Neurophysiology: Neurons And ANS Flashcards

1
Q

who developed the NIssl stain

A

German neurologist Franz Nissl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

when was the nissl stain eveloped

A

late 19th century

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

who developed the golgi stain

A

Camillo golgi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

when was the golgi stain developed

A

1873

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

the golgi stain was developed from»>

A

silver reagents used in photography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

whose research brought about the neuron doctrine

A

Santiago Ramon Y. Cajal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when was the neuron doctrine brought

A

1939

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

when did golgi and cajal win the noble prize

A

1906

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

the brains are composed of 2 cell types

A

-Neurons
-Glial cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the glial cells of the CNS

A

-Astrocytes
-Oligodendrocytes
-Ependymal cells
-Microglia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are the glial cells of the PNS

A

-Schwann cells
-satellite cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are the oligodendrocytes

A

They myelinate the axons of the CNS and provide structural framework

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what are the microglial cells

A

Remove cell debris, wastes and pathogens by phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Draw a neuron

A

check the book.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are the differences between the neuron and the common cell
-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
26
comment on the microtubules of a neuron
they are 20nm, made of a polymer protein called tubulin
27
comment on neurofilaments
they are 10nm, made of glial fibrillary acidic protein
28
comment on microfilaments
they are 5nm, made of protein actin
29
comment on the dendrites
👉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.
30
comment on the axons
👉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
31
comment on alzheimers disease
👉 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)
32
who first described Alzheimer's diseases
It was first described in 1907 by the German physician A. Alzheimer.
33
what year was alzheimer's discovered
1907
34
by 2030, how many people are projected to have alzheimer's
14million
35
why is norepinephrine production affected in alzheimer's disease
locus ceruleus degenration
36
why is acetylcholine production affected in alzheimer's disease
the enzyme choline acetyltransferase
37
acording to the number of dendrites and axons, what are te classes of neurons
👉Unipolar 👉Bipolar 👉multipolar 👉pseudounipolar
38
draw the 4 types of neurons (according to number of dendrites/axons)
check your booklet
39
comment on unipolar neurons
👉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.
40
are there unipolar neurons in human
no
41
what neurons are in human, instead of unipolar neurons
pseudounipolar neuron
42
what is a pseudounipolar neuron
👉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.
43
where is the pseudounipolar neuron seen
dorsal root ganglia of the spinal cord
44
comment on the bipolar neuron
👉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
45
comment on multipolar neurons
👉they have numerous poles, 👉one gives rise to the axon, many others give rise to the dendrites
46
based on function, what are the classifications of neurons
👉Afferent (sensory) neurons 👉Efferent (motor) neurons 👉Interneurons
47
comment on interneurons
👉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
48
comment on efferent (motor neurons)
👉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.
49
comment on the afferent (sensory neurons)
👉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
50
draw a diagram to show the classification of neurons (according to function)
check the book
51
what is voltage
It is the measure of potential energy between two points generated by a charge separation
52
what is membrane potential
It is the voltage difference between the inside and outside of a cell
53
what is resting membrane potential
👉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
54
what are the causes of resting membrane potential
👉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
55
80% of resting membrane potential is attributed to:
👉80% caused by selective permeability of the cell membrane to K+
56
20% to resting membrane potential is attributed to:
Na+/K+ pump
57
what keeps Na/K concentrations different across the cell
the sodium/potassium pump which is dependent on ATP
58
when the electrode is outside the cell, the record reference potential is recorded as
0mV
59
when the electrode is in the cell, the record reference potential is
it drops to -70mV (resting membrane potential)
60
what is equilibrium potential
it is the membrane potential that exactly opposes the concentration of the ion that the cell is permeable to. Eion = ENa, ECl, EK .
61
so, for instance, what would potassium equilibrium potential be defined as
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+
62
equilibrium is calculated using:
👉Nernst equation 👉Goldman equation
63
what is the equilibrium potential of sodium
+60mV
64
what is the equilibrium potential of potassium
-90mV
65
What ion drives resting membrane potential
Potassium (K+)
66
What is Nernst equation used for
👉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
67
state the nernst equation
E = (61/z) * log([ion]outside/[ion]inside)
68
what does the value of 61 in nernst equation mean
The value 61 in the Nernst equation refers to the constant (RT/zF) at room temperature (25°C
69
what is Goldman's equation used for
👉Used to calculate overall membrane potential when multiple ions are involved. 👉Incorporates permeability of each ion.
70
state the goldmans equation
Em = (60mV * log((P[K+]o + P[Na+]o + P[Cl-]i) / (P[K+]i + P[Na+]i + P[Cl-]o)) -Em= membrane potential
71
What would happen to the resting membrane potential of a cell poisoned with a substance, that is an inhibitor of the Na –K – ATPase
👉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.
72
comment on the concept of excitability
👉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
73
what cells exhibit excitability
👉all neirons 👉muscle cells 👉some endocrine cells (e.g beta cells of the islets of langerhans) 👉some immune cells 👉some reproductive cells
74
what are the 2 forms that excitability occurs
👉action potential 👉graded potential
75
give 10 differences between graded potential and action potential
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.
76
does the graded potential summate?
yes, but action potential doesn't
77
do graded potentials last longer than action potential?
yes they do, depending on the strength of the stimulus. action potentials are only for a few milliseconds
78
do action potentials travel in any direction
no they don't, they only travel down the axon. graded potentials though travel in any direction
79
do graded potentials have a fixed amplitude
no they don't, their amplitude depends on their distance to the cell body. it ios action potential that has a fixed amplitude
80
do graded potentials have a refractory period
no they don't, that is action potential. graded potentials can be generated repeatedly
81
do graded potentials have a specific threshold
no they don't, they can be transmitted by any strength of stimulus. Action potentials though have a threshold
82
are graded potentials generated in the axonal hillock only
nahh fam, that is action potential. graded potentials are generated anywhere on the neuron (dendrites, cell body, axon)
83
what are the major factors contributing to membrane potential
👉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.
84
comment on the 'concentration of ions across the membrane' factor that contributes to membrane potential
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.
85
comment on 'membrane permeability to these ions' factor that contributes to membrane potential
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.
86
what does it mean to say that a membrane is depolarized
The membrane is depolarized when its potential becomes less negative i.e more positive (closer to zero) than the resting level.
87
what is an overshoot
Overshoot refers to a reversal of the membrane potential polarity, that is when the inside of a cell becomes positive relative to the outside
88
what is repolarization
When a membrane potential that has been depolarized is returning toward the resting value, it is repolarizing
89
what is hyperpolarization
The membrane is hyperpolarized when the potential is more negative than the resting level.
90
a large stimulus on graded potential will...
create a strong graded potential
91
a small stimulus on graded potential will
create a weak graded potential
92
what is graded potential
👉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)
93
List some types abi examples of graded potentials
1. End plate potential in neuromuscular junction 2. Electronic potential in nerve fibers 3. Receptor potential 4. Excitatory postsynaptic potential 5. Inhibitory postsynaptic potential
94
what is end plate potential in a neuromuscular junction
👉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.
95
what factors affect the magnitude of the end plate potential
-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
what is the usually amplitude of the end plate potential
40-50mV
97
what is electric potential in nerve fibers
👉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
what is the implication of the changes of electric potential
-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
what is receptor potential
👉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
what other graded potentials is receptor potential similar to?
👉excitatory postsynaptic potential (EPSP) in synapse, 👉endplate potential in neuromuscular junction and \ 👉electrotonic potential in the nerve fiber.
101
receptor potential responds to stimulus from
-mechanoreceptors -nociceptors -thermoreceptors -chemoreceptors -electromagnetic receptors(vision)
102
what are the properties of receptor potential
-Receptor potential is non­propagated; it is confined within the receptor itself -It does not obey all­ or ­none law.
103
draw a diagram to explain receptor potential
check the booklet
104
what is the 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.
105
what are the similarities between graded potential and action potential
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
What is an excitatory postsynaptic potential
Excitatory postsynaptic potential (EPSP) is the non-propagated electrical potential that develops during the process of synaptic transmission
107
what are the steps for the development of excitatory postsynaptic potential
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
what are the steps for the development of excitatory postsynaptic potential
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
what other graded potentials is excitatory postsynaptic potential similar to?
-receptor potential -endplate potential.
110
what are the properties of excitatory postsynaptic potential
1. It is non­propagated 2. It does not obey all­or­none law.
111
what is the significance of excitatory postsynaptic potential
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
what is inhibitory postsynaptic potential
Inhibitory postsynaptic potential (IPSP) is the electrical potential in the form of hyperpolarization that develops during postsynaptic inhibition
113
what are the steps for the development of inhibitory postsynaptic potential
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
pacemaker cell exhibit what kind of graded potential
pacemaker potential
115
outline the steps for a pacemaker potential
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
what are some properties of graded potential
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
what is action potential
An AP is a regenerating depolarization of membrane potential that propagates (conducted without decrement) along an excitable tissue capable of action potential
118
The threshold of most excitable membranes is about ___mV less negative than the RMP
15mV
119
btw what is excitability
Excitability is defined as the physiochemical change that occurs in a tissue when stimulus is applied.
120
the local membrane is brought to threshold voltage by
depolarizing stimulus
121
what is the threshold potential of a neuron
-55mV
122
draw a diagram to show action potential
check the book
123
what are the differences between action potential in muscle and in neurons
👉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
outline the process of action potential
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
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?
👉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
what are voltage-gated channels
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
what diseases could be caused by a mutation of the voltage gated channels
Mutations in voltage-gated channels can lead to a range of neurological and neuromuscular disorders, including epilepsy, migraine, and myotonia.
128
what voltage-gated channels open first
Na+
129
voltage gated channels are important for physiological processes like
-muscle contraction, -hormone secretion, and -sensory perception.
130
what volatge gated channel is responsible for depolarization
Na+ volatge gated channels
131
what voltage gated channel is responsible for repolarization
K+ voltage gated channels
132
what volatge gated channel is responsible for refractory period
K+ volatge channels
133
what is the function of Ca2+ voltage gated channels
neurotransmitter release
134
explain the propagation of the action potential
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
btw what are some factors that inhibit Na+ permeability in the cell
-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
draw a diagram to show the action of Na+ voltage gated channels
check the book
137
draw a diagram to show the action of K+ voltage gated channels
check the book
138
draw a diagram to show the action of K+ voltage gated channels
check the book
139
draw a diagram to show the 'extra depolarization' of action potential propagation
check the book
140
what is saltatory conduction
👉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
what are the 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
142
draw a diagram to explain saltatory conduction
check your book
143
what are some applications of AP
-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
explain the 'local anaesthetic' application of the AP
-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
what drugs prevent the generation of AP's as an anesthetic
-procaine -lidocaine
146
how do the drugs that prevent AP generation work
these drugs block voltage-gated Na+ channels, preventing them from opening in response to depolarization
147
what part does AP have to play in sensations to the brain
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
comment on the production of toxins by animals which block AP.
-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
what toxin does the pufferfish secrete that blocks AP
Tetrodotoxin, binds to voltage-gated Na+ channels and prevents the Na+ component of the AP
150
outline properties of AP
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
what is the latent period of a nerve
it is a period corresponding to the time taken from the site of stimulation till the recording electrode.
152
what is the all-or-none law
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
what is refractory period
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
what is absolute refractory period
-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
what is relative refractory period
-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
what are the significance/ uses of the refractory periods
-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
what causes relative refractory period
is due to the slow recovery of potassium channels and the continued hyperpolarization of the membrane potential.
158
what causes absolute refractory period
is due to the inactivation of sodium channels and the slow recovery of potassium channels
159
explain how refractory period helps the AP travel in only one direction
-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
Functions of Action potentials
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
The velocity at which an AP propagates down the axon is dependent on...
👉the diameter of the axon 👉if the axon is myelinated or not
162
A larger diameter fibre will propagate faster?
👉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
Why will a larger diameter fibre propagate faster
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
What are the downsides of large diameter fibre
👉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
Give a comparison between neurons that shows the importance of myelin
a 6mm diameter myelinated axon has the same velocity as a 500mm unmyelinated axon
166
How many times bigger does an unmyelinated axon need to get to conduct with the same velocity of a myelinated axon
83X
167
What is myelin
👉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
Functions of myelin
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
What is a demyelinating disease
👉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
Comment on multiple sclerosis
👉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
Cause of multiple sclerosis
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
What are the signs and symptoms of multiple sclerosis
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
What are the common initial symptoms of MS
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
What are the progressive symptoms of MS
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
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.
Large diameter myelinated fibres
176
Who discovered the synapse
Charles Sherrington near the end of the 19th century.
177
What's the length of a synapse
20-30 nM
178
What is a synapse
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
What are the 2 major classifications of the synapse
👉 Anatomical classification 👉 Physiological classification
180
What is the anatomical classification of the synapse
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
What are some similar 'synapse like junctions
Autoreceptors Neuromuscular junction Neuroendocrine/Neurosecetory junction
182
What is the functional classification of the synapse
Functional classification of synapse is on the basis of mode of impulse transmission 1. Electrical synapse 2. Chemical synapse
183
draw diagrams for the anatomical classification of the synapse
check the book
184
what is an electrical synapse
👉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
draw a diagram to show the electric synapse
check the book
186
what is a chemical synapse
👉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
draw a chemical synapse
check your book
188
comment on the synchronization property of the electrical potential
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
who won the nobel prize for discovering neurotransmitters
Otto Loewi and Sir Henry Dale, 1936
190
what are the differences between chemical synapses and electrical synapses
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
what are some properties of chemical synapse
👉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
what are some properties of electrical synapse
👉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
describe the presynaptic terminal
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
describe the postsynaptic terminal
- comprises of receptors and -enzymes that assist in degradation of the neurotransmitters.
195
outline the steps to neurotransmitter release
👉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
comment on the postsynaptic receptors
-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
opening of the Na+ ion channel results in
Excitatory Postsynaptic Potential
198
opening of Cl- ion channel results in
Inhibitory Postsynaptic potential
199
opening of K+ ion channel results in
Inhibitory postsynaptic potential
200
opening of Ca2+ ion channel results in
neurotransmitter release
201
comment on postsynaptic potentials
-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
comment on epsp
-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
comment on ipsp
-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
comment on termination of postsynaptic potentials
-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
list the inhibitory NT's
-GABA -Glycine
206
list 7 excitatory NT's
-Acetylcholine -Aspartate -Dopamine -Histamine -Norepinephrine -Epinephrine -Glutamate
207
what are the properties of NT's
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
where is acetylcholine produced
CNS and Parasympathetic nerves
209
what is acetylcholine derived from
choline
210
what is Serotonin5-Hydroxytryptamine (5-HT) derived from
Tryptophan
211
where is Serotonin5-Hydroxytryptamine (5-HT) produced
-CNS, -Chromaffin cells of the gut, -Enteric cells
212
Where is GABA produced
CNS
213
WHAT is GABA derived from
glutamate
214
what is histamine derived from
histidine
215
where is histamine derived from
hypothalamus
216
where is histamine derived from
hypothalamus
217
what is Epinephrine derived from
tyrosine
218
what is norepinephrine derived from
tyrosine
219
where is epinephrine produced from
-adrenal medulla, -some CNS cells
220
where is norepinephrine produced from
-CNS, -sympathetic nerves
221
where is dopamine produced from
CNS (dopaminergic neurons on substantia nigra)
222
what is dopamine derived from
tyrosine
223
what is Nitric oxide derived from
arginine
224
where is Nitric oxide produced
-CNS -GIT
225
outline the steps to a synapse
-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
draw a proper diagram to show the process of a synapse
check your book
227
draw a proper diagram to show the process of synapse with Ach as the neurotransmitter
check your book
228
outline the steps to a synapse with acetylcholine
- 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
significance of synaptic inhibition
-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
What is summation
-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
What factors affect the strength of transmission of the synapse at the postsynaptic terminal
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
The amount of neurotransmitter remaining in the synaptic cleft is determined by
Rate of release -(minus) rate of removal
233
Comment on the rate of release is determined by
Release determined by frequency of APs
234
Comment on the rate of removal
Removal determined by: -Passive diffusion out of synapse -Degradation by synaptic enzymes -Uptake by surrounding cells
235
What is a synaptic delay
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.