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MHD2 > Block 8 (Neuro) - L1, L5, L8 > Flashcards

Block 8 (Neuro) - L1, L5, L8 Flashcards

1
Q

What is the specialized zone between neurons at which communication takes place?

A

Synapse

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2
Q

What are the two types of synapses?

A
  1. Electrical

2. Chemical

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3
Q

What is an electrical synapse?

A

A low resistance, high conductance channel utilizing direct connections between cells called gap junctions

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4
Q

What is a chemical synapse?

A

Chemical NT are released from synaptic vesicles in the presynaptic cell and diffuse across the synaptic cleft and bind to specialized receptors in the postsynaptic cell

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5
Q

Compare the distance between pre- and post-synaptic cell membranes of electric and chemical synapses.

A

Electrical: shorter (3.5 nm)
Chemical: longer (20-40 nm)

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6
Q

Which type of synapse maintains cytoplasmic continuity between pre- and post-synaptic cells?

A

Electrical

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7
Q

Compare the ultrastructural components of electric and chemical synapses.

A

Electrical: gap junctions
Chemical: presynaptic vesicles and active zones; postsynaptic receptors

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8
Q

Compare the agent of transmission of electric and chemical synapses.

A

Electrical: ion current
Chemical: chemical transmitter

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9
Q

Compare the synaptic delay of electric and chemical synapses.

A

Electrical: virtually absent
Chemical: significant

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10
Q

Compare the direction of transmission of electric and chemical synapses.

A

Electrical: usually bidirectional
Chemical: unidirectional

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11
Q

Where do synapses occur within cells?

A

Active zones - specialized regions that function as docking sites for synaptic vesicles

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12
Q

Describe the mechanism of NT release from the presynaptic terminal.

A
  1. NT is synthesized and stored in vesicles
  2. An AP invades the presynaptic terminal
  3. Depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels
  4. Influx of Ca2+ through channels
  5. Ca2+ causes vesicles to fuse with the presynaptic membrane
  6. NT is released into synaptic cleft via exocytosis
  7. NT binds to receptor molecules in the postsynaptic membrane
  8. Opening or closing of postsynaptic channels
  9. Postsynaptic current causes excitatory or inhibitory postsynaptic potential that changes the excitability of the postsynaptic cell
  10. Removal of NT by glial uptake or degradation
  11. Retrieval of vesicular membrane from plasma membrane
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13
Q

What two factors determine the grade of chemical synapses?

A
  1. Amount of NT released

2. Number of receptors available

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14
Q

What determines the action of a NT?

A

The properties of the receptor (NOT the NT)

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15
Q

What are the two common features of all chemical receptors?

A
  1. Membrane-spanning proteins

2. Carry out an effector function in the postsynaptic cell by directly or indirectly gating some type of response

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16
Q

Describe the structure and function of a directly gated channel.

A

This channel is typically a single macromolecule made up of several protein subunits that form both the receptor and the ion channel.

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17
Q

What is an ionophoric receptor?

A

Single macromolecule that forms both the receptor and the ion channel

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18
Q

Directly gated responses are ___ (speed) but ___ (time). What types of responses do they tend to mediate?

A

Fast-acting; short-lived; behavioral types of responses

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19
Q

Describe the structure and function of an indirectly gated channel.

A

The receptor complex is separate from the effector complex (ion channel). Communication between the receptor and the channel is accomplished by G proteins and second messengers.

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20
Q

Which component of an indirectly gated receptor complex is NOT loosely bound to the postsynaptic membrane?

A

Second messengers (this allows them to affect distant sites within the cell)

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21
Q

Indirectly gated responses are ___ (speed) but ___ (time). What types of responses do they tend to mediate?

A

Slow-acting; long-lasting or permanent; responses related to learning and memory

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22
Q

___ of synaptic input occurs at the axon hillock. In the CNS, no single synaptic event is usually sufficient to produce an AP. Therefore, you need to ___ many potentials.

A

Integration; summate

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23
Q

What factors affect the production of synaptic potentials?

A
  1. Size of the cell
  2. Location of the synapse (axon, dendrite, soma)
  3. Shape
  4. Proximity
  5. Strength (time and length constants)
  6. Sign (EPSP vs. IPSP) of the input
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24
Q

At the axon hillock, the membrane potential is greatly reduced. Why and what effect does this have on threshold?

A

Due to higher density of voltage-gated sodium channels; increases the likelihood of surpassing threshold

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25
Q

At all sites within the cell beside the axon hillock, neuronal integration depends on what two passive properties of the membrane?

A
  1. Time constant

2. Length constant

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26
Q

A long time constant means a better chance for integration via ___ summation.

A

Temporal (multiple inputs from a single source)

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27
Q

A long length constant means a better chance for integration via ___ summation.

A

Spacial (simultaneous single inputs from multiple sources)

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28
Q

What are the three types of synapses?

A
  1. Axosomatic
  2. Axodendritic
  3. Axoaxonic
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29
Q

Axosomatic synapses are typically ___ and occur via ___ channels.

A

Inhibitory; chloride

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30
Q

Axodendritic synapses are typically ___.

A

Excitatory

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31
Q

Axoaxonic synapses are typically ___ and control the amount of ___ released.

A

Modulatory; NT

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32
Q

Which synapses affect the production of an AP and which do not?

A

Axosomatic and axodendritic are mediating, occur before the axon hillock, and can aid in the production of an AP. Axoaxonic synapses are modulatory and have no influence on the production of an AP. They can modulate its effectiveness at the presynaptic terminal.

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33
Q

The propagation of the AP to the presynaptic terminal requires what types of channels? At the terminal, the presence of these channels is not essential to NT release. What ion is essential?

A

Na; K

Ca

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34
Q

The opening of the voltage-gated Ca channels has a slower activation kinetics than that of Na. What is the implication of this?

A

There is some synaptic delay between the arrival of the AP and the opening of the Ca channels (this opening occurs near the peak of the AP, a 0.2ms delay)

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35
Q

___ of the AP is critical to the calcium influx.

A

Duration

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36
Q

Changes in the levels of calcium do NOT affect the amount of NT in a vesicle. What does it affect?

A

The probability of release of that vesicle from the presynaptic terminal

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37
Q

What are omega figures?

A

Deformations in the presynaptic membrane seen during active transmission - they are the vesicles releasing NT via exocytosis

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38
Q

What are the 7 basic steps for synaptic release and retrieval and what is required for almost every phase?

A
  1. Translocation
  2. Attachment to active zone
  3. Contact to the docking protein at the presynaptic membrane via calcium-dependent proteins
  4. Fusion to the membrane protein
  5. Opening of the vesicle (exocytosis) and extrusion of contents into synaptic cleft
  6. Collapse of the vesicle into the plasm membrane
  7. Retrieval of the vesicle via calcium-dependent proteins
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39
Q

What two toxins can affect the SNARE proteins associated with NT release and lead to paralysis?

A

Botulinum and tetanus

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40
Q

What mediates endocytosis of vesicles?

A

Clathrin

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41
Q

What are 3 diseases leading to a defect in ACh resynthesis or packaging?

A
  1. Familial infantile myasthenia
  2. Congenital paucity of presynaptic vesicles and reduced quantal release
  3. Black widow spider venom
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42
Q

What are 3 diseases leading to a defect in ACh release?

A
  1. Lambert-Eaton myasthenic syndrome
  2. Botulism
  3. Aminoglycoside antibiotics
  4. Magnesium intoxication
  5. Snake venom
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43
Q

What 4 criteria define a NT?

A
  1. Synthesized in a neuron
  2. Present in the presynaptic terminal and released in amounts sufficient to exert its intended action on the postsynaptic cell
  3. If applied exogenously in reasonable concentrations, it mimics exactly the action of the endogenously released substance.
  4. A specific mechanism exists for its removal from the synaptic cleft
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44
Q

What are the major categories of small molecule NTs?

A
  1. ACh
  2. Biogenic amines
  3. Amino acids
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45
Q

How is ACh built?

A

Acetyl CoA + choline

NB: choline is derived only from your diet

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46
Q

Where is ACh used?

A
  1. All NMJs
  2. All preganglionic synapses
  3. Parasympathetic postganglionic synapses
  4. Nucleus basalis (CNS)
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47
Q

What are the 3 biogenic amines?

A
  1. Catecholamines
  2. Indolamine
  3. Imidazole
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48
Q

How are catecholamines derived?

A

Tyrosine + O2 -> L-DOPA -> dopamine + CO2 -> NE -> EPI

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49
Q

Dopamine is the essential NT switch for the ___.

A

Basal ganglia

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50
Q

Where is NE used?

A
  1. All sympathetic postganglionic synapses
  2. Hypothalamus
  3. Limbic system
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51
Q

NE typically acts via ___ receptors.

A

Alpha-adrenergic

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52
Q

Where is EPI used?

A
  1. Peripherally

2. Adrenal medulla

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53
Q

EPI typically acts via ___ receptors.

A

Beta-adrenergic

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54
Q

How is indolamine derived?

A

Tryptophan -> 5-HTP -> 5-HT (serotonin)

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55
Q

Serotonin is an essential NT in the ___ and ___.

A

Brainstem and limbic system

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56
Q

How is imidazole derived?

A

Histidine -> histamine

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57
Q

Where does histamine act?

A

Used as a local hormone - it acts on the cell which released it to limit the peripheral effects; found in the hypothalamus

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58
Q

What are some important amino acid NTs?

A

Glutamate, aspartate, glycine, GABA

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59
Q

Amino acid transmitters are derived from universal cellular compartments and must be protected from degradation for other cellular processes - how is this done?

A

Compartmentalized and isolated from the rest of the cell by placing them in a synaptic vesicle - once in a vesicle, they are not able to be returned to the cell

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60
Q

What are secretory proteins processed by the ER and Golgi apparatus, packaged, and sent to the terminal via fast axonal transport mechanisms?

A

Neuroactive peptides (NAPs)

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61
Q

Where does processing of NAP’s take place?

A

In the vesicle

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62
Q

How are NT removed from the synapse?

A
  1. Reuptake
  2. Glial cell uptake
  3. Enzymatic breakdown
63
Q

What factors determine total synaptic conductance at a synapse?

A
  1. N = total number of channels in the cell
  2. P0 = probability that a channel is open
  3. Gamma = conductance of an open channel
  4. Vm - E(epsp) = driving forces acting on the ions
64
Q

What factor affects the total synaptic conductance most significantly?

A

Probability that a channel is open

65
Q

What factor most directly affects whether a channel is open?

A

Concentration of available NT at that synapse

66
Q

How do central synapses differ from the NMJ?

A

NMJ:

  1. Individual muscle fibers are innervated by a single motor neuron.
  2. The synapse is excitatory only.
  3. Transmitter is always ACh via nicotinic receptors
  4. Synapse is highly effective, leading to a 70 mV depolarization and an AP in the sarcolemma ~100% of the time

vs.

CNS:

  1. Central synapses have multiple connections/cell
  2. Synapses can be excitatory OR inhibitory.
  3. Many NT used singly and in combination
  4. Effectiveness of the synapse is variable but typically small and thus depends on the integration of many synapses to reach threshold
67
Q

What disease causes a defect in AChR density?

A
  1. Myasthenia gravis

2. Congenital end-plate AChR deficiency

68
Q

What disease causes a defect in AChR channel kinetics?

A
  1. Slow-channel syndrome

2. High-conductance, fast-channel syndrome

69
Q

What disease causes a defect in AChE?

A
  1. Congenital end-plate deficiency

2. Organphosphates

70
Q

What disease causes a defect in binding of ACh to its receptor?

A
  1. Congenital myasthenic syndrome with abnormal interaction
  2. Curare, succinylcholine, etc.
  3. Snake venom
71
Q

Excitatory synapses generally open what channels? What is the major NT?

A

Na and Ca

Glutamate

72
Q

What types of receptors can be activated by glutamate?

A
  1. AMPA
  2. NMDA
  3. Quisqualate-B
73
Q

Inhibitory synapses generally open what channels? What are the major NTs?

A

K and Cl

GABA and glycine

74
Q

Describe the scheme of second messenger pathways.

A
  1. NT binds to receptor
  2. REceptor binds to and activates a transducer (G-protein)
  3. G-protein translocates and activates the primary effector
  4. Primary effector produces a second messenger
  5. Second messenger activates the secondary effector
  6. This produces a change in the membrane potential of the post-synaptic cell
75
Q

What are the three major systems of second messengers?

A
  1. cAMP
  2. Phosphoinositol
  3. Arachidonic acid
76
Q

Most protein kinases have what two segments?

A
  1. Regulatory subunit

2. Catalytic subunit

77
Q

What is the regulatory subunit?

A

Binding site or switch which activates/inactivates kinase

78
Q

What is the catalytic subunit?

A

Interacts with other proteins

79
Q

Describe the cAMP system.

A
  1. NE binds to a beta-adrenergic receptor.
  2. The receptor activates a Gs protein (transducer).
  3. The Gs protein activates AC (primary effector)
  4. AC leads to the production of cAMP (second messenger)
  5. cAMP activates a cAMP-dependent protein kinase (secondary effector)
80
Q

Describe the phosphoinositol system.

A
  1. ACh binds to a muscarinic ACh receptor.
  2. The receptor activates a Gq protein (transducer).
  3. The Gs protein activates PLC (primary effector)
  4. PLC leads to the production of IP3 and DAG (second messenger)
  5. DAG activates a PKC (secondary effector) and IP3 diffuses into the ER, activating intracellular Ca2+ release.
81
Q

Describe the arachidonic acid system.

A
  1. Histamine binds to a histamine receptor.
  2. The receptor activates a G protein (transducer).
  3. The G protein activates PLA2 (primary effector)
  4. PLA2 leads to the production of arachidonic acid (second messenger) by cleaving inositol phosphate
  5. Arachidonic acid activates 5-lipoxygenase, 12-lipoxygenase, and cyclo-oxygenase (prostaglandins, thromboxanes, leukotrienes)
82
Q

How is kinase activity terminated?

A

Phosphoprotein phosphatases

83
Q

Slow synaptic mechanisms ___ cellular responses; fast synaptic mechanisms ___ cellular responses.

A

Modulate; mediate

84
Q

True or false - G-proteins can act directly on channels without going through a second messenger cascade.

A

True - it also still a form of indirect transmission because the receptor is not part of the channel.

85
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

86
Q

What are the responses to superficial pain?

A
  1. Orientation toward stimulus
  2. Increase CO
  3. Shut down digestion
  4. Increase blood flow to skeletal muscle
  5. Withdraw or escape
87
Q

What are the responses to deep/chronic pain?

A
  1. Social withdrawal
  2. Anorexia
  3. Decrease HR
  4. Decrease blood flow to digestive tract
  5. Decrease blood flow to skeletal muscle
  6. Motor immobility
88
Q

What are the types of nociceptors, the fiber group/name, and the modality?

A
  1. Mechanical - A-delta, III, sharp/pricking pain
  2. Thermal-mechanical - A-delta, III, burning pain
  3. Thermal-mechanical - C, IV, freezing pain
  4. Polymodal - C, IV, slow, burning pain
89
Q

Compare the information transmitted via the DC and STT pathways.

A

DC: discriminative touch, proprioception, vibration

STT: pain, temperature, crude touch

90
Q

Compare the fiber size and myelination of the DC and STT pathways.

A

DC: large fibers, heavily myelinated

STT: small fibers, thin or unmyelinated

91
Q

Compare the point of decussation of the DC and STT pathways.

A

DC: decussate after ascending

STT: decussate before ascending

92
Q

What is the difference between pain and nociception?

A

Pain: perception of aversive sensations originating from a specific area

Nociception: transduction and conveyance of signals from specialized sensory receptors concerning tissue damage

93
Q

What type of nociceptors convey sharp pain?

A

Thermal or mechanical

94
Q

What type of nociceptors convey dull or diffuse pain?

A

Polymodal

95
Q

What type of nociceptors are found in viscera and only respond to inflammation or extreme stretch?

A

Silent

96
Q

What is hyperalgesia?

A

Increased response to a stimulus which is normally painful

97
Q

What causes hyperalgesia?

A

Lowering of the nociceptor’s threshold by peripheral or central mechanisms, resulting in an increase in the number of action potentials sent to the CNS

98
Q

What is primary hyperalgesia?

A

Occurs at the site of the lesion

99
Q

What is secondary hyperalgesia?

A

Occurs during severe or persistent injury - nociceptors fire repeatedly, increasing the firing of neurons in the dorsal horn, leading to long-term changes in the overall excitability of these cells or the target neurons

100
Q

What is central sensitization?

A

The resulting long-term changes in excitability/sensitivity of the dorsal horn neurons undergoing secondary hyperalgesia

101
Q

Stimulation of the pain pathway results in inhibition of ___ and excitation of ___, resulting in the perception of pain.

A

Inhibitory interneurons; Projection neurons

102
Q

By stimulating the ___ of the somatosensory system, you can excite the ___, resulting in a decreased output of the projection fiber and a suppression of the pain.

A

Non-nociceptive AB fibers; inhibitory interneurons

103
Q

What is analgesia?

A

Modulation or reduction of pain

104
Q

What is the gate control theory?

A

A balance exists between myelinated and unmyelinated fibers in the dorsal horn

105
Q

What are the 4 primary classes of spinal neurons which can interact to modulate pain?

A
  1. Unmyelinated nociceptive afferents (pain fibers)
  2. Myelinated non-noceiceptive afferents (somatosensory fibers)
  3. Projections neurons to the CNS
  4. Spontaneously active inhibitory interneurons
106
Q

What is allodynia?

A

Pain due to a stimulus which does not normally provoke pain

107
Q

What is analgesia?

A

Absence of pain in response to stimulation which would normally be painful

108
Q

What is causalgia?

A

A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes

109
Q

What is central pain?

A

Pain initiated or caused by a primary lesion of dysfunction in the CNS

110
Q

What is CRPS?

A

Complex Regional Pain Syndrome

111
Q

What is CRPS I?

A

Reflex sympathetic dystrophy - develops after an initiating noxious event

112
Q

What is CRPS II?

A

Causalgia - develops after a nerve injury

113
Q

What is hyperalgesia?

A

Increased pain from a stimulus that normally provokes pain

114
Q

What is primary hyperalgesia?

A

Occurs at the site of injury when the nociceptive fiber is sensitized or directly stimulated by chemical agents released by the damaged tissue and nearby cells or the neuron itself

115
Q

What is secondary hyperalgesia?

A

Occurs during severe or persistent injury, leads to long-term changes in sensitivity (central sensitization)

116
Q

What is hyperpathia?

A

A painful syndrome characterized by an abnormally painful reaction to a stimulus, especially a repetitive stimulus, as well as an increased threshold

117
Q

What is hypoalgesia?

A

Diminished pain in response to a normally painful stimulus

118
Q

What is neuralgia?

A

Pain in the distribution of a nerve or nerves

119
Q

What is neurogenic pain?

A

Pain initiated or caused by a primary lesion, dysfunction, or transitory perturbation in the peripheral or central nervous system

120
Q

What are the two types of neurogenic pain?

A
  1. Deafferentation pain

2. Sympathetically maintained pain

121
Q

What is deafferentation pain?

A

May be a complication of any injury anywhere along the course of the somatosensory pathway

122
Q

What is sympathetically maintained pain?

A

Simultaneous occurrence of pain, local autonomic dysregulation, and trophic changes in skin, soft tissue, and bone

123
Q

What is neuropathic pain?

A

Pain caused by a lesion of the somatosensory nervous system

124
Q

What is a neuropathy?

A

Disturbance or function or pathological change in a nerve

125
Q

What is nociceptive pain?

A

Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors

126
Q

What is a pain threshold?

A

Minimum intensity of a stimulus that is perceived as painful

127
Q

What is paresthesia?

A

An abnormal sensation, whether spontaneous or evoke

128
Q

What is dysesthesia?

A

An unpleasant abnormal sensation, whether spontaneous or evoked

129
Q

What is sensitization?

A

Increased responsiveness of nociceptive neurons to their normal input and/or recruitment of a response to normally subthreshold inputs

130
Q

What are the two major cell types of the nervous system?

A
  1. Neurons

2. Glia

131
Q

True or false - the vast majority of neurons do not divide in the adult CNS.

A

True

132
Q

Describe the cell body of a neuron.

A
  1. Large euchromatic nucleus with a prominent nucleolus
  2. Nissl bodies (rough ER for storage of Ca2+)
  3. Other organelles
  4. Neuropil
133
Q

What is the neuropil?

A

Fibrous intercellular network surrounding cells of the CNS consisting of processes of neurons and glial cells

134
Q

What are the main signal reception and processing sites of the nervous system?

A

Dendrites

135
Q

What conducts action potentials in the nervous system?

A

Axons

136
Q

What is the plasma membrane of an axon?

A

Axolemma

137
Q

What are the contents of an axon?

A

Axoplasma

138
Q

What is the region of the cell body where the axons originate?

A

Axon hillock

139
Q

In neurons, cellular components are continuously synthesized in the soma and moved to the axon and dendrites by a process of ___. At the same time, worn-out materials are returned to the soma by ___ for degradation in lysosomes. ___ are the structures which support this process.

A

Anterograde transport; retrograde transport; microtubules

140
Q

What are the 4 types of neurons (structure)?

A
  1. Unipolar
  2. Bipolar
  3. Pseudounipolar
  4. Multipolar
141
Q

What are the 3 types of neurons (function)?

A
  1. Sensory (afferent)
  2. Motor (efferent)
  3. Interneuron
142
Q

What are the neuroglia of the periphery?

A
  1. Schwann cell

2. Satellite cell

143
Q

What is the function of Schwann cell?

A

Myelinate axons

144
Q

What is the function of satellite cells?

A

Surround neuronal cell bodies to insulate, nourish, and regulate the local microenvironment

145
Q

What are unmyelinated axons?

A

Axons with just a neurolemma

146
Q

What is a ganglion?

A

Cluster of neuronal cell bodies outside the CNS

147
Q

What is the role of the oligodendrocytes?

A

Myelinate CNS axons

148
Q

What is the role of astrocytes?

A

Control ionic environment (buffer K+), form scar tissue, and help form BBB

149
Q

What is the role of microglia?

A

Phagocytic and immune

150
Q

What is the role of ependymal cells?

A

Line CNS cavities

151
Q

A peripheral nerve is surrounded by ___.

A

Epineurium

152
Q

A fascicle is surrounded by ___.

A

Perineureum

153
Q

A nerve fiber is surrounded by ___.

A

Endoneurium

MHD2 (34 decks)

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