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How does action potential conduct across a branch in a neuron?

How does action potential conduct across a branch in a neuron?


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As the action potential travel in the dendrite towards the cell body, it will encounter many branches. What happens at the branch? What makes it go to the cell body instead of other dendrite?

Also, as the action potential travel from the axon to its branches, does it go to only one or all terminals? If it goes to only one terminal, how is it decided which terminal it has to go?


Awesome question! Thanks for asking it and giving me the motivation to look back at the literature to increase my own understanding!

I do want to point out one issue of semantics before starting. Just to avoid confusion, I'm going to follow the example of some of the well-known experts in this field and distinguish dendritic spikes from action potentials. The main difference is that a voltage spike in a dendrite or dendritic spine will experience attenuation (essentially a weakening of the spike) as it propagates toward the cell body, and it is distinct from the all-or-none voltage response of an action potential. It is generally accepted that action potentials are initiated in the axon (hillock) because that is where dendritic and somatic spikes will ultimately sum to fire the all-or-none voltage response. I just want to clarify what I mean by dendritic spike when I use it during this explanation.

What happens at the branch? So, to answer your first question, you're absolutely correct that when a dendritic spike occurs, that spike will encounter multiple branch points along the dendrite as it proceeds toward the soma. When a spike propagates to a branch point, the properties of the branches determine what happen to the spike. One important property is referred to as the geometric ratio (GR). This property was described Goldstein and Rall in 1974 (manuscript here for review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1334570/) and the gist of the equation is that spike attenuation is dependent upon the diameter of the branch the spike is coming from and the branch the spike is going into. The concept behind this is called impedance mismatch, but that's complex and I won't get into it. Just know that spike propagation is favorable from a large to a small branch, but is not favorable from a small branch to a large branch. If you wish to read more about this concept, I'd recommend the Goldstein and Rall paper referenced earlier and chapter 14 of the textbook "Dendrites" by Spruston, Stuart, and Hausser.

Additionally, the presence of leak or voltage-gated channels in that branch can determine how well the spike will propagate or how much attenuation will occur. This is an easier concept to grasp because the idea is essentially that more channels open when the spike passes through that branch, the more charge leaks across the membrane and causes attenuation of the spike.

All questions regarding preference of flow To sort of attempt to answer all your other questions at once, nothing really forces the spike toward the soma or a specific axon terminal. There are dynamic changes in membrane potential that may prevent spike propagation down one branch or action potential propagation in a certain direction (like how action potentials aren't thought of as propagating from the axon to the soma because of the hyperpolarization and long inactivation of sodium channels at the area that just fired, preventing what is called backpropagation at that particular time).

I think a little reading on neuronal cable theory might be of some help with this question too. This link is to a PDF that gives a pretty brief explanation of this concept https://nanohub.org/resources/20112/download/Lecture1_Passive_Conduction.pdf. This is a pretty math-heavy field, so beware if math isn't your favorite subject!


Neuron Doctrine

The neuron doctrine was based on a series of observations that culminated in the concept of the neuron as the single independent unit in the nervous system. It is clear from the work described above that several important investigators laid important groundwork for the neuron doctrine. Jan Purkinje, Gabriel Valentin, Robert Remak, and Robert Bentley Todd made important contributions from 1836–45. However, none of these scientists directly formulated the neuron doctrine. Nearly half a century later, Wilhelm His, Fridtjof Nansen, and Auguste Forel independently published documents anticipating the neuron doctrine within a span of 1 year (1886–87). Interestingly, these three investigators inferred similar conclusions despite different methodologies such as retrograde degeneration, development of nerve cells, and marine biology. Thus, while Kölliker gets credit for championing Cajal’s work after 1889 and Waldeyer published the neuron doctrine in 1891, it is clear that in the development of neurohistology in the 19th century, these previous scientists played a crucial part.


What happens when the action potential reaches the sarcoplasmic reticulum?

The structures responsible for coupling this excitation to contraction are the T tubules and sarcoplasmic reticulum (SR). As an action potential travels along the T tubule, the nearby terminal cisternae open their voltage-dependent calcium release channels, allowing Ca 2 + to diffuse into the sarcoplasm.

Additionally, how does action potential result in muscle contraction? A Muscle Contraction Is Triggered When an Action Potential Travels Along the Nerves to the Muscles. Muscle contraction begins when the nervous system generates a signal. When the nervous system signal reaches the neuromuscular junction a chemical message is released by the motor neuron.

Moreover, what happens when an action potential reaches a neuromuscular junction?

When an action potential reaches a neuromuscular junction, it causes acetylcholine to be released into this synapse. The acetylcholine binds to the nicotinic receptors concentrated on the motor end plate, a specialized area of the muscle fibre's post-synaptic membrane.


The Frontal Lobes

Randolph F. Helfrich , Robert T. Knight , in Handbook of Clinical Neurology , 2019

Revisiting the Neuron Doctrine

The neuron doctrine is one of the foundations of modern neuroscience and states that the single neuron constitutes the structural and functional unit of the CNS ( Golgi, 1906 ). The doctrine was first conceptualized by Golgi in the 19th century and later received a multitude of experimental support, including the seminal work of Hubel and Wiesel (1962) and Barlow (1953) , who suggested that individual neurons are highly selective and are only tuned to very specific features. While early recordings were only made from one or a few neurons at a time, modern neuroscience enabled scientists to record from tens to hundreds of neurons simultaneously. One intriguing observation was that a surprising number of randomly sampled neurons encoded task-relevant aspects. For example, several microelectrode studies recording from prefrontal cortex suggested that around 90% of the recorded cells are active during one or more task epochs ( Warden and Miller, 2007 Watanabe and Funahashi, 2007 Barak et al., 2010 Stokes et al., 2013 ). Were these groups simply fortunate to have sampled from highly task-active populations, or does this population activity actually support cognitive processing?

In a theoretically different account from Golgi or Barlow, Hebb and others suggested that neuronal assemblies might constitute the functional unit of the nervous system ( Hebb, 1949 ). This notion has received substantial experimental support in recent years by taking full advantage of large-scale recordings and novel methods to analyze network interactions and population-based information coding ( Quian Quiroga and Panzeri, 2009 Yuste, 2015 Eichenbaum, 2017 ). Regarding prefrontal cortex, it has repeatedly been demonstrated that most randomly sampled neurons are task-active and that the same group of neurons exhibits highly context-dependent alterations in their firing rates ( Warden and Miller, 2007 Meyers et al., 2008 Mante et al., 2013 Rigotti et al., 2013 Stokes et al., 2013 ). While information about all task-relevant aspects could be decoded from the population at all times during the task, individual neurons showed complex patterns, which could not be explained by a linear summation of two task-relevant variables ( Meyers et al., 2008 Barak et al., 2010 Rigotti et al., 2013 ). These findings strongly supported the hypothesis that cell assemblies are the functional unit of the brain and code information in high dimensional neuronal representations ( Fusi et al., 2016 ). Similar findings have been reported in the inferotemporal cortex of macaques or the hippocampus in rodents ( Eichenbaum, 2017 ). Despite substantial evidence for population-based coding in rodents and primates, human single-unit research is still largely focused on single neurons and how they respond to one specific task-aspect ( Fried et al., 2014 Kamiński et al., 2017 Kornblith et al., 2017 Mormann et al., 2017 ).


How does action potential conduct across a branch in a neuron? - Biology

What opens first in response to a threshold stimulus?

Voltage-gated Na + channels

What characterizes depolarization, the first phase of the action potential?

The membrane potential changes from a negative value to a positive value.

What characterizes repolarization, the second phase of the action potential?

Once the membrane depolarizes to a peak value of +30 mV, it repolarizes to its negative resting value of -70 mV.

What event triggers the generation of an action potential?

The membrane potential must depolarize from the resting voltage of -70 mV to a threshold value of -55 mV.

What is the first change to occur in response to a threshold stimulus?

Voltage-gated Na + channels change shape, and their activation gates open.

What type of conduction takes place in unmyelinated axons?

An action potential is self-regenerating because __________.

depolarizing currents established by the influx of Na + ‎ flow down the axon and trigger an action potential at the next segment

Why does regeneration of the action potential occur in one direction, rather than in two directions?

The inactivation gates of voltage-gated Na + ‎ channels close in the node, or segment, that has just fired an action potential.

What is the function of the myelin sheath?

The myelin sheath increases the speed of action potential conduction from the initial segment to the axon terminals.

What changes occur to voltage-gated Na + and K + channels at the peak of depolarization?

Inactivation gates of voltage-gated Na + ‎ channels close, while activation gates of voltage-gated K + ‎ channels open.

In which type of axon will velocity of action potential conduction be the fastest?

Myelinated axons with the largest diameter

Ions are unequally distributed across the plasma membrane of all cells. This ion distribution creates an electrical potential difference across the membrane. What is the name given to this potential difference?

Resting membrane potential (RMP)

Sodium and potassium ions can diffuse across the plasma membranes of all cells because of the presence of what type of channel?

On average, the resting membrane potential is -70 mV. What does the sign and magnitude of this value tell you?

The inside surface of the plasma membrane is much more negatively charged than the outside surface.

The plasma membrane is much more permeable to K + than to Na + . Why?

There are many more K + leak channels than Na + leak channels in the plasma membrane.

The resting membrane potential depends on two factors that influence the magnitude and direction of Na + and K + diffusion across the plasma membrane. Identify these two factors.


Shared Flashcard Set

The difference in voltage charge between the inside and outside of the membrane. Such a membrane is referred to as polarized.

in the plasma membrane allow ions to flow across the membrane

What are the 2 types of ion channels?

Passive: nongated, allow leakage of ions both ways, these are always open.

Ligand: channels open when the appropriate neurotransmitter binds, (sodium/pot. gates).

Voltage gated: channels respond to changes in the membrane potential

The process of producing action potentials

Pot. gates open and membrane becomes highly permeable to K+ ions.

-Inside looses pos ions to outside, and outside of membrane gains pos. charge.

Membrane will repspond to another stimulus, but the stimulus threshold is higher than for a resting neuron, corresponding to period of repolarization.

requires a stronger stimulus to complete restoration of the original resting potential.

must be a threshold stimulus if it will trigger depolarization. A stronger stimulus will make no difference, propagation will occur if threshold.

In myelin encased fibers, myelin acts as an insulator, and does not conduct an action potential. Depolarization jumps from node of Ranvier to node.Since the whole nueron does not have to depolarize, energy is conserved.

The action potential is actually carried by local currents.

greatest diameter nerve fiber, always meylinated, have strong ionic pumps and short refractory periods. Speeds up to 130 m/sec Always exhibit saltatatioin. Found where speed is important

1. Afferents connecting sensory receptors that warn the body of danger to the CNS

2. Efferents that do something about it.

medium diameter nerve fiber, myelinated, long refractory perids. Speed around .5 m/sec

1. most of visceral sensory and motor fibers

nuerons do not actually make contact with one another, the impulse is transmitted from the azon ending of one to the dendrite ending of another.

Physical Gap=synaptic cleft.

Pre and postsynaptic clefts

neuron transmitting the impulse

nueron receiving the impulse

*presynaptic nueron secretes nuerotransmitter chemical sucstance diffuses across synaptic cleft where it has an effect on post..dendrite.

If presynaptic nueron is excitatory it secretes a chemical neurotransmitter that can depolarize the dendrite ending of postsynaptic. That neuron cont. to transmit that impulse.

Depolarization is called: excitatory postsynaptic potential(EPSP).

releases an inhibitory neurotransmitter chemical. This chem. causes an increase in the resting polarization of the postsynaptic neuron, thus increasing the threshold stimulus level.

There is no true physical gap, but direcct protein channels connecting the cytosol of the two neurons, resulting in electrical coupling. Provides for synchronization of neuron activity, because the transmission from neuron to neuron is so rapid. Found in regions of the brain controlling rapid stereotyped movements, eg eye movements.

Refers only to receptors. Receptors do not appear to have refractory periods. All or none principle does not apply, and repeated stimuli can increase depolarization, and the strength of stimulus transmitted to the sensory neuron dendrite ending.

Action potentials are not produced in short dendritess or on the membrane of the perikaryon.Local electrical currents set in cytosol of the dendrite or neuron cell body.

- After threshold stimulation at dendrite endings, local currents in cytosol carry the message through the dendrite to the cell body. At axon hillock the local currents, if threshold will trigger an action potential, which then runs the length of the axon as described. Not all or none, depends on strength.


How does myelination speed up action potential?

Myelin can greatly increase the speed of electrical impulses in neurons because it insulates the axon and assembles voltage-gated sodium channel clusters at discrete nodes along its length. Myelin damage causes several neurological diseases, such as multiple sclerosis.

Furthermore, what will most affect the speed of an action potential? There are several factors affecting the rate and speed of an action potential: Diameter of the axon - the larger the diameter of an axon increases the rate and speed of conductance as there is less leakage of ions. 3. Temperature - The higher the temperature the faster the conductance.

Besides, how does myelin sheath speed up transmission?

Most nerve fibres are surrounded by an insulating, fatty sheath called myelin, which acts to speed up impulses. The myelin sheath contains periodic breaks called nodes of Ranvier. By jumping from node to node, the impulse can travel much more quickly than if it had to travel along the entire length of the nerve fibre.

How do nodes of Ranvier speed up conduction?

Nodes of Ranvier. Nodes of Ranvier are microscopic gaps found within myelinated axons. Their function is to speed up propagation of action potentials along the axon via saltatory conduction. The Nodes of Ranvier are the gaps between the myelin insulation of Schwann cells which insulate the axon of neuron.


Supporting information

S1 Fig. Correlation of aEPSC amplitude and waveform between convergent inputs is not associated with changes in series resistance.

Related to Fig 2. (A,B) Rise time and decay time constant values are correlated between the two inputs (rise time: R 2 = 0.82, p = 0.0018, decay time constant: R 2 = 0.77, p = 0.0042). Linear regression line and 95% confidence interval (gray shaded area) are shown. (C–E) aEPSC amplitude (C), rise-time values (D), and decay time constant (E) are not impacted by the differences in series resistance over the range measured during the triple recordings. Underlying data can be found in S1 Data. aEPSC, asynchronous EPSC EPSC, excitatory postsynaptic current.

S2 Fig. SEP-GluA1 and SEP-GluA2 fluorescence signal intensity as a proxy for postsynaptic strengths.

Related to Fig 2. (A) Example traces of mEPSC recordings (left) and amplitude histogram of mEPSCs normalized to the median (right) and fitted by the lognormal function (black curve, R 2 = 0.99). (B–C) Representative images of dendrites from neurons expressing SEP-GluA1 (B, left) or SEP-GluA2 (C, left) and corresponding histograms of normalized integrated intensity of SEP-GluA fluorescence puncta (right) fitted by the lognormal function (black curves: SEP-GluA1, R 2 = 0.93 SEP-GluA2, R 2 = 0.98) (D) Cumulative distributions of normalized mEPSC amplitudes and normalized signal intensity of individual SEP-GluA1 and SEP-GluA2 fluorescence puncta. Underlying data can be found in S1 Data. GluA, AMPA receptor subunit EPSC, excitatory postsynaptic current mEPSC, miniature EPSC SEP, superecliptic pHluorin.

S3 Fig. Changes in aEPSC frequency are not correlated between stimulated and nonstimulated inputs.

Related to Fig 4. Comparison of the extent change in aEPSC frequency before and after the application of CS (1 Hz, 3 min) at stimulated versus nonstimulated synapses. Underlying data can be found in S1 Data. aEPSC, asynchronous EPSC CS, conditioning stimulation EPSC, excitatory postsynaptic current.

S4 Fig. Uniform downscaling of postsynaptic AMPA receptors is calcium dependent.

Related to Fig 4. (A) Representative traces showing mEPSC events before and after the CS recorded from a control neuron (black) or a neuron filled with 10 mM BAPTA (blue). (B) Plots of mEPSC amplitude before versus after the CS for control (left) and BAPTA-filled (right) neurons. Underlying data can be found in S1 Data. AMPA, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid BAPTA, 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid CS, conditioning stimulation EPSC, excitatory postsynaptic current mEPSC, miniature EPSC.

S5 Fig. Relationship between EPSC amplitude, PPR, and SEP-GluA2 signal intensity changes.

Related to Fig 5. Individual recordings showing that LTD of EPSC amplitude (left column) (A,B) is associated with a decrease in SEP-GluA2 fluorescence intensity (right column), whereas LTP of EPSC amplitude (C) is associated with a decrease in PPR (middle column). Opposite changes in PPR and SEP-GluA2 fluorescence intensity (D) are associated with no net change in EPSC amplitude. (E, F) Comparison of EPSC amplitude change versus PPR change (E) and SEP-GluA2 fluorescence change (F). Underlying data can be found in S1 Data. EPSC, excitatory postsynaptic current GluA, AMPA receptor subunit LTD, long-term depression LTP, long-term potentiation PPR, paired-pulse ratio SEP, superecliptic pHluorin.

S6 Fig. Electrophysiological properties of unitary EPSCs at CA3–CA3 recurrent connections.

Related to Fig 6. (A) Summary of EPSC amplitude, PPR, peak EPSC amplitude excluding failures, rise time, decay time constant, and latency at the time of transfection through whole-cell recordings in CA3 neurons. (B) Left: plot showing average maximal EPSC values (peak EPSC amplitude excluding failures) during the first and second patch-clamp recording sessions (n = 10 CA3–CA3 pairs, Wilcoxon matched pairs signed-rank test). Right three panels: the transfection procedure does not produce consistent changes in rise time, decay time constant, and latency of EPSCs (n = 10 pairs, Wilcoxon matched pairs signed-rank test). Underlying data can be found in S1 Data. CA3, Cornu Ammonis 3 EPSC, excitatory postsynaptic current PPR, paired-pulse ratio.

S7 Fig. LTD induction is associated with a consistent change in PPR, whereas LTP induction is not accompanied by consistent changes in PPR nor sEPSC amplitude at unitary CA3 recurrent connections.

Related to Fig 7. (A) Comparison of the PPR change versus initial PPR (PPR0) for LTD experiments in absence or presence of D-AP5 (LTD [without D-AP5]: R 2 = 0.57, p = 0.0115). (B) Comparison of the PPR change versus EPSC amplitude change for LTD experiments in absence of D-AP5 (R 2 = 0.77, p = 0.0042). Linear regression and 95% confidence interval (gray) are shown. (C) Left, representative traces showing synaptic currents in the postsynaptic CA3 neuron evoked by a pair of APs triggered in the presynaptic CA3 neuron (2–3 nA, 50-ms interval), before and 20 min after LTP induction. Right, summary of the time course of EPSC amplitude (n = 8 cell pairs). The gray shaded box represents the LTP induction. (D) Left, plot showing PPR values before and after LTP induction (n = 10 cell pairs, Wilcoxon matched pairs signed-rank test). Right, comparison of the PPR change versus initial PPR (PPR0) (R 2 = 0.77, p = 0.0096). Linear regression and 95% confidence interval (gray) are shown. (E) Left, example traces of sEPSCs recorded from a postsynaptic CA3 neuron before (Pre-stim) and after (Post-stim) LTP induction. Middle, plot showing sEPSC amplitude before and after LTP induction (untreated: n = 7 cell pairs, Wilcoxon matched pairs signed-rank test). Right, cumulative distributions of sEPSC amplitudes before and after LTP induction. Underlying data can be found in S1 Data. AP, action potential CA3, Cornu Ammonis 3 D-AP5, D-2-amino-5-phosphonovalerate EPSC, excitatory postsynaptic current LTD, long-term depression LTP, long-term potentiation PPR, paired-pulse ratio sEPSC, spontaneous EPSC stim, stimulation.

S1 Video. Sequential unloading of the FM dye for the two inputs.

Related to Fig 1. Images were obtained every 1 sec. After a baseline of 5 consecutive planes, 600 APs were delivered in the presynaptic cells at 10 Hz, thus triggering the loss of FM fluorescence at boutons corresponding to input 1 (left) or input 2 (right). AP, action potential.

S2 Video. Imaging synaptic vesicle dynamics along the axon using VGLUT1-pH.

Related to Fig 3. Time-lapse images were obtained before (baseline) or after (20 min) delivering the CS (180 APs at 1 Hz). Consecutive planes were obtained every 1 sec. After 15 consecutive planes, 40 APs (left and middle videos) or 600 APs (right video) were delivered at 20 Hz to mobilize the readily releasable or the total pool of presynaptic vesicles. AP, action potential CS, conditioning stimulation pH, pHluorin VGLUT1, vesicular glutamate transporter 1.

S1 Data. Data underlying figures and Supporting Information figures.


What Are the Stages of Action Potential? (with pictures)

Usually, the stages of action potential are summarized in five steps, the first two of which are the rising and the overshoot phases. The three latter steps would be the falling, the undershoot, and the recovery phases. Some sources, whether physiologists or textbooks, sometimes include an initial resting phase before the rising phase when enumerating the stages of action potential, probably to illustrate the status quo of the neuron before action potential begins.

Action potential is an event that happens between neurons in order to send messages from the brain to the different parts of the body, whether for voluntary or involuntary actions. In the simplest sense, action potential can be described as short electrical pulses that are created inside the cell body of the neuron. These pulses are caused by the exchange of positive and negative ions when potassium and sodium ions exit and enter the cell body. The “spark” from the exchange, then, travels down the axon, or the stem-like part of the neuron, towards another neuron, and the cycle goes on. In many cases, when the brain needs to “send” many “messages,” action potential can occur in a series called a “spike train.”

A neuron usually contains positively-charged potassium ions (+K), while the sodium ions (+Na), also positively charged, reside in the periphery of the neurons. During the resting phase, the neuron is inactive and contains an “electric potential” of -7- millivolts (mV). This negative charge is maintained by the neuron’s sodium-potassium pump that brings in two +K ions in while carrying three +Na ions out of the membrane. When the brain “sends” a message, a significant amount of +Na ions enter the neuron, and the rising and overshoot stages of action potential occur. In these stages, the neuron experiences “depolarization” and becomes positively charged due to the entrance of +Na ions.

The neuron reaches the overshoot stage when its positive charge exceeds 0 mV. The more positively charged the neuron becomes, the more sodium channels begin to open, and more +Na ions rush in, making it harder for the potassium-sodium pump to carry the ions out. To let out positive ions, the potassium channels will open as soon as the sodium channels close, and the falling and undershoot stages of action potential take place. In these phases, the neuron experiences “repolarization” and becomes more negatively charged, so much so that the charge will hit below -70 mV in the undershoot stages, also known as “hyperpolarization.”

After both potassium and sodium channels close, the sodium-potassium pump functions more effectively in bringing in +K ions and carrying out +Na ions. In this final recovery stage, the neuron returns to its normal state of -7 mV, until another episode of action potential occurs. It is very interesting to know that all these stages of action potential occur in as short as two milliseconds.


How does action potential conduct across a branch in a neuron? - Biology

Unmyelinated fibers conduct impulses faster than myelinated fibers.

In multiple sclerosis, the cells that are the target of an autoimmune attack are the _________.

neurons
muscle cells
Schwann cells
oligodendrocytes

Local anesthetics block voltage-gated Na+ channels, but they do not block mechanically gated ion channels. Sensory receptors for touch (and pressure) respond to physical deformation of the receptors, resulting in the opening of specific mechanically gated ion channels. Why does injection of a local anesthetic into a finger still cause a loss of the sensation of touch from the finger?

The local anesthetic prevents Na+ from causing the initial depolarization of this sensory receptor.
The local anesthetic prevents any type of repolarization of this sensory receptor.
Touch stimulation of this sensory receptor requires that there be a simultaneous opening of voltage-gated Na+ channels and mechanically gated ion channels.
Touch stimulation of this sensory receptor will open the mechanically gated ion channels, but action potentials are still not initiated because propagation of an action potential requires the opening of voltage-gated Na+ channels

Touch stimulation of this sensory receptor will open the mechanically gated ion channels, but action potentials are still not initiated because propagation of an action potential requires the opening of voltage-gated Na+ channels



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