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Bio 465 - Physio > Chapter 7 - The Nervous System > Flashcards

Chapter 7 - The Nervous System Flashcards

1
Q

What is the main difference between the Central Nervous System (CNS) and Peripheral Nervous System (PNS)?

A
  • The CNS consists of the brain and spinal cord
  • The PNS consists of the cranial nerves arising from the brain, and the spinal nerves arising from the spinal cord.
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2
Q

What is a “Nissl Body?”

A
  • Located within the cell body of nuerons, and are composed of large stacks of rough endoplasmic reticulum that are needed for the synthesis of membrane protiens.
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3
Q

Which neuron transmits impulses from the CNS to an effector organ, like a muscle?

A

Efferent neuron (Motor Neuron)

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4
Q

Which neuron transmits impulses from a sensory receptor into the CNS?

A

Afferent Neuron (sensory neuron)

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5
Q

What are interneurons?

A
  1. also called Association Neurons
  2. located entirely within the CNS and serve the associative, or integrative, functions of the nervous system
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6
Q

What are the 2 types of motor neurons?

A

Somatic

Autonomic

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7
Q

Somatic Neurons innervate…?

A

skeletal muscles, or muscles we can voluntarily control

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8
Q

Autonomic Neurons innervate…?

A
  • involuntary effectors
    • smooth muscles, cardiac muscles, glands
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9
Q

What are the 2 subdivisions of autonomic nerves?

A

Sympathetic

parasympathetic

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10
Q

Why are sensory neurons considered - Pseudounipolar?

A
  • Technically sensory neurons originate with 2 processes - one receiving stimuli and creatig nerve impulses and one taking the message to the CNS
  • Even though they are branched from the cell body, the 2 processes act as one long axon continuously conducting actino potentials
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11
Q

What are bipolar neurons?

A
  • The have a process at either end of the cell body
  • Normally found in the retine
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12
Q

What are multipolar neurons?

A
  • Have several dendrites and one axon extending away from the cell body
  • Example - motor neurons
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13
Q

What are the 2 types of neuroglia (glial) cells in the PNS?

A
  1. Schwann Cells (neurolemmocyte) - form myelin sheath around peripheral axons
  2. Satellite Cells (or ganglionic gliocytes) - support neuron cell bodies within the ganglia of the PNS
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14
Q

What are the 4 types of neuroglial cells in the CNS?

A
  1. Oligodendrocytes - form myelin sheath around axons of CNS
  2. Microglia - migrate through CNS and phagocytose foreign and degenerated material
  3. Astrocyte - help regulate the external environment of neurons in the CNS
  4. Ependymal Cells - epithelial cells that line the ventricles (Cavities) of the brain and central canal of the Spinal cord
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15
Q

What are some of the functions of microglia?

A
  • kill exogenous pathogens
  • remove damaged dendrites, axon terminals, myelin and other debris within CNS
  • release anti inflammatory chemicals
  • Overactive microglia can release free radicals…can contribute to neurodegenerative diseases.
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16
Q

Which type of axon will usually receive a myelin sheath?

A
  • larger axons.
  • Axons smaller than 2 micrometers are usually unmyelinated
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17
Q

Are unmyelinated axons still surrounded by neurilemma?

A

Yes, even unmyelinated axons are surround by neurilemma. They just do not have the multiple wrappings of Schwann cells and their plasma membrane - creating the myelin sheath.

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18
Q

Describe the difference between white matter and grey matter in the CNS.

A
  1. White matter - portions of the CNS where there is a higher concentration of oligodendrocytes creating myelin sheaths around the Axons
  2. Grey matter - composed of high concentrations of cell bodies and dendrites, which lack myelin sheaths
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19
Q

These proteins, produced predominantly by oligodendrocytes, inhibit axon regeneration in the CNS…?

A

Nogo proteins

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20
Q

This neurotrophin is a regulatory molecule produced by neurons that promotes the survival and growth of sympathetic and sensory neurons in teh developing fetal brain….

A

NGF - nerve growth factor

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21
Q

What are some of the roles of neurotrophins?

  1. maintenance of [] ganglia
  2. mature sensory neurons to [] after injury
  3. Regulate the survival and [] of adult neural stem cells in part of the brain in volved in learning and []
A
  1. In adult nervous system
    1. sympathetic
    2. regenerate
    3. differntiation, memory
      • growth of dendrites, axons, formation of synapses and synaptic change during learning
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22
Q

Which is the most abundant glial cell in the CNS?

A

Astrocyte

(90% of nervous tissue in some areas of the brain)

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23
Q

How can an increase Ca2+ caused by neuronic APs, increase blood flow to the brain? (Hint - Astrocytes involved)

A
  • Rise in Ca2+ promotes the production of prostaglandin E2 , which is released from an Astrocyte surrounding cerebral blood vessels and stimulates vasodillation.
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24
Q

What is neuron-glia crosstalk?

A
  • Action potentials in neurons can provoke a rise in Ca2+ within a localized region of an astrocyte, which in turn stimulates the release of ATP and other gliotransmitters that affect the synaptic transmission of neurons
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25
Q

How are molecules within brain capillaries moved through the endothelial cells? Why is this the case?

A
  1. Diffusion, active transport, endocytosis, and exocytosis
  2. Endothelial cells of the brain are not connected to adjecent cells by pores…but by tight junctions. This creates the blood-brain barrier.
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26
Q

How does plasma glucose enter the brain?

A

The carrier protein GLUT1.

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27
Q

How are the endothelial cells of the brain and the astrocytes interconnected?

A
  • Astrocytes secrete molecules to stimulate the endothelial cells to produce the proteins of the tight junctions - holding the blood-brain barrier together
    • also stimulate the production of the proteins of carriers, ion channels, and enzymes that destory toxic molecules
  • Endothelial cells in-turn secrete regulators that promote the growth and differentiation of astrocytes.
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28
Q

Do all cells have the same RMP? What is a neurons RMP?

A
  1. no
  2. -70 mV
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29
Q

What are the 3 main causes of the RMP, listed in order of influence?

A
  1. Permeability of membranes to K+ / Na+ (K+ more!)
  2. Na+/K+ Pumps
  3. Negatively charged anions in the cytoplasm pull cations in, if possible
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30
Q

If (+) ions flood into a cell, the membrane potential will become more positive…this is called

A

Depolarization (hypopolarization)

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31
Q

What is caused if (-) ions were to rush into a cell?

A

hyperpolarization

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32
Q

Does depolarization excite or inhibit? Why?

A
  • Depolarization excites a dendrite or cell body because it causes the RMP to become more positive…trying to reach that -55 threshold to hit an action potential!! EXCITING!
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33
Q

What are the three states of the ion channels in Axons?

A
  1. Closed - resting membrane potential
  2. Open - depolarization
  3. Inactive - refractory period
34
Q

Depolarization to a threhold level on an axon causes which ion gates to open first?

A

Na+

35
Q

What are the Na+ and K+ ion channels considered to be voltage-gated?

A
  1. They are open/closed in response to specific membrane potentials
    1. Closed at -70mV
    2. Open in responde to a depolarization to threshold (-55 mV usually)
36
Q

In terms of axon action potentials - which molecule’s movement produces positive/negative feedback?

A
  • The inflow of Na+ produces a depolarization which causes more Na+ to flow in momentarily….positive feedback
  • The outflow of K+ causes the initial depolarization to repolarize…negative feedback
37
Q

How does a neuron return to RMP after a depolarization?

A
  • Repolarization - K+ voltage-gated channels open allowing K+ to rush out of the cell. Making the inside of the cell more negative again and returning it to the -70 mV RMP
38
Q

How can a stronger stimulus increase the frequency of action potentials?

A
  • 1 single action potential is triggered if the stimulus meets the depolarization threshold
  • However, different stimuli can effect different types of axons in a nerve. So a “lighter” stimuli may recruit axons with lower thresholds.
  • Therefore, a strong stimulus will recruit all of the types of axons in a nerve.
39
Q

The strength of a stimulus will result in a weak or stronger action potential?

A
  1. Neither
  2. The strength of the stimulus does not create a stronger stimulus. The strength of the stimulus will recruit more and more axons, firing action potentials. This will lead to an increased number of action potentials and greater reaction to the stimulus.
40
Q

Why does the action potential at the end of an axon have a lower amplitude than the action potential that started the “wave” of action potentials?

A
  • This question is false to begin with. APs at the end of an axon have the same amplitude as the AP that started everything.
  • This is referred to as conducted without decrement (
41
Q

What 2 properties increase the speed of action potential?

A
  • Increased axon diameter
  • Myelination
42
Q

What is an example of a neuromuscular junction?

A

The connection between a neuron from the PNS - and the possibly another neuron, or an effector cell within a muscle or gland

43
Q

How can two cells communicate electrically, instead of chemically through neurotransmitters?

A
  • If they are connected via gap junctions
  • Each cells plasma membrane has half of the junction, hemichannel. When joined it become the gap junction
    • allows ions and molecules to pass from one cell to another.
  • Found in cardiac cells/smooth cells…so everything can ctonract together.
44
Q

Which proteins found in the pre and post-synaptic clefts bind to each other, essentially holding the cleft together?

A

Cell Adhesion Molecules (CAMs)

45
Q

For neurotransmitters to be released, Action Potentials must stimulate the exit of Ca2+ out of the axon terminal through Na/Ca pumps. T/F?

A

False - action potentials stimulate the entry of Ca2+ INTO the axon terminal through voltage-gated Ca2+ channels.

46
Q

How are receptor proteins in a post-synaptic cell chemically regulated?

A
  • These gates only open/respond when bound to a specific ligand - the neurotransmitter
47
Q

Fill in the Blank

  • Voltage-gated channels open in response to a []
  • Chemically regulated channels open in response to the binding of a [] receptor proteins to their neurotransmitter []
A
  1. depolarization
  2. postsynaptic, ligand
48
Q

How is a graded potential formed?

A
  • Triggered by either EPSP or IPSP
49
Q

What causes and EPSP to produce a graded potential?

A
  • The EPSP is an excitatory postsynaptic potential caused by the opening of specific channels - like Na+ and Ca2+ that make the inside of the cell more positive
50
Q

What causes and IPSP to produce a graded potential?

A
  • The IPSP is an - inhibitory postsynaptic potential caused by channels that allow, for example, Cl- to enter into the cell. Making the inside of the cell more negative…or inhibiting it from reaching the threshold needed for an action potential
51
Q

Where are IPSP and EPSP started and where do they end?

A

Started in the dendrites of a post-synaptic cell and end in that cell’s Axon Hillock…or more specifically the axon initial segment

52
Q

How can Acetylcholine (ACh) be used as an IPSP and an EPSP?

A
  1. Excitatory neurotransmitter - in CNS and by somatic motor neurons at neuromuscular junctions
  2. Excitatory or inhibitory - at autonomic nerve endings…..depending on the organ invovled.
53
Q

What are the 2 types of Cholinergic Receptors?

A
  1. Nicotinic ACh receptors
  2. Muscarinic ACh receptors
54
Q

What are typical places to find Nicotinic ACh Receptors? What do these control?

A
  • Regions of the brain, Autonomic ganglia,
  • Skeletal muscle fibers
    • stimulate skeletal muscle contraction
55
Q

Where do you typically find Muscarinic ACh receptors? What do they do?

A
  • plasma membrane of smooth muscle cells, cardiac muscle cells, and cells of particular glands.
  • required for regulation of cardio vascular system, digestive system, and other systems.
56
Q

How does the binding of ACh to its nicotinic ACH receptor effect the polarization of the post synaptic cell?

A
  • Since the binding of ACh to its nicotinic receptr opens the channel for Na+ to rush in and K+ to rush out…the cell depolarizes due to Na+ having a steeper electrochemical gradient.
57
Q

If a Nicotinic receptor opens, causing an EPSP, will the cell need to repolarize through inactivation?

A

No….EPSPs do not have a refractory period….so they can be graded.

58
Q

How are muscarinic ACh receptors different than nicotinic receptors?

A
  • Muscarinic
    • only binds to 1 molecule of ACh
    • do not contain ion channels
      • Ion channels are seperate proteins
    • binding of ACH to muscarinic receptor causes it to activate complex of proteins in membrane known as G-proteins.
59
Q

What is an example of the Alpha subunit, of G-proteins, binding to the ion channel protein?

A
  • The smooth muscles in the stomach that cause stomach contractions
  • Here the Alpha subunit binds to the K+ channel closing the channel. Reducing the outward flow of K+ and therefore causing a depolarization.
60
Q

How is acetlycholine stopped from producing mass amounts of graded potentials?

A
  • The enzyme acetylcholinesterase, or AChE is located in the postsynaptic membrane (or very close to it.
  • This enzyme breaks down ACh into acetate and choline which can be taken back up into the presynaptic cell and resynthesied into acetylcholine.
61
Q

What is an end-plate potential?

A

An EPSP made by ACh in the skeletal muscle fiber

62
Q

What are the major monoamine neurotransmitters found in the CNS?

A
  • (Catecholamines)
    • dopamine - neurotransmitter
    • Norepinephrine - neurotransmitter and hormone
    • Epinephrine (adrenaline) - primary hormone
  • Serotonin - neurtotransmitter
  • Histamine - neurotransmitter
63
Q

How is the action of monoamine neurotransmitters stopped within the synapse?

A
  1. reuptake of neurotransmitter molecules from the synaptic cleft into the presynaptic axon terminal
  2. degradation of the monoamine by an enzyme within the axon terminal called monoamine oxidase (MAO).
64
Q

What do monoamine neurotransmitters use to open ion channels?

A
  • Secondary messengers within cell cytoplasm
  • cAMP is an example
65
Q

How do SSRIs help to treat depression?

A
  • These drugs reduce the production of serotonin transporter proteins (SERT). Thereby reducing the ability of SERT proteins in the presynaptic neuron plasma membrane to clear serotonin from the synaptic cleft. This increases the ability of serotonin to stimulate its receptors in the postsynaptic membrane.
66
Q

Neurons that use dopamine as a neurotransmitter are called….what?

A

dopaminergic neurons

67
Q

Adrenergic Receptors utilizes which neurotransmitter?

A

norepinephrine

68
Q

How is norepinphrine used as a neurotransmitter in the PNS and CNS?

A
  • PNS
    • sympathetic neurons use norepinephrine at their synapse with smooth muscles, cardiac muscle and glands
  • CNS
    • these neurons seem to be involved in general behavioral arousal
69
Q

Which amino acid is the major excitatory neurotransmitter in the brain?

A
  • Glutamate
    • 80% of synapses in cerebral cortex
70
Q

Glutamate receptor encloses an ion channel - what other ACh receptor is this similar to?

What are the 3 subtypes of glutamate receptors?

A
  • Nicotinic ACh receptor
  • NMDA receptor, AMPA receptor, kainate receptor
71
Q

What 2 requirements are necessary for the NMDA receptors to open their channel pores? (channel pore is blocked by Mg2+

A
  1. NMDA receptor must also bind to glutamate (produced by astrocyte)
  2. membrane must be partially depolarized at this time by a different neurotransmitter molecule that binds to a different receptor
    1. ex: glutamate binding to the AMPA receptor nearby
      1. this could cause Na+ to rush into the cell depolarizing it
    2. This depolarization causes Mg2+ to be released from NMDA channel unblocking the channel and allowing Ca2+ and Na+ into the postsynaptic dendrites
72
Q

What 2 amino acid neurotransmitters are EPSPs and What 2 amino acid neurotransmitters are IPSPs

A
  1. Glutamic Acid and Aspartic Acid = EPSP
  2. GABA and Glycine = IPSP
73
Q
  1. What type of channels do glycine and GABA receptors open when binded to their respective neurotransmitter?
  2. What type of ACh receptor do their channels mimic?
  3. What does this do to the post synaptic cell?
A
  1. They have Cl- channels
  2. Nicotinic ACh channels
  3. This hyperpolarizes the cell –> IPSP
74
Q
A
75
Q

What do benzodiazepines (Valium and Xanax) do?

A
  • Try to promote sleep and treat anxiety
  • these drugs bind to a subgroup of GABA receptors, increasing the permeability of Cl-.
  • The inflow of Cl- into the postsynaptic neuron enhances the inhibitory effect of GABA at their synapses in the brain and spinal cord
76
Q

Occurs due to the convergence of axon terminals from different presynaptic axon (up to a thousand sometimes!) on the dendrites and cell body of a posynaptic neuron

A

Spatial Summation

77
Q

Successive rapid bursts of activity of a single presynaptic axon can cause corresponding bursts of neurotransmitter release, resulting in successive waves of EPSPs (or IPSPs) that summate with each other as they travel to the initial segment of the axon

A

Temporal Summation

78
Q

The ability of synapses to change in response to activity

A

synaptic plasticity

79
Q

In regards to synaptic plasticity - Insertion of AMPA receptors promotes what?

A

long term potentiation of synaptic trasnmission (makes them better)

80
Q

LTP - long term potentiation- what is it?

Where is it mostly observed?

A
  • The improved efficacy of synaptic transmission
  • Observed in the hippocampus of the brain - implicated in memory storage
81
Q

What neurotransmitter is used in Long-term potentiation in the brain, and what is its receptor?

A
  1. Glutamate
  2. NMDA
    1. Usually comes with icreased AMPA - since the depolarization caused by glutamate binding to AMPA causes NMDA to active its channels

Bio 465 - Physio (16 decks)

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