intracellular concentration (mM) Ratio outside/inside
Na + 145 12 12
K+ 4 155 0.026
Cl − 120 4 30
Organic anions (A−) 100

Action Potential

A neuron can receive input from other neurons and, if this input is strong enough, send the signal to downstream neurons. Transmission of a signal between neurons is generally carried by a chemical called a neurotransmitter. Transmission of a signal within a neuron (from dendrite to axon terminal) is carried by a brief reversal of the resting membrane potential called an action potential. When neurotransmitter molecules bind to receptors located on a neuron’s dendrites, ion channels open. At excitatory synapses, this opening allows positive ions to enter the neuron and results in depolarization of the membrane—a decrease in the difference in voltage between the inside and outside of the neuron. A stimulus from a sensory cell or another neuron depolarizes the target neuron to its threshold potential (-55 mV). Na + channels in the axon hillock open, allowing positive ions to enter the cell ([link] and [link]). Once the sodium channels open, the neuron completely depolarizes to a membrane potential of about +40 mV. Action potentials are considered an "all-or nothing" event, in that, once the threshold potential is reached, the neuron always completely depolarizes. Once depolarization is complete, the cell must now "reset" its membrane voltage back to the resting potential. To accomplish this, the Na + channels close and cannot be opened. This begins the neuron's refractory period, in which it cannot produce another action potential because its sodium channels will not open. At the same time, voltage-gated K + channels open, allowing K + to leave the cell. As K + ions leave the cell, the membrane potential once again becomes negative. The diffusion of K + out of the cell actually hyperpolarizes the cell, in that the membrane potential becomes more negative than the cell's normal resting potential. At this point, the sodium channels will return to their resting state, meaning they are ready to open again if the membrane potential again exceeds the threshold potential. Eventually the extra K + ions diffuse out of the cell through the potassium leakage channels, bringing the cell from its hyperpolarized state, back to its resting membrane potential.

Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K + through voltage-gated K + channels. Which part of the action potential would you expect potassium channels to affect?

This video presents an overview of action potential.

Myelin and the Propagation of the Action Potential

For an action potential to communicate information to another neuron, it must travel along the axon and reach the axon terminals where it can initiate neurotransmitter release. The speed of conduction of an action potential along an axon is influenced by both the diameter of the axon and the axon’s resistance to current leak. Myelin acts as an insulator that prevents current from leaving the axon this increases the speed of action potential conduction. In demyelinating diseases like multiple sclerosis, action potential conduction slows because current leaks from previously insulated axon areas. The nodes of Ranvier, illustrated in [link] are gaps in the myelin sheath along the axon. These unmyelinated spaces are about one micrometer long and contain voltage gated Na + and K + channels. Flow of ions through these channels, particularly the Na + channels, regenerates the action potential over and over again along the axon. This ‘jumping’ of the action potential from one node to the next is called saltatory conduction. If nodes of Ranvier were not present along an axon, the action potential would propagate very slowly since Na + and K + channels would have to continuously regenerate action potentials at every point along the axon instead of at specific points. Nodes of Ranvier also save energy for the neuron since the channels only need to be present at the nodes and not along the entire axon.

Synaptic Transmission

The synapse or “gap” is the place where information is transmitted from one neuron to another. Synapses usually form between axon terminals and dendritic spines, but this is not universally true. There are also axon-to-axon, dendrite-to-dendrite, and axon-to-cell body synapses. The neuron transmitting the signal is called the presynaptic neuron, and the neuron receiving the signal is called the postsynaptic neuron. Note that these designations are relative to a particular synapse—most neurons are both presynaptic and postsynaptic. There are two types of synapses: chemical and electrical.

Chemical Synapse

When an action potential reaches the axon terminal it depolarizes the membrane and opens voltage-gated Na + channels. Na + ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated Ca 2+ channels to open. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, containing neurotransmitter molecules to fuse with the presynaptic membrane. Synaptic vesicles are shown in [link], which is an image from a scanning electron microscope.

Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes, as illustrated in [link]. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane.

The binding of a specific neurotransmitter causes particular ion channels, in this case ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane, as detailed in [link]. For example, when acetylcholine is released at the synapse between a nerve and muscle (called the neuromuscular junction) by a presynaptic neuron, it causes postsynaptic Na + channels to open. Na + enters the postsynaptic cell and causes the postsynaptic membrane to depolarize. This depolarization is called an excitatory postsynaptic potential (EPSP) and makes the postsynaptic neuron more likely to fire an action potential. Release of neurotransmitter at inhibitory synapses causes inhibitory postsynaptic potentials (IPSPs), a hyperpolarization of the presynaptic membrane. For example, when the neurotransmitter GABA (gamma-aminobutyric acid) is released from a presynaptic neuron, it binds to and opens Cl - channels. Cl - ions enter the cell and hyperpolarizes the membrane, making the neuron less likely to fire an action potential.

Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can “reset” and be ready to receive another signal. This can be accomplished in three ways: the neurotransmitter can diffuse away from the synaptic cleft, it can be degraded by enzymes in the synaptic cleft, or it can be recycled (sometimes called reuptake) by the presynaptic neuron. Several drugs act at this step of neurotransmission. For example, some drugs that are given to Alzheimer’s patients work by inhibiting acetylcholinesterase, the enzyme that degrades acetylcholine. This inhibition of the enzyme essentially increases neurotransmission at synapses that release acetylcholine. Once released, the acetylcholine stays in the cleft and can continually bind and unbind to postsynaptic receptors.

Neurotransmitter Function and Location
Neurotransmitter Example Location
Acetylcholine CNS and/or PNS
Biogenic amine Dopamine, serotonin, norepinephrine CNS and/or PNS
Amino acid Glycine, glutamate, aspartate, gamma aminobutyric acid CNS
Neuropeptide Substance P, endorphins CNS and/or PNS

Electrical Synapse

While electrical synapses are fewer in number than chemical synapses, they are found in all nervous systems and play important and unique roles. The mode of neurotransmission in electrical synapses is quite different from that in chemical synapses. In an electrical synapse, the presynaptic and postsynaptic membranes are very close together and are actually physically connected by channel proteins forming gap junctions. Gap junctions allow current to pass directly from one cell to the next. In addition to the ions that carry this current, other molecules, such as ATP, can diffuse through the large gap junction pores.

There are key differences between chemical and electrical synapses. Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is unidirectional. Signaling in electrical synapses, in contrast, is virtually instantaneous (which is important for synapses involved in key reflexes), and some electrical synapses are bidirectional. Electrical synapses are also more reliable as they are less likely to be blocked, and they are important for synchronizing the electrical activity of a group of neurons. For example, electrical synapses in the thalamus are thought to regulate slow-wave sleep, and disruption of these synapses can cause seizures.

Signal Summation

Sometimes a single EPSP is strong enough to induce an action potential in the postsynaptic neuron, but often multiple presynaptic inputs must create EPSPs around the same time for the postsynaptic neuron to be sufficiently depolarized to fire an action potential. This process is called summation and occurs at the axon hillock, as illustrated in [link]. Additionally, one neuron often has inputs from many presynaptic neurons—some excitatory and some inhibitory—so IPSPs can cancel out EPSPs and vice versa. It is the net change in postsynaptic membrane voltage that determines whether the postsynaptic cell has reached its threshold of excitation needed to fire an action potential. Together, synaptic summation and the threshold for excitation act as a filter so that random “noise” in the system is not transmitted as important information.

Brain-computer interface Amyotrophic lateral sclerosis (ALS, also called Lou Gehrig’s Disease) is a neurological disease characterized by the degeneration of the motor neurons that control voluntary movements. The disease begins with muscle weakening and lack of coordination and eventually destroys the neurons that control speech, breathing, and swallowing in the end, the disease can lead to paralysis. At that point, patients require assistance from machines to be able to breathe and to communicate. Several special technologies have been developed to allow “locked-in” patients to communicate with the rest of the world. One technology, for example, allows patients to type out sentences by twitching their cheek. These sentences can then be read aloud by a computer.

A relatively new line of research for helping paralyzed patients, including those with ALS, to communicate and retain a degree of self-sufficiency is called brain-computer interface (BCI) technology and is illustrated in [link]. This technology sounds like something out of science fiction: it allows paralyzed patients to control a computer using only their thoughts. There are several forms of BCI. Some forms use EEG recordings from electrodes taped onto the skull. These recordings contain information from large populations of neurons that can be decoded by a computer. Other forms of BCI require the implantation of an array of electrodes smaller than a postage stamp in the arm and hand area of the motor cortex. This form of BCI, while more invasive, is very powerful as each electrode can record actual action potentials from one or more neurons. These signals are then sent to a computer, which has been trained to decode the signal and feed it to a tool—such as a cursor on a computer screen. This means that a patient with ALS can use e-mail, read the Internet, and communicate with others by thinking of moving his or her hand or arm (even though the paralyzed patient cannot make that bodily movement). Recent advances have allowed a paralyzed locked-in patient who suffered a stroke 15 years ago to control a robotic arm and even to feed herself coffee using BCI technology.

Despite the amazing advancements in BCI technology, it also has limitations. The technology can require many hours of training and long periods of intense concentration for the patient it can also require brain surgery to implant the devices.

Watch this video in which a paralyzed woman use a brain-controlled robotic arm to bring a drink to her mouth, among other images of brain-computer interface technology in action.

Synaptic Plasticity

Synapses are not static structures. They can be weakened or strengthened. They can be broken, and new synapses can be made. Synaptic plasticity allows for these changes, which are all needed for a functioning nervous system. In fact, synaptic plasticity is the basis of learning and memory. Two processes in particular, long-term potentiation (LTP) and long-term depression (LTD) are important forms of synaptic plasticity that occur in synapses in the hippocampus, a brain region that is involved in storing memories.

Long-term Potentiation (LTP)

Long-term potentiation (LTP) is a persistent strengthening of a synaptic connection. LTP is based on the Hebbian principle: cells that fire together wire together. There are various mechanisms, none fully understood, behind the synaptic strengthening seen with LTP. One known mechanism involves a type of postsynaptic glutamate receptor, called NMDA (N-Methyl-D-aspartate) receptors, shown in [link]. These receptors are normally blocked by magnesium ions however, when the postsynaptic neuron is depolarized by multiple presynaptic inputs in quick succession (either from one neuron or multiple neurons), the magnesium ions are forced out allowing Ca ions to pass into the postsynaptic cell. Next, Ca 2+ ions entering the cell initiate a signaling cascade that causes a different type of glutamate receptor, called AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors, to be inserted into the postsynaptic membrane, since activated AMPA receptors allow positive ions to enter the cell. So, the next time glutamate is released from the presynaptic membrane, it will have a larger excitatory effect (EPSP) on the postsynaptic cell because the binding of glutamate to these AMPA receptors will allow more positive ions into the cell. The insertion of additional AMPA receptors strengthens the synapse and means that the postsynaptic neuron is more likely to fire in response to presynaptic neurotransmitter release. Some drugs of abuse co-opt the LTP pathway, and this synaptic strengthening can lead to addiction.

Long-term Depression (LTD)

Long-term depression (LTD) is essentially the reverse of LTP: it is a long-term weakening of a synaptic connection. One mechanism known to cause LTD also involves AMPA receptors. In this situation, calcium that enters through NMDA receptors initiates a different signaling cascade, which results in the removal of AMPA receptors from the postsynaptic membrane, as illustrated in [link]. The decrease in AMPA receptors in the membrane makes the postsynaptic neuron less responsive to glutamate released from the presynaptic neuron. While it may seem counterintuitive, LTD may be just as important for learning and memory as LTP. The weakening and pruning of unused synapses allows for unimportant connections to be lost and makes the synapses that have undergone LTP that much stronger by comparison.

Section Summary

Neurons have charged membranes because there are different concentrations of ions inside and outside of the cell. Voltage-gated ion channels control the movement of ions into and out of a neuron. When a neuronal membrane is depolarized to at least the threshold of excitation, an action potential is fired. The action potential is then propagated along a myelinated axon to the axon terminals. In a chemical synapse, the action potential causes release of neurotransmitter molecules into the synaptic cleft. Through binding to postsynaptic receptors, the neurotransmitter can cause excitatory or inhibitory postsynaptic potentials by depolarizing or hyperpolarizing, respectively, the postsynaptic membrane. In electrical synapses, the action potential is directly communicated to the postsynaptic cell through gap junctions—large channel proteins that connect the pre-and postsynaptic membranes. Synapses are not static structures and can be strengthened and weakened. Two mechanisms of synaptic plasticity are long-term potentiation and long-term depression.

Art Connections

[link] Potassium channel blockers, such as amiodarone and procainamide, which are used to treat abnormal electrical activity in the heart, called cardiac dysrhythmia, impede the movement of K+ through voltage-gated K+ channels. Which part of the action potential would you expect potassium channels to affect?

[link] Potassium channel blockers slow the repolarization phase, but have no effect on depolarization.

Review Questions

For a neuron to fire an action potential, its membrane must reach ________.

  1. hyperpolarization
  2. the threshold of excitation
  3. the refractory period
  4. inhibitory postsynaptic potential

After an action potential, the opening of additional voltage-gated ________ channels and the inactivation of sodium channels, cause the membrane to return to its resting membrane potential.

What is the term for protein channels that connect two neurons at an electrical synapse?

  1. synaptic vesicles
  2. voltage-gated ion channels
  3. gap junction protein
  4. sodium-potassium exchange pumps

Free Response

How does myelin aid propagation of an action potential along an axon? How do the nodes of Ranvier help this process?

Myelin prevents the leak of current from the axon. Nodes of Ranvier allow the action potential to be regenerated at specific points along the axon. They also save energy for the cell since voltage-gated ion channels and sodium-potassium transporters are not needed along myelinated portions of the axon.

What are the main steps in chemical neurotransmission?

An action potential travels along an axon until it depolarizes the membrane at an axon terminal. Depolarization of the membrane causes voltage-gated Ca 2+ channels to open and Ca 2+ to enter the cell. The intracellular calcium influx causes synaptic vesicles containing neurotransmitter to fuse with the presynaptic membrane. The neurotransmitter diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane. Depending on the specific neurotransmitter and postsynaptic receptor, this action can cause positive (excitatory postsynaptic potential) or negative (inhibitory postsynaptic potential) ions to enter the cell.

Glossary


Watch the video: The Chemical Mind: Crash Course Psychology #3 (September 2022).


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