Neurophysiology: Neurons And ANS Flashcards

1
Q

who developed the NIssl stain

A

German neurologist Franz Nissl

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2
Q

when was the nissl stain eveloped

A

late 19th century

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3
Q

what did the nissl stain show

A

The stain was a basic dye. it stained clumps of material surrounding the nuclei- called Nissl bodies

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4
Q

who developed the golgi stain

A

Camillo golgi

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5
Q

when was the golgi stain developed

A

1873

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6
Q

the golgi stain was developed from»>

A

silver reagents used in photography

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7
Q

what did the golgi stain show

A

Golgi stain shows neurons have at least 2 distinguishable parts: a central region that contains the cell nucleus and numerous thin tubes that radiate away from the central region called neurites

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8
Q

what did golgi propound from what he saw in his stain

A

He concluded that the neurites of different cells are fused together to form a continuous reticulum, or network, similar to the arteries and veins of the circulatory system.

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9
Q

whose research brought about the neuron doctrine

A

Santiago Ramon Y. Cajal

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10
Q

when was the neuron doctrine brought

A

1939

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11
Q

what was Cajal’s observation on the neuron

A

cajal said that the neurons were individual units (they existed as discrete entities). That is, neurons communicate by contact not continuity

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12
Q

when did golgi and cajal win the noble prize

A

1906

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13
Q

when was the neuron doctrine proved, and why?

A

The Neuron Doctrine was not proved until the development of in the 1950s. Neurons primarily communicate with one another at contacts called synapses (the exceptions being gap junctions).

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14
Q

the brains are composed of 2 cell types

A

-Neurons
-Glial cells

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15
Q

what are the glial cells

A

They outnumber the neurons 10:1. They insulate, support, and nourish injuries. They also remove degeneration debris

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16
Q

what are the glial cells of the CNS

A

-Astrocytes
-Oligodendrocytes
-Ependymal cells
-Microglia

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17
Q

what are the glial cells of the PNS

A

-Schwann cells
-satellite cells

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18
Q

what are the astrocytes

A

They are glial cells in the CNS that:
-maintain the blood-brain barrier
-provide structural support
-regulate ions
-regulate nutrients and dissolved gas concentrations
-They absorb and recycle neurotransmitter from scar tissue

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19
Q

what are the oligodendrocytes

A

They myelinate the axons of the CNS and provide structural framework

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20
Q

what are the ependymal cells

A

they line the ventricles of the brain and the central spinal canal. They participate in the production regulation and monitoring of CSF

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21
Q

what are the microglial cells

A

Remove cell debris, wastes and pathogens by phagocytosis

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22
Q

what are the satellite cells

A

they surround the cell bodies in the ganglia and regulate, the O2, CO2, nutrients and neurotransmitter levels around those neurons in the ganglia

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23
Q

what are the schwann cells

A

They surround all the axons in the PNS, myelinate them and take part in the process of repair after injury

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24
Q

Draw a neuron

A

check the book.

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25
Q

what are the differences between the neuron and the common cell

A

-Nissl bodies: they are the organelles containing the ribosomes.
-Mitochondria: they are numerous in neurons because energy is required to maintain the resting membrane potential
-There is a neuronal membrane
-Cytoskeleton are; microtubules, neurofilaments, microfilaments.
-Dendrites
-Axon

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26
Q

comment on the microtubules of a neuron

A

they are 20nm, made of a polymer protein called tubulin

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27
Q

comment on neurofilaments

A

they are 10nm, made of glial fibrillary acidic protein

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28
Q

comment on microfilaments

A

they are 5nm, made of protein actin

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29
Q

comment on the dendrites

A

👉The dendrite is the branched process of neurons and it is
branched repeatedly.
👉Dendrite may be present or absent. If present, it may be one or many in number.
👉Dendrite has Nissl granules and neurofibrils.
👉Dendrite transmits impulses towards the nerve cell
body(the receiving portion).
👉Usually, the dendrite is shorter than axon.

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30
Q

comment on the axons

A

👉It conducts impulses away from the cell body
👉It has no nissl bodies
👉it joins the soma at a cone shaped elevation- the axonal hillock
👉The first part of the axon is the initial segment
👉Most electrical impulses arise from the junction of the axonal hillock and the initial segment, it is called the TRIGGER ZONE

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31
Q

comment on alzheimers disease

A

👉 Alzheimer’s disease is a progressive neurodegenerative
disease.
👉It is due to degeneration, loss of function and
death of neurons in many parts of brain, particularly:
-cerebral hemispheres,
-hippocampus and
-pons.
👉There is a reduction in the synthesis of most of the
neurotransmitters, especially acetylcholine.
👉Synthesis of acetylcholine decreases due to lack of enzyme
choline acetyltransferase.
👉Norepinephrine synthesis decreases because of degeneration of locus ceruleus.
👉It results in memory loss, such that the patient may not even remember family members
👉Over time, cognitive functions are lost, and in the final stages of the disease the patient can no longer communicate
👉The diagnosis is made through the patients declining cognitive abilities in mental examinations (dementia)

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32
Q

who first described Alzheimer’s diseases

A

It was first described in 1907 by the German physician A. Alzheimer.

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33
Q

what year was alzheimer’s discovered

A

1907

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34
Q

by 2030, how many people are projected to have alzheimer’s

A

14million

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35
Q

why is norepinephrine production affected in alzheimer’s disease

A

locus ceruleus degenration

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36
Q

why is acetylcholine production affected in alzheimer’s disease

A

the enzyme choline acetyltransferase

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37
Q

acording to the number of dendrites and axons, what are te classes of neurons

A

👉Unipolar
👉Bipolar
👉multipolar
👉pseudounipolar

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38
Q

draw the 4 types of neurons (according to number of dendrites/axons)

A

check your booklet

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39
Q

comment on unipolar neurons

A

👉These are neurons with only one pole.
👉from that single pole, both the dendrite and axon arise
👉This type of neuron is only present in the embryonic stage of humans.

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40
Q

are there unipolar neurons in human

A

no

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41
Q

what neurons are in human, instead of unipolar neurons

A

pseudounipolar neuron

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42
Q

what is a pseudounipolar neuron

A

👉A pseudounipolar neuron is a type of sensory neuron found in the dorsal root ganglia of the spinal cord.
👉They have a single process that splits into 2 branches, but unlike unipolar neurons, the single process is actually a fusion of two processes that arise from opposite sides of the cell body, which is at one side.
👉One branch carries sensory information from the periphery to the central nervous system, while the other branch extends to the periphery and acts as an axon.

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43
Q

where is the pseudounipolar neuron seen

A

dorsal root ganglia of the spinal cord

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44
Q

comment on the bipolar neuron

A

👉they are neurons with 2 poles,
👉the dendrite arises from one pole, the axon from the other pole
👉they are the retina, inner ear and olfactory bulb

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45
Q

comment on multipolar neurons

A

👉they have numerous poles,
👉one gives rise to the axon, many others give rise to the dendrites

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46
Q

based on function, what are the classifications of neurons

A

👉Afferent (sensory) neurons
👉Efferent (motor) neurons
👉Interneurons

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47
Q

comment on interneurons

A

👉They function as integrators and signal changers.
👉They act to integrate groups of sensory and afferent neurons into reflex circuits
👉They lie entirely in the CNS and account for 90% of all neurons
👉The number of interneurons between specific afferent and efferent neurons varies according to the complexity of the action they control.
👉Interneurons {millions} are involved in memories such as when you smell a perfume or song and it evokes memories

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48
Q

comment on efferent (motor neurons)

A

👉They transmit information out of the CNS to effector cells, particularly muscles, glands, neurons and other cells
👉Their Cell bodies have multiple dendrites and
👉a small segment of the axon is in the CNS but most of the axon is in the PNS
👉Generally, each motor neuron has a long axon and short dendrites.

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49
Q

comment on the afferent (sensory neurons)

A

👉They transmit information into the CNS from receptors at their peripheral endings
👉They have single processes from the cell body split into a long peripheral process (axon) that is in the PNS and a short central process that enters the CNS
👉Generally, each sensory neuron has a short axon and long dendrites

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50
Q

draw a diagram to show the classification of neurons (according to function)

A

check the book

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51
Q

what is voltage

A

It is the measure of potential energy between two points generated by a charge separation

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52
Q

what is membrane potential

A

It is the voltage difference between the inside and outside of a cell

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53
Q

what is resting membrane potential

A

👉it is the potential difference recorded across the cell membrane at rest.
➡️Causes:
👉80% caused by selective permeability of the cell membrane to K+. The K+ diffuses out of the cell & Na+ diffuses into the cell according to the concentration gradient. The K+ permeability is 50-75 folds more than Na+
👉20% is caused by the Na+/K+ pump. It is an active process that needs energy taken from ATP. This is very important to maintain the concentration gradient across the cell membrane

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54
Q

what are the causes of resting membrane potential

A

👉80% caused by selective permeability of the cell membrane to K+. The K+ diffuses out of the cell & Na+ diffuses into the cell according to the concentration gradient. The K+ permeability is 50-75 folds more than Na+

👉20% is caused by the Na+/K+ pump. It is an active process that needs energy taken from ATP. This is very important to maintain the concentration gradient across the cell membrane

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55
Q

80% of resting membrane potential is attributed to:

A

👉80% caused by selective permeability of the cell membrane to K+

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56
Q

20% to resting membrane potential is attributed to:

A

Na+/K+ pump

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57
Q

what keeps Na/K concentrations different across the cell

A

the sodium/potassium pump which is dependent on ATP

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58
Q

when the electrode is outside the cell, the record reference potential is recorded as

A

0mV

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59
Q

when the electrode is in the cell, the record reference potential is

A

it drops to -70mV (resting membrane potential)

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60
Q

what is equilibrium potential

A

it is the membrane potential that exactly opposes the concentration of the ion that the cell is permeable to.
Eion = ENa, ECl, EK .

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61
Q

so, for instance, what would potassium equilibrium potential be defined as

A

Potassium equilibrium potential (Ek) is the membrane potential at which the chemical and electrical gradients are equal in magnitude and opposite in direction, resulting in no net movement of K+

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62
Q

equilibrium is calculated using:

A

👉Nernst equation
👉Goldman equation

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63
Q

what is the equilibrium potential of sodium

A

+60mV

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64
Q

what is the equilibrium potential of potassium

A

-90mV

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65
Q

What ion drives resting membrane potential

A

Potassium (K+)

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66
Q

What is Nernst equation used for

A

👉Use to calculate the membrane potential of an ion at equilibrium
👉Represents the electrical potential necessary to maintain a certain concentration gradient of a permeable solute

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67
Q

state the nernst equation

A

E = (61/z) * log([ion]outside/[ion]inside)

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68
Q

what does the value of 61 in nernst equation mean

A

The value 61 in the Nernst equation refers to the constant (RT/zF) at room temperature (25°C

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69
Q

what is Goldman’s equation used for

A

👉Used to calculate overall membrane potential when multiple ions are involved.

👉Incorporates permeability of each ion.

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70
Q

state the goldmans equation

A

Em = (60mV * log((P[K+]o + P[Na+]o + P[Cl-]i) / (P[K+]i + P[Na+]i + P[Cl-]o))

-Em= membrane potential

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71
Q

What would happen to the resting membrane potential of a cell poisoned with a substance, that is an inhibitor of the Na –K – ATPase

A

👉Inhibition of the Na-K ATPase pump would lead to an accumulation of sodium ions inside the cell and a depletion of potassium ions inside the cell.
👉This would cause the inside of the cell to become more positively charged, leading to depolarization of the membrane potential.
👉The degree of depolarization would depend on the severity and duration of the inhibition, as well as the initial state of the resting membrane potential.

👉Depolarization of the membrane potential can have a range of effects on cellular function, including:
- changes in ion channel activity,
- alterations in synaptic transmission, and
- changes in gene expression.
- In severe cases, depolarization can lead to cellular dysfunction or death.

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72
Q

comment on the concept of excitability

A

👉All living cells have a resting membrane potential due to the presence of ion pumps and leak channels in the cell membrane.
👉This difference in charge can be measured as potential energy- measured in millivolts.
👉In addition, however, some cells have another group of ion channels that can be gated (opened or closed) under certain conditions. Such channels give a cell the ability to produce electrical signals that can transmit information between different regions of the membrane.
👉This property is known as Excitability and such membranes are called excitable membranes

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73
Q

what cells exhibit excitability

A

👉all neirons
👉muscle cells
👉some endocrine cells (e.g beta cells of the islets of langerhans)
👉some immune cells
👉some reproductive cells

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74
Q

what are the 2 forms that excitability occurs

A

👉action potential
👉graded potential

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75
Q

give 10 differences between graded potential and action potential

A

Action potentials and graded potentials are both types of electrical signals that occur in neurons, but they have several key differences. Here are 10 differences between action potentials and graded potentials:

  1. Definition: An action potential is an all-or-nothing electrical signal that is generated when a neuron depolarizes to a certain threshold. A graded potential is a small, variable change in membrane potential that can be either depolarizing or hyperpolarizing.
  2. Magnitude: Action potentials are typically the same size and duration regardless of the strength of the stimulus that triggered them. Graded potentials vary in magnitude depending on the strength of the stimulus.
  3. Threshold: Action potentials have a specific threshold that must be reached in order to be generated. Graded potentials do not have a specific threshold and can be generated by any strength of stimulus.
  4. Location: Action potentials are generated at the axon hillock and propagate down the axon of the neuron. Graded potentials can occur anywhere on the neuron, including the dendrites, cell body, and axon.
  5. Duration: Action potentials are very brief, typically lasting only a few milliseconds. Graded potentials can last for varying lengths of time depending on the strength of the stimulus.
  6. Direction: Action potentials always travel in one direction, from the cell body down the axon to the axon terminal. Graded potentials can travel in any direction, depending on the location of the stimulus.
  7. Amplitude: Action potentials have a fixed amplitude that does not vary with distance from the cell body. Graded potentials have a variable amplitude that decreases with distance from the site of stimulation.
  8. Summation: Action potentials do not summate or add together. Graded potentials can summate, meaning that multiple graded potentials occurring close together in time can add together to create a larger signal.
  9. Refractory period: Action potentials have a refractory period during which they cannot be generated again. Graded potentials do not have a refractory period and can be generated repeatedly.
  10. Role: Action potentials are used for long-distance communication within the nervous system, allowing neurons to transmit signals over long distances. Graded potentials are used for short-distance communication within the neuron, allowing neurons to integrate information and make decisions about whether or not to generate an action potential.
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76
Q

does the graded potential summate?

A

yes, but action potential doesn’t

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77
Q

do graded potentials last longer than action potential?

A

yes they do, depending on the strength of the stimulus. action potentials are only for a few milliseconds

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78
Q

do action potentials travel in any direction

A

no they don’t, they only travel down the axon. graded potentials though travel in any direction

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79
Q

do graded potentials have a fixed amplitude

A

no they don’t, their amplitude depends on their distance to the cell body. it ios action potential that has a fixed amplitude

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80
Q

do graded potentials have a refractory period

A

no they don’t, that is action potential. graded potentials can be generated repeatedly

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81
Q

do graded potentials have a specific threshold

A

no they don’t, they can be transmitted by any strength of stimulus. Action potentials though have a threshold

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82
Q

are graded potentials generated in the axonal hillock only

A

nahh fam, that is action potential. graded potentials are generated anywhere on the neuron (dendrites, cell body, axon)

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83
Q

what are the major factors contributing to membrane potential

A

👉The concentration of ions across the membrane: Normally, sodium (Naᶧ), Chloride (Cl⁻), and calcium (Ca²ᶧ) are more concentrated in the extracellular fluid than in the intracellular fluid, while potassium (Kᶧ) is more concentrated in the intracellular fluid than in the extracellular fluid.

👉Membrane permeability to these ions: The resting cell membrane is much more permeable to Kᶧ than to Naᶧ or Ca²ᶧ. This makes Kᶧ the major ion contributing to the resting membrane potential.

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84
Q

comment on the ‘concentration of ions across the membrane’ factor that contributes to membrane potential

A

Normally, sodium (Naᶧ), Chloride (Cl⁻), and calcium (Ca²ᶧ) are more concentrated in the extracellular fluid than in the intracellular fluid, while potassium (Kᶧ) is more concentrated in the intracellular fluid than in the extracellular fluid.

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85
Q

comment on ‘membrane permeability to these ions’ factor that contributes to membrane potential

A

The resting cell membrane is much more permeable to Kᶧ than to Naᶧ or Ca²ᶧ. This makes Kᶧ the major ion contributing to the resting membrane potential.

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86
Q

what does it mean to say that a membrane is depolarized

A

The membrane is depolarized when its potential becomes less negative i.e more positive (closer to zero) than the resting level.

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87
Q

what is an overshoot

A

Overshoot refers to a reversal of the membrane potential polarity, that is when the inside of a cell becomes positive relative to the outside

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88
Q

what is repolarization

A

When a membrane potential that has been depolarized is returning toward the resting value, it is repolarizing

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89
Q

what is hyperpolarization

A

The membrane is hyperpolarized when the potential is more negative than the resting level.

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90
Q

a large stimulus on graded potential will…

A

create a strong graded potential

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91
Q

a small stimulus on graded potential will

A

create a weak graded potential

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92
Q

what is graded potential

A

👉Graded potential is a mild local change in the membrane potential that develops when stimulated in receptors, synapses or neuromuscular junction.
👉It is also called graded membrane potential, graded depolarization or
local potential.
👉It is non­propagative and characterized by mild depolarization or hyperpolarization.
👉In most cases, the graded potential is responsible for generating an action potential.
👉However, in some cases the graded potential hyperpolarizes the membrane potential (more negativity than resting membrane potential) and inhibits the generation of action potential (as in inhibitory synapses)

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93
Q

List some types abi examples of graded potentials

A
  1. End plate potential in neuromuscular junction
  2. Electronic potential in nerve fibers
  3. Receptor potential
  4. Excitatory postsynaptic potential
  5. Inhibitory postsynaptic potential
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94
Q

what is end plate potential in a neuromuscular junction

A

👉The end-plate potential is a type of graded potential that occurs at the neuromuscular junction, which is the synapse between a motor neuron and a muscle fiber.
👉It is a depolarization of the muscle fiber caused by the release of acetylcholine from the motor neuron, which binds to nicotinic acetylcholine receptors on the muscle fiber and allows positively charged ions to enter.
👉The magnitude of the EPP depends on:
-The amount of ACh released by the motor neuron,
-The sensitivity of the nicotinic Ach receptors on the muscle fiber, and
-The number of nAChRs that are activated.
👉The End plate potential can vary in size and duration, but is typically around 40-50 mV in amplitude and lasts for several milliseconds.
👉The End plate potential is important for initiating muscle contraction by triggering an action potential in the muscle fiber.

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95
Q

what factors affect the magnitude of the end plate potential

A

-The amount of ACh released by the motor neuron,
-The sensitivity of the nicotinic Ach receptors on the muscle fiber, and
-The number of nAChRs that are activated.

96
Q

what is the usually amplitude of the end plate potential

A

40-50mV

97
Q

what is electric potential in nerve fibers

A

👉The electric potential in nerve fibers refers to the difference in electrical charge that exists across the cell membrane of a neuron.
👉This charge difference is maintained by the selective movement of ions (sodium, potassium and chlorine) across the membrane through ion channels.
👉At rest, the neuron has a negative charge inside relative to the outside, with a resting membrane potential of around -70 millivolts.
👉Changes in electric potential can:
-trigger the release of neurotransmitters,
-activate ion channels, and
-generate action potentials that allow neurons to communicate with each other and with other cells in the body.

98
Q

what is the implication of the changes of electric potential

A

-trigger the release of neurotransmitters,
-activate ion channels, and
-generate action potentials that allow neurons to communicate with each other and with other cells in the body.

99
Q

what is receptor potential

A

👉Receptor potential is a non­propagated transmembrane potential difference that develops when a receptor is stimulated. It is also called generator potential.
👉Receptor potential is short lived and hence, it is called transient receptor potential.
👉Receptor potential is not action potential. It is a graded potential .
👉It is similar to excitatory postsynaptic potential (EPSP) in synapse, endplate potential in neuromuscular junction and electrotonic potential in the nerve fiber.
👉Receptor potential responds to stimulus from:
-mechanoreceptors
-nociceptors
-thermoreceptors
-chemoreceptors
-electromagnetic receptors(vision)

=>Properties of Receptor Potential
-Receptor potential is non­propagated; it is confined within the receptor itself
-It does not obey all­ or ­none law.

=>Significance of Receptor Potential
When receptor potential is sufficiently strong (when the magnitude is about 10 mV), it causes the development of action potential in the sensory nerve.

100
Q

what other graded potentials is receptor potential similar to?

A

👉excitatory postsynaptic potential (EPSP) in synapse,
👉endplate potential in neuromuscular junction and \
👉electrotonic potential in the nerve fiber.

101
Q

receptor potential responds to stimulus from

A

-mechanoreceptors
-nociceptors
-thermoreceptors
-chemoreceptors
-electromagnetic receptors(vision)

102
Q

what are the properties of receptor potential

A

-Receptor potential is non­propagated; it is confined within the receptor itself
-It does not obey all­ or ­none law.

103
Q

draw a diagram to explain receptor potential

A

check the booklet

104
Q

what is the significance of receptor potential

A

When receptor potential is sufficiently strong (when the magnitude is about 10 mV), it causes the development of action potential in the sensory nerve.

105
Q

what are the similarities between graded potential and action potential

A

Action potentials and graded potentials are both types of electrical signals that occur in neurons, and they share several similarities. Here are 10 similarities between action potentials and graded potentials:

  1. Both are changes in the electric potential of a neuron that result from the movement of ions across the cell membrane.
  2. Both can be either depolarizing or hyperpolarizing, depending on the direction of ion movement.
  3. Both can be initiated by a variety of stimuli, including neurotransmitters, sensory input, and mechanical forces.
  4. Both involve the opening and closing of ion channels in the cell membrane.
  5. Both can be influenced by the concentration gradients of ions inside and outside the cell.
  6. Both can be affected by the presence of drugs or other chemicals that alter ion channel activity.
  7. Both can be modified by the activity of other neurons or synaptic inputs.
  8. Both can exhibit temporal and spatial summation, meaning that multiple signals occurring close together in time or space can add together to create a larger signal.
  9. Both can be used by neurons to integrate information and make decisions about whether or not to generate an action potential.
  10. Both are important for communication within the nervous system, allowing neurons to transmit signals over short or long distances depending on their type.
106
Q

What is an excitatory postsynaptic potential

A

Excitatory postsynaptic potential (EPSP) is the non-propagated electrical potential that develops during the process of synaptic transmission

107
Q

what are the steps for the development of excitatory postsynaptic potential

A
  1. Action potential: An action potential reaches the presynaptic terminal of the neuron, causing voltage-gated calcium channels to open and allowing calcium ions to enter the cell.
  2. Neurotransmitter release: The influx of calcium ions triggers the release of neurotransmitter molecules, such as glutamate and acetylcholine, into the synaptic cleft.
  3. Neurotransmitter binding: The neurotransmitter molecules diffuse across the synaptic cleft and bind to their specific receptors on the postsynaptic membrane of the receiving neuron.
  4. Ion channel opening: The binding of the neurotransmitter to their specific receptors causes ion channels to open, allowing positively charged ions, such as sodium ions, to enter the postsynaptic neuron.
  5. Depolarization: The influx of positively charged ions depolarizes the postsynaptic membrane, making it more positive.
  6. EPSP generation: The resulting depolarization of the postsynaptic membrane is called an EPSP. The magnitude of the EPSP depends on the amount of neurotransmitter released by the presynaptic neuron, the sensitivity of the ionotropic receptors on the postsynaptic membrane, and the number of receptors that are activated.
  7. Integration: The EPSP can summate with other EPSPs or IPSPs (inhibitory postsynaptic potentials) occurring close together in time or space, allowing neurons to integrate information and make decisions about whether or not to generate an action potential.
  8. Action potential generation: If the EPSP is large enough to depolarize the postsynaptic membrane to its threshold potential, voltage-gated ion channels in the membrane will open, allowing an action potential to be generated and propagate down the axon of the postsynaptic neuron.

Overall, EPSPs are important for communication between neurons and for many functions of the nervous system, including perception, movement, and cognition.

108
Q

what are the steps for the development of excitatory postsynaptic potential

A
  1. Action potential: An action potential reaches the presynaptic terminal of the neuron, causing voltage-gated calcium channels to open and allowing calcium ions to enter the cell.
  2. Neurotransmitter release: The influx of calcium ions triggers the release of neurotransmitter molecules, such as glutamate and acetylcholine, into the synaptic cleft.
  3. Neurotransmitter binding: The neurotransmitter molecules diffuse across the synaptic cleft and bind to their specific receptors on the postsynaptic membrane of the receiving neuron.
  4. Ion channel opening: The binding of the neurotransmitter to their specific receptors causes ion channels to open, allowing positively charged ions, such as sodium ions, to enter the postsynaptic neuron.
  5. Depolarization: The influx of positively charged ions depolarizes the postsynaptic membrane, making it more positive.
  6. EPSP generation: The resulting depolarization of the postsynaptic membrane is called an EPSP. The magnitude of the EPSP depends on the amount of neurotransmitter released by the presynaptic neuron, the sensitivity of the ionotropic receptors on the postsynaptic membrane, and the number of receptors that are activated.
  7. Integration: The EPSP can summate with other EPSPs or IPSPs (inhibitory postsynaptic potentials) occurring close together in time or space, allowing neurons to integrate information and make decisions about whether or not to generate an action potential.
  8. Action potential generation: If the EPSP is large enough to depolarize the postsynaptic membrane to its threshold potential, voltage-gated ion channels in the membrane will open, allowing an action potential to be generated and propagate down the axon of the postsynaptic neuron.

Overall, EPSPs are important for communication between neurons and for many functions of the nervous system, including perception, movement, and cognition.

109
Q

what other graded potentials is excitatory postsynaptic potential similar to?

A

-receptor potential
-endplate potential.

110
Q

what are the properties of excitatory postsynaptic potential

A
  1. It is non­propagated
  2. It does not obey all­or­none law.
111
Q

what is the significance of excitatory postsynaptic potential

A

When EPSP is strong enough, it causes the opening
of voltage ­gated sodium channels in the initial segment
of axon. Now, due to the entrance of sodium ions, the
depolarization occurs in the initial segment of axon
and thus, the action potential develops. From here, the
action potential spreads to other segments of the axon.

112
Q

what is inhibitory postsynaptic potential

A

Inhibitory postsynaptic potential (IPSP) is the electrical
potential in the form of hyperpolarization that develops
during postsynaptic inhibition

113
Q

what are the steps for the development of inhibitory postsynaptic potential

A

The steps involved in an inhibitory postsynaptic potential (IPSP) at a synapse between two neurons can be summarized as follows:

  1. Action potential: An action potential reaches the presynaptic terminal of the neuron, causing voltage-gated calcium channels to open and allowing calcium ions to enter the cell.
  2. Neurotransmitter release: The influx of calcium ions triggers the release of neurotransmitter molecules, such as GABA (gamma-aminobutyric acid),or dopamine into the synaptic cleft.
  3. Neurotransmitter binding: The neurotransmitter molecules diffuse across the synaptic cleft and bind to ionotropic or metabotropic receptors on the postsynaptic membrane of the receiving neuron.
  4. Ion channel opening: The binding of GABA to ionotropic receptors causes ion channels to open, allowing negatively charged ions, such as chloride ions, to enter the postsynaptic neuron or positively charged ions, such as potassium ions, to leave the postsynaptic neuron. Alternatively, binding of GABA to metabotropic receptors can activate signaling pathways that lead to ion channel opening or closing.
  5. Hyperpolarization: The influx of negatively charged ions or efflux of positively charged ions hyperpolarizes the postsynaptic membrane, making it more negative.
  6. IPSP generation: The resulting hyperpolarization of the postsynaptic membrane is called an IPSP. The magnitude of the IPSP depends on the amount of neurotransmitter released by the presynaptic neuron, the sensitivity of the receptors on the postsynaptic membrane, and the number of receptors that are activated.
  7. Integration: The IPSP can summate with other IPSPs or EPSPs occurring close together in time or space, allowing neurons to integrate information and make decisions about whether or not to generate an action potential.
  8. Action potential inhibition: If the IPSP is large enough to hyperpolarize the postsynaptic membrane to a level that is more negative than the resting potential, it can prevent the generation of an action potential.

Overall, IPSPs are important for communication between neurons and for many functions of the nervous system, including regulation of muscle tone, control of reflexes, and modulation of sensory information processing.

114
Q

pacemaker cell exhibit what kind of graded potential

A

pacemaker potential

115
Q

outline the steps for a pacemaker potential

A
  1. Resting membrane potential: The pacemaker cells have a resting membrane potential of -60 to -70 mV, which is more positive than the resting potential of most other cardiac cells.
  2. Slow depolarization: The pacemaker potential begins with a slow depolarization caused by a gradual increase in the permeability of the cell membrane to sodium ions (Na+). This is due to the opening of funny channels (If channels) that allow Na+ to enter the cell.
  3. Threshold potential: As the membrane potential reaches a certain threshold level (-40 mV), voltage-gated calcium channels (Ca2+) open, allowing an influx of calcium ions into the cell.
  4. Rapid depolarization: The influx of calcium ions causes a rapid depolarization of the cell membrane, which triggers the opening of voltage-gated potassium channels (K+).
  5. Repolarization: The efflux of potassium ions out of the cell causes repolarization of the membrane, which leads to the closure of the calcium channels and the opening of the potassium channels.
  6. Hyperpolarization: The efflux of potassium ions continues, causing hyperpolarization of the membrane potential, which brings it back to the resting state.
  7. Reaching threshold again: The slow depolarization caused by the funny channels starts again, and the cycle repeats itself.
116
Q

what are some properties of graded potential

A
  1. Graded potentials are localized: Graded potentials occur only at the site of the stimulus and are not propagated along the length of the axon or dendrite.
  2. Graded potentials are decremental: Graded potentials decrease in amplitude as they spread away from the site of the stimulus. This is due to the leakage of ions across the membrane.
  3. Graded potentials can be summated: Graded potentials can add up to produce a larger depolarization or hyperpolarization. T
  4. Graded potentials are non-regenerative: Graded potentials do not regenerate themselves and cannot trigger an action potential. They are simply local changes in membrane potential that can either increase or decrease the likelihood of an action potential occurring.
  5. Graded potentials can have different durations: Graded potentials can last for different lengths of time depending on the type of stimulus and the properties of the membrane.
117
Q

what is action potential

A

An AP is a regenerating depolarization of membrane potential that propagates (conducted without decrement) along an excitable tissue capable of action potential

118
Q

The threshold of most excitable membranes is about ___mV less negative than the RMP

A

15mV

119
Q

btw what is excitability

A

Excitability is defined as the physiochemical change
that occurs in a tissue when stimulus is applied.

120
Q

the local membrane is brought to threshold voltage by

A

depolarizing stimulus

121
Q

what is the threshold potential of a neuron

A

-55mV

122
Q

draw a diagram to show action potential

A

check the book

123
Q

what are the differences between action potential in muscle and in neurons

A

👉Resting membrane potential: -70mV in nerves and -90mV in muscle
👉Threshold potential: -55mV in nerves and -75mV in muscle
👉end of depolarisation: +35mV in nerves, +55mV in muscle

124
Q

outline the process of action potential

A
  1. Resting potential: The neuron is at rest, with a negative charge inside and a positive charge outside, the value is -70mV
  2. Depolarization: A stimulus causes the membrane potential to become less negative, (more positive), as positive ions {sodium ions} enter the neuron.
  3. Threshold: If the depolarization reaches a certain threshold (-55mV), an action potential is triggered.
  4. Current through opening voltage-gated Na+ channels rapidly depolarizes the membrane, causing more Na+ channels to open.
    Inactivation of Na+ channels and delayed opening of voltage-gated K+ channels halt membrane depolarization
  5. Repolarization: Outward current through open voltage-gated K+ channels repolarizes the membrane back to a negative potential.
  6. Hyperpolarization: Persistent current through slowly closing voltage-gated K+ channels hyperpolarizes the membrane toward the equilibrium potential of potassium (Ek); Sodium channels return from inactivated state to the closed state (without opening).
    Closure of voltage-gated K+ channels returns the membrane potential to its resting value.
  7. Refractory period: The neuron is temporarily unable to fire another action potential, as the ion channels reset.
  8. Propagation: The action potential travels down the axon, as the depolarization triggers adjacent sections of the membrane to depolarize and fire their own action potentials.
  9. Synaptic transmission: When the action potential reaches the end of the axon, it triggers the release of neurotransmitters, which cross the synapse and bind to receptors on the next neuron.
125
Q

The pyrethrin insecticides, derived from chrysanthemums, disable the inactivation gates of Na+ channels so that the channels remain open. In neurons poisoned with pyrethrins, what would you predict would happen to the membrane potential?

A

👉In neurons poisoned with pyrethrins, the inactivation gates of Na+ channels would be disabled so that the channels remain open.
👉This would result in an increased influx of Na+ ions into the neuron, leading to depolarization of the membrane potential.
👉The membrane potential would become less negative, and if the depolarization reached the threshold, an action potential would be triggered.
👉The continued influx of Na+ ions would prevent the membrane potential from repolarizing and returning to its resting state, leading to the continuous firing of action potentials and hyperexcitability of the neuron. 👉This could potentially lead to seizures, tremors, and other neurological symptoms.

126
Q

what are voltage-gated channels

A

Voltage-gated channels are specialized ion channels that are found in the membranes of neurons and other excitable cells, such as muscle cells. These channels are activated by changes the membrane potential.

Voltage-gated channels are selective for specific ions:
-such as sodium (Na+),
-potassium (K+), or
-calcium (Ca2+),
and they open or close in response to changes in the membrane potential. When the membrane potential reaches a certain threshold, voltage-gated channels open, allowing ions to flow across the membrane and generating an action potential.

Voltage-gated channels are important for a variety of physiological processes, including:
-muscle contraction,
-hormone secretion, and
-sensory perception.

Mutations in voltage-gated channels can lead to a range of neurological and neuromuscular disorders, including epilepsy, migraine, and myotonia.

127
Q

what diseases could be caused by a mutation of the voltage gated channels

A

Mutations in voltage-gated channels can lead to a range of neurological and neuromuscular disorders, including epilepsy, migraine, and myotonia.

128
Q

what voltage-gated channels open first

A

Na+

129
Q

voltage gated channels are important for physiological processes like

A

-muscle contraction,
-hormone secretion, and
-sensory perception.

130
Q

what volatge gated channel is responsible for depolarization

A

Na+ volatge gated channels

131
Q

what voltage gated channel is responsible for repolarization

A

K+ voltage gated channels

132
Q

what volatge gated channel is responsible for refractory period

A

K+ volatge channels

133
Q

what is the function of Ca2+ voltage gated channels

A

neurotransmitter release

134
Q

explain the propagation of the action potential

A

an action potential travels down the axon without a decrement in its amplitude.
This is because the voltage change in an action potential is more than 5 times the voltage needed to exceed the threshold potential.
This extra depolarization in AP causes the membrane adjacent to the AP to also depolarize and produce the next Action potenti

135
Q

btw what are some factors that inhibit Na+ permeability in the cell

A

-Inactivation of Na+ channels
-The direction of electrical gradient of Na+ is reversed during overshoot because the membrane potential is reversed
-Opening of the their voltage gated K+ channels because of K+ which leaves along its concentration gradient

136
Q

draw a diagram to show the action of Na+ voltage gated channels

A

check the book

137
Q

draw a diagram to show the action of K+ voltage gated channels

A

check the book

138
Q

draw a diagram to show the action of K+ voltage gated channels

A

check the book

139
Q

draw a diagram to show the ‘extra depolarization’ of action potential propagation

A

check the book

140
Q

what is saltatory conduction

A

👉Saltatory conduction is the mode of transmission of impulses along a myelinated nerve.
👉In a myelinated nerve, the depolarization (action potential) jumps from one node of ranvier to the next.
👉this is becbecause I ause tthe heis intervening myelin acts as an insulatory sheath so no ions can pass through them. Therefore the action potential is propagated node to node.
👉The action potential flows through the ECF and axoplasm from node to node, exciting the successive nodes, one after the other.

👉ADVANTAGES OF SALTATORY CONDUCTION
-velocity of conduction is faster than unmyelinated nerve of the same diameter. this is because the action potential simply jumps from node to node, instead of travelling across the axon of the cell.
-It requires less energy for the conduction of impulse. As only the nodes are depolarised and repolarised, it requires movement of a small amount of ions during conduction

141
Q

what are the advantages of saltatory conduction

A

-velocity of conduction is faster than unmyelinated nerve of the same diameter. this is because the action potential simply jumps from node to node, instead of travelling across the axon of the cell.

-It requires less energy for the conduction of impulse. As only the nodes are depolarised and repolarised, it requires movement of a small amount of ions during conduction

142
Q

draw a diagram to explain saltatory conduction

A

check your book

143
Q

what are some applications of AP

A

-local anaesthetics
-without action potentials, graded potentials generated from stimuli in sensory receptor cannot reach the brain.
-some toxins produced by animals block the action potential

144
Q

explain the ‘local anaesthetic’ application of the AP

A

-Local anesthetics are drugs that temporarily block action potentials in axons.
-They are called Local because they are injected directly into the tissue where anesthesia (the absence of sensation) is desired.
-The generation of APs is prevented by local anesthetics such as procaine and lidocaine, because these drugs block voltage-gated Na+ channels, preventing them from opening in response to depolarization

145
Q

what drugs prevent the generation of AP’s as an anesthetic

A

-procaine
-lidocaine

146
Q

how do the drugs that prevent AP generation work

A

these drugs block voltage-gated Na+ channels, preventing them from opening in response to depolarization

147
Q

what part does AP have to play in sensations to the brain

A

Without AP, graded signals generated in sensory neurons in response to injury, for example, cannot reach the brain and give rise to the sensation of pain.

148
Q

comment on the production of toxins by animals which block AP.

A

-Some animals produce toxins (poisons) that work by interfering with nerve conduction in the same way that local anesthetics do.

-For example, some organs of the pufferfish produce an extremely potent toxin, tetrodotoxin, that binds to voltage-gated Na+ channels and prevents the Na+ component of the AP

149
Q

what toxin does the pufferfish secrete that blocks AP

A

Tetrodotoxin, binds to voltage-gated Na+ channels and prevents the Na+ component of the AP

150
Q

outline properties of AP

A
  1. All-or-none: Action potentials are triggered when the membrane potential reaches a certain threshold, and once triggered, they occur at a fixed amplitude and duration, regardless of the strength of the stimulus that triggered them.
  2. Self-propagating: Once an action potential is triggered, it propagates down the axon without losing strength, due to the positive feedback loop created by the influx of sodium ions.
  3. Non-decremental: Action potentials do not weaken as they travel down the axon, unlike graded potentials, which weaken with distance.
  4. Reversible: While the depolarization phase of the action potential is irreversible, the repolarization and hyperpolarization phases can be reversed by another stimulus, if the membrane potential is still in the appropriate range.
  5. Refractory period: After an action potential is fired, the neuron enters a refractory period during which it is temporarily unable to fire another action potential, due to the inactivation of sodium channels and the slow recovery of potassium channels.
  6. Frequency coding: The frequency of action potentials can encode the intensity of a stimulus, with stronger stimuli resulting in more frequent firing of action potentials.
  7. It has a conduction velocity (m/sec)
151
Q

what is the latent period of a nerve

A

it is a period corresponding to the time taken from the site of stimulation till the recording electrode.

152
Q

what is the all-or-none law

A

All-or-none law states that when a nerve is stimulated by a threshold level of stimulus it gives maximum response or does not give response at all.
- Further increase in the intensity of a stimulus produces no increment or other changes in action potential.
- The action potential failed to occur if the stimulus is sub-threshold, it produces only local changes with no propagation.

153
Q

what is refractory period

A

Refractory period is the period at which the nerve does
not give any response to a stimulus.
It is of two types:
-absolute refractory period
-relative refractory period

154
Q

what is absolute refractory period

A

-In absolute refractory period of a membrane, a second stimulus, no matter how strong, will not produce a second AP.

-is due to the inactivation of sodium channels and the slow recovery of potassium channels.

-Absolute refractory period corresponds to the
period from the time when firing level is reached till
the time when one third of repolarization is completed.

The Absolute refractory period ensures that:
- a second AP will not occur before the first has finished.
- AP cannot overlap and cannot travel backward because of their refractory periods.

155
Q

what is relative refractory period

A

-It is the period, during which the nerve fiber shows
response, if the strength of stimulus is increased to
maximum.

  • is due to the slow recovery of potassium channels and the continued hyperpolarization of the membrane potential.

-The relative refractory period allows the neuron to respond to strong stimuli, but also prevents it from firing too frequently and becoming overexcited.

-while absolute refractory period corresponds to the
period from the time when firing level is reached till
the time when one third of repolarization is completed.
Relative refractory period extends through rest of the
repolarization period

156
Q

what are the significance/ uses of the refractory periods

A

-Ensuring unidirectional propagation: The absolute refractory period ensures that action potentials are propagated in a one-way direction, from the cell body to the axon terminals, and prevents the action potential from traveling back in the opposite direction.

-Preventing overexcitation: The relative refractory period prevents the neuron from firing too frequently and becoming overexcited, which could lead to damage or death of the neuron.

-Encoding information: The refractory period can encode information about the strength and timing of stimuli, as the frequency and timing of action potentials can indicate the intensity and duration of the stimulus.

-Regulating neuronal activity: The refractory period can regulate the activity of neurons and prevent them from firing too frequently or inappropriately, which could disrupt normal brain function

157
Q

what causes relative refractory period

A

is due to the slow recovery of potassium channels and the continued hyperpolarization of the membrane potential.

158
Q

what causes absolute refractory period

A

is due to the inactivation of sodium channels and the slow recovery of potassium channels

159
Q

explain how refractory period helps the AP travel in only one direction

A

-The Na+ gated channel is activated in depolarisation
-the depolarization spreads (propagates) to the adjacent patch of membrane
-After this the initial Na+ channel becomes inactivated (refractory period) and this an AP cannot be conducted through it again. i.e if an action potential has just passed through a section of the axon, that section of the axon is temporarily unable to generate another action potential.
-this ensures that the action potential doesn’t flow backwards, but from the cell body and down the axon

160
Q

Functions of Action potentials

A
  1. Transmission of Information: Action potentials are the means by which neurons communicate with each other and with other cells in the body. They allow information to be transmitted rapidly over long distances in the nervous system.
  2. Integration of Information: Action potentials can integrate information from multiple inputs, allowing neurons to make complex decisions about whether and how to transmit signals to other neurons or cells.
  3. Encoding of Information: The frequency and pattern of action potentials can encode information about the strength and type of stimuli that neurons are responding to, allowing the nervous system to distinguish between different sensory inputs.
  4. Propagation of Signals: Action potentials are self-propagating, meaning that they can travel down the length of the axon without losing strength. This allows signals to be transmitted rapidly and efficiently over long distances.
  5. Regulation of Synaptic Plasticity: Action potentials can trigger the release of neurotransmitters at synapses, which can lead to changes in the strength of synaptic connections. This process, known as synaptic plasticity, is thought to underlie learning and memory.
  6. Control of Muscle Contraction: Action potentials can also trigger the release of calcium ions in muscle cells, which can lead to muscle contraction. This allows the nervous system to control movement and other physiological processes.
  7. In non-nervous tissue APs are the initiators of a range of cellular responses
    muscle contraction,
    secretion (eg. Adrenalin from chromaffin cells of medulla)
161
Q

The velocity at which an AP propagates down the axon is dependent on…

A

👉the diameter of the axon
👉if the axon is myelinated or not

162
Q

A larger diameter fibre will propagate faster?

A

👉The larger the fiber diameter the faster the AP propagates.
👉This is because a large fiber offers less internal resistance to local current
More ions will flow in a given time, bringing adjacent regions of the membrane to threshold

163
Q

Why will a larger diameter fibre propagate faster

A

large fiber offers less internal resistance to local current. More ions will flow in a given time, bringing adjacent regions of the membrane to threshold

164
Q

What are the downsides of large diameter fibre

A

👉They take up a lot of space that limits the amount of neurons that could be packed into a system

👉They have large volumes of cytoplasm making them difficult to produce and maintain

👉Vulnerability to Injury: Large diameter fibers are more vulnerable to injury than smaller diameter fibers, particularly in conditions such as diabetic neuropathy, where damage to the myelin sheath that surrounds the fibers can occur. This can lead to decreased nerve conduction velocity and impaired function

👉Limited Adaptability: Large diameter fibers are less adaptable than smaller diameter fibers, meaning they are less able to change their properties in response to changes in the environment or physiological conditions. This limits their usefulness in certain situations where adaptability is important, such as in the development of new neural pathways following injury or disease.

165
Q

Give a comparison between neurons that shows the importance of myelin

A

a 6mm diameter myelinated axon has the same velocity as a 500mm unmyelinated axon

166
Q

How many times bigger does an unmyelinated axon need to get to conduct with the same velocity of a myelinated axon

A

83X

167
Q

What is myelin

A

👉Myelin sheath is a thick lipoprotein sheath that insulates
the myelinated nerve fiber.
👉Myelin sheath is not a continuous sheath. It is absent at regular intervals.
👉The area where myelin sheath is absent is called node of
Ranvier.
👉Segment of the nerve fiber between two nodes
is called internode.
👉Myelin sheath is responsible for
white color of nerve fibers
👉It is secreted by Schwann cells in the PNS, and oligodendrocytes in the CNS

168
Q

Functions of myelin

A
  1. Faster conduction
    Myelin sheath is responsible for faster conduction of
    impulse through the nerve fibers. In myelinated nerve
    fibers, the impulses jump from one node to another
    node. This type of transmission of impulses is called
    saltatory conduction
  2. Insulating capacity
    Myelin sheath has a high insulating capacity. Because
    of this quality, myelin sheath restricts the nerve impulse
    within single nerve fiber and prevents the stimulation of
    neighboring nerve fibers.
  3. Size requirement is diminished
  4. Reduced cell energy requirement
169
Q

What is a demyelinating disease

A

👉In demyelinating disease, the loss of myelin from vertebrate neurons can have devastating effects on neural signaling.
👉In central and peripheral nervous system, the loss of myelin slows the conduction of APs.
👉In addition, when ions leak out of the uninsulated regions of membrane between the channel rich-rich nodes of Ranvier, the depolarization that reaches a node may not be above threshold and conduction may fail.

170
Q

Comment on multiple sclerosis

A

👉Multiple sclerosis (MS) is a chronic and progressive
inflammatory disease characterized by demyelination
in brain and spinal cord.
👉It affects the myelinated
nerve fibers of brain, spinal cord and optic nerve
and causes gradual destruction of myelin sheath
(demyelination).
👉When the disease progresses, there
is transection of axons in patches throughout brain
and spinal cord. The term sclerosis refers to scars
(scleroses) in the myelin sheath.

👉Cause of multiple sclerosis is unknown. It is hypothesized
that multiple sclerosis occurs due to combination and
interaction of environmental factors (chemicals, bacteria
and virus) and genetic factors resulting in abnormal
reactions of immune system. During the process, the
immune system attacks the myelin sheath.

👉Signs and symptoms
Initial attack by multiple sclerosis is often mild or
asymptomatic. As the disease progresses variety o

171
Q

Cause of multiple sclerosis

A

Cause of multiple sclerosis is unknown. It is hypothesized
that multiple sclerosis occurs due to combination and
interaction of environmental factors (chemicals, bacteria
and virus) and genetic factors resulting in abnormal
reactions of immune system. During the process, the
immune system attacks the myelin sheath.

172
Q

What are the signs and symptoms of multiple sclerosis

A

Common initial symptoms:
1. Mild disturbance in the sensations on face, arms
and legs
2. Weakness and disturbances in maintenance of
posture
3. Double vision followed by partial blindness.
Other symptoms when the disease progresses:
1. Tremor, fatigue and muscle spasms
2. Speech difficulty
3. Difficulty in performing day-to-day activities
4. Bowel problems
5. Bladder dysfunction
6. Emotional outbursts like anxiety, anger and
frustration
7. Short-term memory loss
8. Complete blindness
9. Development of suicidal tendency

173
Q

What are the common initial symptoms of MS

A

Common initial symptoms:
1. Mild disturbance in the sensations on face, arms
and legs
2. Weakness and disturbances in maintenance of
posture
3. Double vision followed by partial blindness.

174
Q

What are the progressive symptoms of MS

A

Other symptoms when the disease progresses:
1. Tremor, fatigue and muscle spasms
2. Speech difficulty
3. Difficulty in performing day-to-day activities
4. Bowel problems
5. Bladder dysfunction
6. Emotional outbursts like anxiety, anger and
frustration
7. Short-term memory loss
8. Complete blindness
9. Development of suicidal tendency

175
Q

In which of the following would the velocity of nerve impulse conduction be the greatest
a) Large-diameter unmyelinated fibers
b) Small-diameter unmyelinated fibers
c) Large-diameter myelinated fibers
d) Small-diameter myelinated fibers.

A

Large diameter myelinated fibres

176
Q

Who discovered the synapse

A

Charles Sherrington near the end of the 19th century.

177
Q

What’s the length of a synapse

A

20-30 nM

178
Q

What is a synapse

A

Synapse is the junction between two neurons. It
is not an anatomical continuation. But, it is only a
physiological continuity between two nerve cells.

179
Q

What are the 2 major classifications of the synapse

A

👉 Anatomical classification
👉 Physiological classification

180
Q

What is the anatomical classification of the synapse

A

Depending upon ending of axon, synapse is
classified into 3 types:
1. Axoaxonic synapse in which axon of one neuron terminates on axon of another neuron
2. Axodendritic synapse in which the axon of one neuron terminates on dendrite of another neuron
3. Axosomatic synapse in which axon of one neuron
ends on soma (cell body) of another neuron

And a different type:
4. Dendrodendritic synapse in which the dendrites of one neuron terminates on the dendrite of another neuron. It is very important in olfaction (olfactory discrimination and olfactory learninga)

181
Q

What are some similar ‘synapse like junctions

A

Autoreceptors
Neuromuscular junction
Neuroendocrine/Neurosecetory junction

182
Q

What is the functional classification of the synapse

A

Functional classification of synapse is on the basis
of mode of impulse transmission
1. Electrical synapse
2. Chemical synapse

183
Q

draw diagrams for the anatomical classification of the synapse

A

check the book

184
Q

what is an electrical synapse

A

👉Electrical synapse is a synapse in which the physiological continuity between the presynaptic and the post-synaptic neurons is provided by a gap junction between the two neurons
👉There is a direct exchange of ions between the two neurons through the gap junction.
👉Because of this reason, the action potential reaching the terminal portion of presynaptic neuron directly enters the postsynaptic neuron.
👉Important feature of electrical synapse is that the synaptic delay is very less because of the direct flow of
current.
👉Moreover, the impulse is transmitted in either direction through the electrical synapse.
👉This type of impulse transmission occurs in some tissues like:
-the cardiac muscle fibers,
-smooth muscle fibers of intestine and
-the epithelial cells of lens in the eye.

185
Q

draw a diagram to show the electric synapse

A

check the book

186
Q

what is a chemical synapse

A

👉Chemical synapse is the junction between a nerve fiber
and a muscle fiber or between two nerve fibers, through
which the signals are transmitted by the release of
chemical transmitter.
👉In the chemical synapse, there is no continuity between the two neurons because of the presence of a space called synaptic cleft between the two neurons.
👉Action potential reaching the presynaptic
terminal causes release of neurotransmitter substance
from the vesicles of this terminal.
👉Neurotransmitter reaches the postsynaptic neuron through synaptic cleft and causes the production of potential change.

187
Q

draw a chemical synapse

A

check your book

188
Q

comment on the synchronization property of the electrical potential

A

Synchronization of the electrical activity of large populations of neurons; it is bidirectional
- e.g., the large populations of neurosecretory neurons that synthesize and release biologically active peptide neurotransmitters and hormones are extensively connected by electrical synapses.
- e.g., Synchronization may be required for neuronal development, including the development of chemical synapses.
- e.g., Synchronization may be important in functions that require instantaneous responses, such as reflexes.

189
Q

who won the nobel prize for discovering neurotransmitters

A

Otto Loewi and Sir Henry Dale, 1936

190
Q

what are the differences between chemical synapses and electrical synapses

A

Chemical synapses and electrical synapses are two types of synapses that are involved in the transmission of signals between neurons. Here are 10 differences between chemical synapse and electrical synapse:

  1. Transmission method: Chemical synapses transmit signals between neurons using chemical neurotransmitters, while electrical synapses transmit signals through direct electrical coupling between neurons.
  2. Speed: Electrical synapses are faster than chemical synapses, as they allow for the rapid and direct transmission of electrical signals between neurons.
  3. Directionality: Chemical synapses are unidirectional, meaning that signals can only be transmitted in one direction from the presynaptic neuron to the postsynaptic neuron. Electrical synapses are bidirectional, meaning that signals can be transmitted in both directions between neurons.
  4. Synaptic delay: Chemical synapses have a synaptic delay, which is the time it takes for the neurotransmitter to cross the synaptic cleft and bind to the receptors on the postsynaptic neuron. Electrical synapses have no synaptic delay, as the electrical signal is transmitted directly through gap junctions.
  5. Amplification: Chemical synapses allow for signal amplification, as a single action potential in the presynaptic neuron can trigger the release of multiple neurotransmitter molecules, which can then bind to multiple receptors on the postsynaptic neuron. Electrical synapses do not allow for signal amplification.
  6. Modulation: Chemical synapses can be modulated by various factors, such as neuromodulators and drugs, which can affect the release or uptake of neurotransmitters. Electrical synapses are not modulated in the same way.
  7. Energy consumption: Chemical synapses require more energy than electrical synapses, as the process of synthesizing, packaging, and releasing neurotransmitters is energy-intensive.
  8. Selectivity: Chemical synapses are more selective than electrical synapses, as they allow for the precise targeting of specific postsynaptic neurons. Electrical synapses are less selective, as they allow for the direct transmission of signals between all coupled neurons.
  9. Frequency dependence: Chemical synapses are frequency-dependent, meaning that the strength of the synaptic transmission can be modulated by the frequency of action potentials in the presynaptic neuron. Electrical synapses are not frequency-dependent.
191
Q

what are some properties of chemical synapse

A

👉They involve the release of neurotransmitters from the presynaptic neuron into the synaptic cleft.
👉The neurotransmitters bind to specific receptors on the postsynaptic neuron, leading to changes in its membrane potential.
👉The strength of the synaptic connection can be modified through a process called synaptic plasticity, which can be either long-term potentiation (LTP) or long-term depression (LTD).
👉The release of neurotransmitters can be modulated by various factors, including other neurons, hormones, and drugs.
👉Conduction of impulses is in one direction (unidirectional)
👉The speed and reliability of signal transmission can be influenced by factors such as the distance between neurons, the number of synapses involved, and the properties of the neurotransmitter receptors.

192
Q

what are some properties of electrical synapse

A

👉They involve the direct flow of ions (such as sodium, potassium, and calcium) from the presynaptic neuron to the postsynaptic neuron through gap junctions.
👉Impulse conduction is bi-directional
👉The transmission of signals through electrical synapses is very fast and reliable, with little to no delay or distortion.
👉Electrical synapses are often found in areas of the brain and body where rapid and synchronized activity is needed, such as in reflex circuits and cardiac muscle cells.
👉Unlike chemical synapses, the strength of electrical synapses is not modifiable through synaptic plasticity.
👉The direction of signal flow through electrical synapses can be bidirectional, meaning that signals can be transmitted in both directions between neurons.

193
Q

describe the presynaptic terminal

A

the swollen axon terminal has two important structures:
i. Mitochondria, which help in the synthesis of
neurotransmitter substance
ii. Synaptic vesicles, which store neurotransmitter
substance.

194
Q

describe the postsynaptic terminal

A
  • comprises of receptors and
    -enzymes that assist in degradation of the neurotransmitters.
195
Q

outline the steps to neurotransmitter release

A

👉Vesicles lie “docked” near the presynaptic membrane
👉The arrival of an action potential at the axon terminal opens voltage-dependent Ca++ channels
👉Ca++ ions flow into the axon
👉Ca++ ions change the structure of the proteins that bind the vesicles to the presynaptic membrane
👉A fusion pore is opened, which results in the merging of the vesicular and presynaptic membranes
👉The vesicles release their contents (neurotransmitters) into the synapse by exocytosis
👉Released transmitter then diffuses across cleft to interact with postsynaptic membrane receptors

196
Q

comment on the postsynaptic receptors

A

-Molecules of neurotransmitter (NT) bind to receptors located on the postsynaptic membrane
-Receptor activation opens postsynaptic ion channels
-Ions flow through the membrane, producing either depolarization or hyperpolarization
-The resulting postsynaptic potential (PSP) depends on which ion channel is opened

197
Q

opening of the Na+ ion channel results in

A

Excitatory Postsynaptic Potential

198
Q

opening of Cl- ion channel results in

A

Inhibitory Postsynaptic potential

199
Q

opening of K+ ion channel results in

A

Inhibitory postsynaptic potential

200
Q

opening of Ca2+ ion channel results in

A

neurotransmitter release

201
Q

comment on postsynaptic potentials

A

-PSPs are either excitatory (EPSP) or inhibitory (IPSP)
-Opening Na+ ion channels results in an EPSP
-Opening K+ ion channels results in an IPSP
-PSPs are conducted down the neuron membrane
-Neural integration involves the algebraic summation of PSPs
-A predominance of EPSPs at the axon will result in an action potential
-If the summated PSPs do not drive the axon membrane past threshold, no action potential will occur

202
Q

comment on epsp

A

-A depolarizing graded post-synaptic voltage change increases the probability that the post-synaptic neuron will generate an action potential and therefore is called an Excitatory Post-Synaptic Potential (EPSP).

-Synaptic activation of
=>Ach-gated and
=>glutamate gated ion channels causes EPSPs.

Outlined steps have already been stated man

203
Q

comment on ipsp

A

-A graded post synaptic voltage change that results in a hyperpolarization of the post-synaptic membrane, making the post-synaptic neuron less likely to generate an action potential and therefore less excitable, is called an Inhibitory Post-Synaptic Potential (IPSP).

-Synaptic activation of
=>glycine-gated or
=>GABA-gated ion channels cause an IPSP.

outlined steps have already been stated man

204
Q

comment on termination of postsynaptic potentials

A

-The binding of NT to postsynaptic receptor results in a postsynaptic potential
-Termination of PSPs is accomplished via
=>Reuptake: the NT molecule is transported back into the cytoplasm of the presynaptic membrane to be reused
=>Enzymatic deactivation: an enzyme destroys the NT molecule

205
Q

list the inhibitory NT’s

A

-GABA
-Glycine

206
Q

list 7 excitatory NT’s

A

-Acetylcholine
-Aspartate
-Dopamine
-Histamine
-Norepinephrine
-Epinephrine
-Glutamate

207
Q

what are the properties of NT’s

A
  1. They are chemical messengers that transmit signals between neurons and other cells.
  2. They are synthesized and packaged within the presynaptic neuron.
  3. They are released into the synaptic cleft in response to an action potential.
  4. They bind to their specific receptors on the postsynaptic neuron or other target cell.
  5. The binding of neurotransmitters to receptors can lead to changes in the membrane potential of the target cell, which can either excite or inhibit its activity.
  6. The effects of neurotransmitters on the target cell can be modulated by various factors, including the type and number of receptors present, the concentration of neurotransmitters in the synaptic cleft, and the presence of other molecules that can affect receptor activity.
  7. The activity of neurotransmitters can be terminated by various mechanisms, including reuptake into the presynaptic neuron, enzymatic degradation, and diffusion away from the synapse.
  8. Different neurotransmitters can have different effects on the same target cell, depending on the type and distribution of receptors present.
  9. Some neurotransmitters can also act as neuromodulators, which can modulate the activity of other neurons or synaptic connections e.g dopamine, serotonin, acetylcholine, and norepinephrine.
208
Q

where is acetylcholine produced

A

CNS and Parasympathetic nerves

209
Q

what is acetylcholine derived from

A

choline

210
Q

what is Serotonin5-Hydroxytryptamine (5-HT) derived from

A

Tryptophan

211
Q

where is Serotonin5-Hydroxytryptamine (5-HT) produced

A

-CNS,
-Chromaffin cells of the gut,
-Enteric cells

212
Q

Where is GABA produced

A

CNS

213
Q

WHAT is GABA derived from

A

glutamate

214
Q

what is histamine derived from

A

histidine

215
Q

where is histamine derived from

A

hypothalamus

216
Q

where is histamine derived from

A

hypothalamus

217
Q

what is Epinephrine derived from

A

tyrosine

218
Q

what is norepinephrine derived from

A

tyrosine

219
Q

where is epinephrine produced from

A

-adrenal medulla,
-some CNS cells

220
Q

where is norepinephrine produced from

A

-CNS,
-sympathetic nerves

221
Q

where is dopamine produced from

A

CNS (dopaminergic neurons on substantia nigra)

222
Q

what is dopamine derived from

A

tyrosine

223
Q

what is Nitric oxide derived from

A

arginine

224
Q

where is Nitric oxide produced

A

-CNS
-GIT

225
Q

outline the steps to a synapse

A

-action potential arrives at axon terminal
-voltage gated Ca2+ channels open
-Ca2+ enters the cell
-Ca2+ signals the vesicles
-vesicles move to the membrane
-docked vesicles release neurotransmitter by exocytosis
-neurotransmitter diffuses across the synaptic cleft and bind to receptors of the postsynaptic terminal
-binding of the neurotransmitter to receptor, activates signal transduction pathways

226
Q

draw a proper diagram to show the process of a synapse

A

check your book

227
Q

draw a proper diagram to show the process of synapse with Ach as the neurotransmitter

A

check your book

228
Q

outline the steps to a synapse with acetylcholine

A
  • acetyl-CoA is synthesized in the mitochondria
  • choline acetyltransferase catalyzes the conversion of choline and acetyl-CoA
  • The Ach is packaged into synaptic vesicles
  • Ach is released into the synaptic cleft
  • Ach binds to its receptor on the postsynaptic cell
  • Acetylcholinesterase breaks down choline and acetate, terminating the signal in the postsynaptic cell.
  • The presynaptic cell takes up and recycles the choline, and the acetate diffuses out of the synapse
229
Q

significance of synaptic inhibition

A

-Synaptic inhibition in CNS limits the number of impulses
going to muscles and enables the muscles to act
properly and appropriately.

-Thus, the inhibition helps to select exact number of impulses and to omit or block the excess ones.

-When a poison like strychnine is introduced into the body, it destroys the inhibitory function at synaptic level resulting in continuous and
convulsive contraction even with slight stimulation.

-In the nervous disorders like parkinsonism, the inhibitory
system is impaired resulting in rigidity.

230
Q

What is summation

A

-Summation is the fusion of effects or progressive increase in the excitatory postsynaptic potential in post ­
synaptic neuron when many presynaptic excitatory
terminals are stimulated simultaneously or when single
presynaptic terminal is stimulated repeatedly.
-Increased
EPSP triggers the axon potential in the initial segment
of axon of postsynaptic neuron

231
Q

What factors affect the strength of transmission of the synapse at the postsynaptic terminal

A
  1. Neurotransmitter availability: The amount of neurotransmitter released by the presynaptic neuron affects the strength of the synapse. The more neurotransmitter released, the stronger the synapse.
  2. Receptor density: The number of receptors on the postsynaptic membrane can affect the strength of the synapse. The more receptors there are, the stronger the response to the neurotransmitter.
  3. Receptor affinity: The affinity of the receptors for the neurotransmitter can affect the strength of the synapse. High-affinity receptors will respond more strongly to the same amount of neurotransmitter.
  4. Presynaptic activity: The frequency and timing of action potentials in the presynaptic neuron can affect the strength of the synapse. High-frequency stimulation can lead to stronger synaptic responses.
  5. Postsynaptic potential: The current state of the postsynaptic neuron can affect the strength of the synapse. If the neuron is already depolarized, it may be more difficult to induce an action potential.
  6. Neuromodulators: Other chemicals in the synaptic cleft, such as neuromodulators, can affect the strength of the synapse by either enhancing or inhibiting the response to the neurotransmitter.
  7. Calcium concentration: The concentration of calcium ions in the presynaptic terminal can affect the strength of the synapse. Calcium influx is required for the release of neurotransmitter.
  8. Distance from the synapse: The distance between the synapse and the postsynaptic terminal can affect the strength of the synapse. The further away the synapse, the weaker the response.
  9. Glial cells: Glial cells can affect the strength of the synapse by regulating neurotransmitter levels and receptor expression.
  10. Aging: The strength of synapses can decline with age, leading to decreased cognitive function and memory.
232
Q

The amount of neurotransmitter remaining in the synaptic cleft is determined by

A

Rate of release -(minus) rate of removal

233
Q

Comment on the rate of release is determined by

A

Release determined by frequency of APs

234
Q

Comment on the rate of removal

A

Removal determined by:
-Passive diffusion out of synapse
-Degradation by synaptic enzymes
-Uptake by surrounding cells

235
Q

What is a synaptic delay

A

Synaptic delay is a short delay that occurs during the
transmission of impulses through the synapse. It is due
to the time taken for:
i. Release of neurotransmitter
ii. Passage of neurotransmitter from axon terminal
to postsynaptic membrane
iii. Action of the neurotransmitter to open the ionic
channels in postsynaptic membrane.
Normal duration of synaptic delay is 0.3 to 0.5
millisecond. Synaptic delay is one of the causes for
reaction time of reflex activity.