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Physiology > Neurophyiosology > Flashcards

Neurophyiosology Flashcards

1
Q

Neuro lectures

A

Synaptic transmission
Cortex anatomy
Hippocampus anatomy
Thalamus anatomy
DSA Dennis hypothalmic RF and Limbic systems
PHYSICIAN neurotransmitters, chemical messengers, and excitotoxicity

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2
Q

Declarative memory

A

Available to consciousness

-daily episodes, worlds and their meanings, history

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3
Q

Non declarative memory

A 
Generally not available to consciousness
Motor skills
Associations
Priming cues
Puzzle solving skills
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4
Q

Working memory

A

Short term

Recollection of a fact or memory for use

Answering a test question

Functions a lot like short term memory

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5
Q

Declarative memory

A

Explicit memory
The conscious recognition/recollection of learned facts and experiences

Episodic-events
Semantic-words, language, rules

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6
Q

Procedural memory

A

Non declarative memory
Skilled memory
Implicit memory
Reflexive memory

Complex activity repeated over and over again until all of the relevant neural systems work together to autonomically produce the activity

Riding a bike , tying shoes

Basal ganglia-motor skills
Cerebellum-motor skill
Nucleus accumbens-nonmotor skills

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7
Q

Neuroplasticity

A

The ability of the brain to form and reorganize synaptic connections, espicially response to to learning or experience or following injury

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8
Q

Synaptic neuroplasticity -altering function of synapses

A

Post titanic potetiation (PTP)

Long term potentiation (LTP)

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9
Q

Structural neuroplasticity-changing the shape of synapses

A

Gain or loss synapses
Dendritic structural
Soma structural changes

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10
Q

Synaptic facilitation

A

An increase in synaptic strength that occurs when two or more action potentials invade the presynaptic terminal within milliseconds of eachther

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11
Q

Synaptic potentiation

A

Activity dependent form of plasticity that enhances synaptic transmission due to increase in neurotransmitter released in response to presynaptic action potentials and results from persistent calcium cations within presynaptic terminals

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12
Q

Synaptic augmentation

A

Increases the probability of releasing synaptic vesicles during and after repetitive stimulation

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13
Q

Post tetanic potentiation

A

Short lived
Results in increased frequency of miniature excitatory postsynaptic potentials or currents with no effect on amplitude in the spontaneous postsynaptic potential

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14
Q

Long term potentiation

A

Persistent strengthening of synapses based on recent patterns of activity

Produce long lasting increase in signal transmission between two neurons

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15
Q

Bc potentiation acts over a time course of seconds to minutes, it often outlasts the high frequency trains of action potentials that evoke it, leading to __

A

PTP

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16
Q

What does PTP require

A

High frequency , brief discharge of the pre-synaptic neuron
Pulses increased neurotransmitter release for 60 seconds
Results in increased probability of action potentials in the post synaptic cell

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17
Q

Mechanism of PTP

A

Leading theory depends on abundance of calcium

  • action potential opens Ca channels (more enters than can be processed-more vesicular release of NT than otherwise seen)
  • Ca causes vesicle fusion and NT release (leads to more activation of receptors than typical)
  • receptor channels open Na enters post synaptic cell (leads to more likelihood of action potential in post synaptic cell)
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18
Q

Long term potentiation

A

Persistent increase in synaptic strength following high frequency stimulation of chemical synapse
-requires repeated strong stimulation

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19
Q

Mechanism of long term potentiation

A

Increased phosphorylation of AMPA receptors and insertion of additional AMPA receptors into post synaptic membrane
Eventually, activation of calcium-calmodulin-CREB mechanism

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20
Q

AMPAR

A

Na enters and depolarized cell. This causes depolarization of opening of NMDAR

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21
Q

NMDAR

A

Mg leaves cell and Ca enters cell

Open by depolarization from Na entry in AMPAR

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22
Q

What happens when ca enters cell STP

A

Binds calcineurin

Binds calmodulin

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23
Q

What does ca bound to calcineurin do

A

Increase NOS and production of NO to presynaptic cell which increases cGMP and NT release

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24
Q

What happens when Ca binds calmodulin

A

Activates adenylyl cyclase, cAMP and phosphorylation of AMPAR

Increases Na influx in response to future ligand binding

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25
Q

What is CREB

A

CAMP response element binding protein , which is a transcription factor targeting CRE (cAMP response elements)
Well documented roles in memory formation, neuroplasticity, and spatial memory

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26
Q

What genes does CREB upregulate the expression of

A 
BDNF
Cytoskeleton structural proteins
Synapse and growth formation 
Enzymes for NT synthesis 
NT receptors
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27
Q

Long term (declarative/explicit) memory is mediated by four types of processing

A

Encoding
Storage
Consolidation
Retrieval

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28
Q

Encoding

A

New information is attended and linked to existing information in memory

Attending to new information or facts:
Focus and attention and linked to existing information in memory

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29
Q

Storage

A

Neural mechanisms and sites by which memory is retrained over time

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30
Q

Consolidation

A

Process of taking temporarily stored information and making it stable

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31
Q

Retreival

A

Process by which stored information is recalled

Subject to distortion

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32
Q

Short term memory has __ capacity

A

Limited

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33
Q

Long term memory capacity

A

Unknown

Unlimited?

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34
Q

Encoding memory utilizes what

A

Perception of something
Focused attention
Linkage to previous knowledge
Emotion enhances encoding

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35
Q

What is encoding memory critically important for

A

How well something is learned

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36
Q

For encoding memory to persist, the information must be deeply encoded. What does this require

A

-attending to the information
Associating the information with knowledge already well established in memory
Even stronger when one is well motivated to remember
REM sleep is important

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37
Q

Long term memory storage is associated with the area of the __ that the memory is most associated with

A

Cortex

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38
Q

Long term visual memory

A

Visual cortex

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39
Q

Long term sound memory

A

Auditory cortex

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40
Q

What happens with widespread damage to the cortex

A

Sig decline in long term memory

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41
Q

Is all short term memory turned into long term memory

A

Nope

A lot is lost

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42
Q

Consolidation of memory

A

Labels memory is stabilized(making a memory permanent)

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43
Q

How does memory consolidation occur

A

LTP and physical changes in synaptic structure

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44
Q

Anatomy of consolidation of memory

A

Hippocampus, temporal lobes, papez circuit, cingulate cortex

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45
Q

__ improves consolidation

A

Sleep

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46
Q

Reconsolidation

A

Long term memory goes back to short term memory

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47
Q

Short term memory is associated with __ synaptic chemical changes

A

More

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48
Q

Long term memory is associated with more ___ changes

A

Structural

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49
Q

What structural changes is long term memory associated with

A

Increased vesicle release sites (active zones)
Increased number of vesicles released
Increased pre synaptic terminals
Increased dendritic spines

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50
Q

Rehersal

A

Short term memory to short term memory

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51
Q

Retreival memory

A

Act of accessing the long term memory: recollection or using the memory
Brings the memory into working memory
-makes the memory susceptible to modification or deletion

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52
Q

What does retreival of memory use

A

Cortex, parahippocampal gyrus, and hippocampus

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53
Q

Memory is reconstructed int he ___

A

Hippocampus

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54
Q

Cortex

A

Site of memory storage and sends it to the parahippocampal gyrus

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55
Q

Parahippocampal gyrus

A

Brings all the components from the cortical memories into working memory
Sends to the hippocampus

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56
Q

Hippocampus

A

Reassembles the full memory and sends back to the parahippocampal gyrus

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57
Q

Parahippocampal gyrus

A

Prolongs the life of the memory trace and sends back to cortex

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58
Q

Cortex

A

Stores memory again

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59
Q

Dentate gyrus

A

Site of adult neurogenesis

  • excitatory principle neuron that adds to mossy fiber circuits between DG and pyramidal cells of CA3
  • low turnover of old neurons
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60
Q

Function of dentate gyrus

A

Time stamping new information to distinguish two pieces of information in time
Aka content

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61
Q

Working short term memory

A

Accessing memories and using what you remember

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62
Q

Three components of working short term memory

A

Phonological loop
Visuospatial loop
Executive control process

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63
Q

Phonological loop

A

Wernickes and Broca’s areas (verbal information )

Provide and interpret the auditory information associated with the memory

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64
Q

Visuospatial loop

A

Occipital cortex (visuospatial information)

Provides and interprets the visual information associated with the memory

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65
Q

Executive control processes

A 
Prefrontal cortex (allocates attention)
Directs, uses and updates memory
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66
Q

Spatial memory

A

Place cells in the hippocampus (specialized pyramidal cells in CA1)

Grid cells in enterohinal cortex (works in conjunction with place cells. Spacing and orientation between fields and a reference point)

Encodes the physical space associated with the memory

Believed to act as an anchor to the entire memory
-speed cells-released function guesses speed

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67
Q

Good cells

A

As a person wanders around a new environment, so called “grid cells” within the brain are thought to provide a base coordinate system

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68
Q

Place cells

A

Related “place cells” response to specific locations such as NY Central Park

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69
Q

Which of the following is another name for short term memory

Working memory
Sensory memory

Episodic memory
Implicit memory

A

Idk

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70
Q

In each of the following determine whether you would use implicit or explicit memory

  1. speaking your native tongue
  2. Remembering what present you bought for your aunt
  3. Opening a present
  4. Writing with pen and paper
  5. Remembering that time you fell out of a tree when you were 5
  6. Climbing a tree
  7. Knowing the work for flower in anoth language
  8. Hearing a French speaker and later noticing French food more often wherever you go
  9. Knowing the state capital of Missouri
  10. Solving a geometry problem
A

Ok

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71
Q

Compare and contract implicit and explicit memory

A

Explicit-intentionally and consciously recalled (formula for statistics), declarative. Dates for history class
-recall phone number, dates for class, what time meeting a friend

Implicit-not consciously recalled (ride a bike )
Nondeclarative
Procedural swinging a bat
Singing a familiar song, ride bike

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72
Q

Two types of explicit memory

A

Episodic and semantic

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73
Q

Episodic memory

A

Long term memories of specific events such as what you did yesterday’s or your high school graduation

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74
Q

Semantic memory

A

Facts, concepts, names, and other general knowledge

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75
Q

A 27 year old man with severe epilepsy, characterized by major convulsions and lapses of consciousness every few minutes, underwent experimental neurosurgery to help relieve seizures. The operation has a significant , beneficial effect not he epilepsy, but led to a devastating memory deficit. He had normal procedural memory, maintained long term memory for events that occurred prior to surgery, and high short term memory was intact, but he could not commit new events to long term memory (loss of declarative memory). Which of the following areas of the brain was bilaterally respected in this patient

Cerebral cortex
Cingulate gyrus
Hypothalamus
Parietal lobe
Temporal lobe
A

Idk

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76
Q

What cells does the brain (BBB) capillary have apart from the general capillary

A

Astrocyte
Pericyte=contractile
Endothelial cell

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77
Q

Pathways across the BBB

A 
Paracellular aqueous pathway
Transcellular lipophilic path
Transport proteins
Endocytosis
Passive discussion
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78
Q

What agents are transported with paracellular pathway

A

Water soluble agents (rare)

Through tight junction

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79
Q

What agents cross the transcellular lipophilic path

A

Lipid soluble agents

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80
Q

What sort of agents cross the transport proteins

A

Glucose, aa, nucleosides, vinca alkaloids, ciclosporin A, AZt

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81
Q

What agents use endocytosis

A

Insulin, transferrin, albumin, other plasma proteins

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82
Q

Agents of passive diffusion

A

H20, CO2, O2, unbound steroid hormones, lipid soluble stuff

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83
Q

GLUT1

A

Transports glucose from blood through BBB

Not insulin dependent

2 isoforms (45kD and 55kD)

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84
Q

NaK2Cl

A

Transports ions from CSF to blood

Expression tied to endothelium 1 and 3

Endothelium production ties to astrocyte signals

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85
Q

P-glycoprotein

A

Moves drugs that don’t belong that crossed BBB back into blood

Similar to MRPI in GI

Some drugs target this signaling path

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86
Q

The BBB and blood CSF layer is not present in _____

A

Circumventricular organs (CVO)

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87
Q

What are the circumventricular organs

A

Area postrema, OVLY, SFO, and posterior pituitary

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88
Q

How does blood CSF barrier work in CVO

A

Facilitated transport carries necessary molecules across the barrier

Majority of capillaries lack the typical slit pores

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89
Q

What are CVE highly permeable to

A

Water, CO2, O2, and lipid soluble substances

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90
Q

What are CVO slightly permeable to

A

Na, Cl and K

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91
Q

What are CVO nearly permeable to

A

Plasma proteins and non lipid soluble organic molecules

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92
Q

What is the posterior pituitary

A

Secretory, endocrine

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93
Q

What is the area postrema

A

Sensory; initiation of vomiting in response to chemotactic triggers

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94
Q

What is the organum vasculosum of the lamina terminalis

A

Sensory; regulation of total body water and thirst-target of angiotensin II

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95
Q

What is the subcortical organ

A

Sensory

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96
Q

What are the sensory CVO

A

Subcortical organ, OVLT, area postrema

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97
Q

What are the secretory CVO

A

Median eminence, posterior pituitary , pineal gland

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98
Q

Metabolic glutamate receptors (mGluR’s)

A

8 subtypes, GPCR
Modulates synaptic signaling of other receptors
Modulates transmitter release

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99
Q

Inotropy glutamate receptors-has a glutamate binding domain

A

NMDAR’s

Non-NMDA receptors(AMPAR, KAR)

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100
Q

The NMDA receptor is activated by what

A

Exogenous N-methyl-D-aspartate

Glutamate and aspartate

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101
Q

What happens when NMDA receptor is activated

A

Allows Ca influx

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102
Q

Modulators sites of the NMDA receptor

A

Glycine binding site
Mg binding site
PCP binding site

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103
Q

Activation of the NMDA receptors leads to what

A

EPSP in post synaptic cell

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104
Q

NMDA has a ___ onset and __ duration

A

Slow

Prolonged

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105
Q

Glycine binding site of the NMDA receptor

A

Serves as a coagonist
Required for EAA to have an affect
Can’t open the channel on its own

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106
Q

Magnesium binding site of the NMDA receptor

A

Inside the channel
Mg blocks the channel
To open the channel, Mg must leave
Depolarization forces Mg out of channel

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107
Q

PCP binding site of NMDA receptor

A

Inside the channel
Internal to Mg binding site
Blocks the channel

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108
Q

Most glutamatergic synapses have both _ and _ receptors

A

AMPA and NMDA

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109
Q

The rise time for NMDA receptor currents are much slower than those of non NMDA receptors

A

10-50ms

.2-.4 ms

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110
Q

Deactivateion is also much slower for NMDA receptors than non NMDA receptors

A

10-50 ms vs .2-.4 ms

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111
Q

AMPA provides fast cell depolarization and NMDA receptors determine the duration of that deporization

A

Ok

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112
Q

For NMDA receptor, ESPs show longer duration and longer latency. Why

A

Ca influx is slower

Takes time to remove Mg

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113
Q

Non-NMDA receptors are almost exclusively __ receptors

A

Post synaptic

Similar to NMDAR

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114
Q

Non NMDA receptors cause _ influx and small amount of _ influx

A

Na Ca

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115
Q

Two types of non NMDA receptors

A

AMPA

Kainate

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116
Q

Activation of Non-NMDA receptors lead to what

A

EPSP

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117
Q

Non-NMDA receptors often co-localize at the same synapses as __

A

NMDARs

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118
Q

Binding sites on non-NMDA receptor : AMPA receptor

A 
EAA binding site
Benzodiazepine site (inhibitors response to NT)
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119
Q

What does the AMPA receptor allow

A

Na influx

Small amount of Ca influx

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120
Q

When Na enters through the AMPA receptor what happens

A

Depolarization of cell

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121
Q

What does depoaliraztaion of a cell (caused by Na entry from AMPA) cause

A

Mg out of NMDA and Ca in at NMDA

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122
Q

Binding sites on NMDA

A

Glutamate binding site

Glycine binding site

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123
Q

Both inotropy and metabotropic receptors can be activated by __

A

Excitatory neurotransmitters

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124
Q

What are the inotropic receptors and what do they allow influx of

A

NMDA Ca influx

AMPA Na influx

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125
Q

Both __ and ___ receptors can be activated by eaa

A

Inotropic and metabotropic

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126
Q

Metabotropic aa receptors

A

Both pre and post synaptic location

Presynaptic : controls NT release

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127
Q

What are the uptake systems that get rid of EAA

A

Neurons and glia

  • Na dependent secondary active transport
  • high affinity
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128
Q

Glia uptake system

A

Converts to glutamine

Release into ECF

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129
Q

Neurons take up glutamine

A

Converts back to glutamate

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130
Q

Glutamate enters glial cell after being release from extrasynaptic NMDARS. What happens

A

Glutamine synthetase turns it to glutamine

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131
Q

Glutamine leaves the glial cell and enters the neuron. What happens then

A

Glutaminase turns it to glutamate

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132
Q

Glutamate is released from the presynaptic neuron. What happens

A

Binds mGluR (metabotropic),

kaintae, AMPAR, and NMDAR
Inotropic

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133
Q

What happens when neuron is depolarized

A

ATP levels rapidly fall to 0 inside the neurons
NaKATPase function ceases
Cell depolarizes
Leads to action potential and excessive release of NT (including EAA)

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134
Q

Lots of EAA accumulate int he synapse after neuron depolarization

A

Ok

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135
Q

EAA reuptake is _ dependent

A

Na

*but there is less Na around in synaptic cleft
EAAs accumulate outside the cell

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136
Q

What does NMDAR activation from glutamate lead to

A

Ca influx

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137
Q

Increased intracellular Ca initiates

A

Activation of phospholipase A2
Activation of calcineurin (phosphatase)
Activation of Mu calpain (protease)
Activation of apoptosis pathway

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138
Q

Activation of phospholipase A2

A

Release o arachidonate from membrane and causes physical damage to the membrane

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139
Q

What does arachidonte from the membrane do

A

Acts at Ryan’s dine receptor on ER, which releases Ca from intracelllular stores

  • ER:unfolded protein response-stops making protein
  • activation of elFa-kinase
  • mitochondria: impaired function
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140
Q

What happens with u-calpain (protease) activation

A

Proteolysis
-spectrin (more structural damage to cell)
-elF4G (eukaryotic induction factor 4G-protein synthesis)
Others-metabolic impairment

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141
Q

Activation of calcineurin

A

Phosphatase
Activates NOS
Increases NO synthesis

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142
Q

The disruption of mitochondrial and ER function further increases free cytosolic __

A

Calcium

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143
Q

As mitochondrial membranes are disrupted, __ pathways are activated

A

Apoptosis

Cytochrome C and caspase 9 activate caspase 3

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144
Q

Caspase 3

A

Proteolytic enzyme

Apoptotic

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145
Q

What activates cytochrome C and caspase 9

A

Bcl2 enzymes

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146
Q

What turns on Bcl2 enxymes

A

Excitotoxicity ????

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147
Q

What does calcium release cause

A

Caspase 3/9 activation and calpain activation

148
Q

What does caspase 3/9 and calpain activation lead to

A

Cell death

149
Q

What system is crucial for increasing general excitaability of cortical ceurons

A

RAS-PBN EAA

150
Q

The ___ system adds to the general excitation

A

Cholinergic

151
Q

The __ and __ systems move us from being awake to being more generally aware of incoming information

A

Noradrenergic and serotonergic

152
Q

The __ pathways modulate the activity of noradrenergic and serotonergic systems

A

Histiminergic

153
Q

The __ system adds to that awareness , particularly focused awareness associated with novel stimuli, but its role is not as well defined

A

Dopaminergic

154
Q

Alertness

A

Cognitive, motor, emotion, novel stimuli

DA

Agonists improve cognitive function

155
Q

Awareness

A

Moving beyond awake into general awareness of environment

NE, 5-HT

Startle and awareness

156
Q

Arousal (wakefulness)

A

General excitation of cortex

EAA, Ach

Hyperpolarization and memory

157
Q

Dopamine

A

Substantia Nigra, ventral tegmental area

158
Q

EAA

A

Dorsal and ventral pathways (to cortex)

159
Q

Norepinephrine

A

Locus coeruleus

160
Q

Serotonin

A

Raphe nuclei

161
Q

Acetylcholine

A

Pedunculopontine tegmetnal and laterodorsal nuclei

162
Q

Histamine

A

Tuberomammillary nucleus of the hypothalamus

163
Q

Describe the steps of the neuromuscular junction

A
  1. NT in vesicles
  2. Action potential
  3. Ca enters cell
  4. Vesicles fuse
  5. NT released
  6. Post-synaptic receptors activated
  7. Neurotransmission ends
164
Q

The descending systems are __ motor neurons

A

Upper

165
Q

What are the descending systems (upper motor neurons)

A

Motor cortex

Brainstem centers

166
Q

What does the motor cortex do

A

Planning, initiating, directing voluntary movements

167
Q

What does the brainstem center do

A

Rhythmic, stereotyped movements and postural control

168
Q

What do the descending systems (UMN) get information from

A

Basal ganglia and cerebellum

169
Q

What does the basal ganglia do

A

Initiation of intended movement and suppression of unwanted movement

170
Q

What does the cerebellum do

A

Coordination of ongoing movement

171
Q

What does the descending system UMN send information to

A

Local circuit neurons and motor neuron pools

172
Q

Local circuit neurons

A

Sensorimotor integration and central pattern generators (CPGs)

173
Q

Motor neuron pools

A

Lower motor neurons

174
Q

What do local circuit neurons get information from

A

UMN and sensory inputs

175
Q

What do motor neuron pools give information to

A

Skeletal muscles

176
Q

Where are local circuit neurons and motor neuron pools

A

Spinal cord and brainstem circuits

177
Q

Basic function of cortico and rubrospinal tracts

A
  1. Transmission of commands for skilled movements

2. Corrections of motor patterns generated by the spinal cord

178
Q

Reticulospinal tract

A
  1. Activation of spinal motor programs for stepping and other stereotypic movements
  2. Control of upright body posture
179
Q

Vestibulospinal tract

A

Generation of tonic activity in antigravity msucles

180
Q

Premotor cortex

A

Determines whether its okay to move

Identifies the goal and the motion required to meet that goal

181
Q

Supplementary motor cortex

A

Postural control

Identifies the specific motor sequence required and plans the motion

Changes tactics if necessary

182
Q

Primary motor cortex

A

Codes the individual motions. Required to reach the goal and activate muscles

183
Q

Vestibulocerebellum

A

To vestibular nuclei

*coordinated balance and eye movement. Postural control for future movements

184
Q

Cerebrocerebellum

A

To motor cortices

*planning, coordinating, properly times movement sequences, motor memory

185
Q

Spinocerebellum (medial and lateral)

A

To descending brainstem and Corticospinal pathways

*proper execution of coordinated movements, postural control, correct ongoing motion

186
Q

Basal ganglia get input from what

A

Striatum receives input from nearly all of the cerebral cortex

187
Q

Basal ganglia send output

A

From GPi and SNpr is inhibitory and projects to motor areas in brainstem and thalamus (releases GABA; then on to cortex)

188
Q

Damage to any basal ganglia structure may cause what

A

Slowness of voluntary movement, involuntary movement, involuntary postures, or a combination of these

189
Q

Damage to SNpc

A

Causes tremor at rest, slowness of movement, rigidity, and postural instability, which are the main features of PD

190
Q

Striatum

A

Caudate

Putamen

191
Q

Globes pallidus

A

External segment

Internal segment

192
Q

Substantia nigra

A

Pars compacta

Pars reticulate

193
Q

Subthalmic nucleus

A

Ok

194
Q

Where does striatum receive most of its information from

A

Basal ganglia

  • from cortex regions (glutamate)
  • also receives input from dopaminergic neurons of substantia nigra pars compacts (loss of which—>parkinsons)
195
Q

90% of neurons are striatum

A

Medium spiny neurons (GABAnergic)

Output is inhibitory

196
Q

Output from striatum to basal ganglia is ___

A

Inhibitory

197
Q

Intrastriatal system is ___

A

Cholinergic and stimulators

198
Q

Subthalamic nucleus receives input form

A

Frontal lobe

199
Q

Output from subthalamic nucleus

A

Excitatory (glutamate) to other basal ganglia nuclei

200
Q

Subthalamic nucleus is typically kept under tonic inhibition by ___, disinhibition is seen in __ disease

A

GPe

Parkinsons

201
Q

Globes pallidus

A

Has external and internal segments

Function

202
Q

Substantia nigra

A

Has two divisions (pars reticulata and pars compacta)

Dopaminergic neurons project to other basal ganglia nuclei (see nigrostriatal path)
-stimulates D1 (+) and D2 (-) receptors

203
Q

Normally the direct pathway allows _ and indirect pathway prevents __

A

Motion motion

204
Q

Dopamine helps motion occur by two mechanisms

A
  1. turn on/amplify the direct pathway

2. turn off/dampen the indirect pathway

205
Q

In parkinson disease, the __ input is abolished resulting in a loss of dopaminergic tone in the basal ganglia..characterized by bradykinesia

A

SNPC

206
Q

What are the effects of loss of dopaminergic tone

A
  1. Direct pathway becomes difficult to activate (but it still can due to the presence of excitatory glutamatergic and cholinergic circuits in the striatum)
  2. The indirect pathway becomes overactive (due to loss of D2 mediated inhibitory tone

Therefore difficulty in initiating motion

207
Q

In __ disease, the indirect pathway is abolished, resulting in excessive movement

A

Huntington

208
Q

Why is there excess movement in Huntington disease

A

Ach activates GABAergic input in those local intrastriatal loops

When active and functional, this inhibits motion

Therefore the loss of Ach tone results in excess motion

209
Q

Following deflection of stereocilia, _ ions enter cell and depolarize it

A

K

210
Q

Describe the steps of depolarization of hair cells

A
  1. Ion channels (TRPA1) on stereocilia tips are opened when the tip links joining the stereocilia are stretched
  2. Entry of K depolarize the hair cell which opens voltage gated calcium channels
  3. Incoming Ca leads to the release of glutamate from synaptic vesicles ,which then diffuses to the postsynaptic afferent neuron from the spiral ganglion
211
Q

Adelta peripheral nerves

A

Afferent type III, 1-5 micrometer diameter, 5-30 m/s conduction velocity, skin mechanoreceptors, thermal receptors, and nociceptors

212
Q

C peripheral nerves

A

Type IV
.2-1.5 micrometer diameter
.5-2 (slow)

Skin mechanoreceptors, thermal receptors, and nociceptors

213
Q

Location of pain

A

Somatic or cutaneous pain
Muscle pain
Deep pain
Visceral pain

214
Q

Modality of pain

A

Thermal, mechanical, chemical

Many subtypes of each
Can be polymodal (respond to more than one modality)
Silent nociceptors are related to the phenomenon of phenotype switching

215
Q

Cutaneous pain

A

Skin, superficial structures (cutes, burns, bruises

Fast pain (sharp) and slow pain (dull and achy, throbbing)

216
Q

Deep pain

A

Periosteum ligaments, bone

Usually dull and achy

Associated with muscle spasm

217
Q

Muscle pain

A

Injury of ischemia

Both fast pain and slow pain

218
Q

Visceral pain

A

Internal organs:GI tract, stomach, bladder, prostate, reproductive tract, kidneys, heart

Poor localization, very sensitive to stretch. (Distension). Associated with referred pain

219
Q

Free nerve endings

A

Lacks specialized receptor cells or encapsulateions

Characterization can further be broken down by various molecular markers

220
Q

Peptidergic free nerve endings

A

Expresses neuropeptides

  • substance P
  • CGRP(calcitonin gene-related peptide)
Responsive to NGF (nerve growth factor)
Most visceral afferent
Half cutaneous afferent
-chronic inflammation 
-visceral pain
221
Q

Non-peptidergic free nerve ending

A

Does NOT express these neuropeptides
Responsive to GDNF
Half cutaneous afferent
-diabetic neuropathy

222
Q

Sensing noxious stimuli with __ receptors

A

TRP

Transient receptor potential family

223
Q

TRPVI

A

Capsaicin , heat

224
Q

TRPAI

A

Mustard

Cool

225
Q

TRPM8

A

Menthol

Cool

226
Q

Ligand gated non-selective cation channel is permeable to _, _ and _

A

Ca Na K

227
Q

Nav1.7

A

Mechanosensitive sodium channel

  • I type off mutation results in pain insensitive individuals (rare)
  • other mutation results in paroxysmal extreme pain disorder (channel doesn’t inactivate properly)
228
Q

Other signaling modalities

A 
Nav1.7
ATP receptor
Acid-sensing channel-activated by H+
SP and CGRP
Histamine
Minions (bradykinin)
229
Q

Referred pain

A

Brain requires some experience to localize pain, visceral pain is not experienced often enough in early development ot train the brain to localize it

Afferent converge in the dorsal horn

Antidromic signaling further diffuses visceral pain across multiple organs

230
Q

Central processing of pain is done by what

A

Cortex, thalamus, raphe nuclei, insular cortex

231
Q

Information cortex

A
  • pain inputs widely distributed

- damage to these areas may impact perception of pain, but not the emotional processing associated with the pain

232
Q

Cortex details

A

SI and PTO-receive initial input and also involved in higher processing

233
Q

Thalamus information

A

-damage to thalamus would greatly impact perception of pain-damage to a specific nucleus would impact some but not all features of pain

234
Q

Thalamus details

A

Nociceptors inputs do synapse in the thalamus, intralaminar nucleus in particular

235
Q

Raphe nuclei information

A

Descending pathway

236
Q

Raphe nuclei details

A

Serotonergic signaling results in opoid Eric signaling in dorsal horn

237
Q

Insular cortex information

A

Relays nociceptors input to Limbic system

-damage decreases emotional component of pain

238
Q

Details of insular cortex

A

Emotional component of pain

239
Q

Membrane potential: seizure disorders

A

Held stable at a negative Vm compared to the outside of a cell

240
Q

Nerve and muscle relationship

A

The bigger the nerve and muscle, the more negative

Skeletal-large neurons are usually listed as -70,-90 mV

Smooth muscle-small neurons -50mV

241
Q

How is the membrane potential maintained

A

Na/K ATPase

  • electrogenic (pumps three sodium out for every 2 K in)
  • creates the concentration gradients for sodium and potassium (this is critical to Vm in large muscle and nerve cells)
242
Q

How is membrane potential maintained

A

By selective permeability of the membrane (ions don’t cross readily without a channnel)

-twoions cross at rest bc they have channels that allow it
K leak channel
Chloride ClC1 channel

243
Q

The action potential is involved in what

A

Seizure disorders, MS and other demyelination diseases

244
Q

Fast action potential

A
  • rapid depolarization-opening of voltage gated sodium channels
  • repolarization(inactivation of sodium channels, opening of voltage gated K channels)
  • at completion-both sodium and k Channels are closed
  • activity of the NaK ATPas returns concentration gradients
245
Q

Refractory periods

A

Lots of cardiac drugs affect these

246
Q

Absolute refractory period

A

Can’t elicit an AP
Voltage gated Na channels are open or inactive
Occurs during an on going potential

247
Q

Relative refractory period

A
  • requires greater stimulation to produce an AP
  • at least some voltage gated Na channels are closed (others are in inactive state-that’s why its harder)
  • occurs during repolarization and a bit after the on going AP has completed
248
Q

Voltage inactivation (depolarization block)

A
  • neuron(or muscle cell) forced to remain in a depolarized state for too long
  • sodium channels end up struck in the inactivated state (or the open state, depending on exactly what happened0
  • cell is depolarized but can no longer generate action potentials (in the inactive state, depolarization no longer opens the Na channels. If the channel is held open, the gradient for Na and/or K is abolished )
  • regardless of cause: although NT release was triggered by the initial depolarization, depolarization block prevents the cell from releasing NT once the block has occurred
  • essentially stuck in the absolute refractory period
249
Q

Salvatore conduction (MS)

A

Occurs in myelinated neurons

250
Q

What is the source of myelin

A

Central:oligodendrocytes
Peripheral:Schwann

251
Q

Action potentials jump from node of ___ to node

A

Ranviee

252
Q

Salvatore conduction _ conduction velocity

A

Increases

253
Q

The myelin sheath prevents the _ from leaving the cell, so the depolarization travels quickly to the next node

A

Na

254
Q

Nodes have __ channels, that the rest of the axon does not have

A

Voltage gated channels

255
Q

What disease are associated with the synapse/neuromuscular junction

A

Myasthenia gravis, botulism, tetanus

256
Q

Describe the presynaptic cell

A

Lots of mitochondria
Presynaptic voltage gated calcium channels
Vesicles containing NTsynaptic docking proteins

257
Q

Describe the postsynaptic cell

A

Post synaptic densities-likely NT receptors

  • ionotropic(ion channel), metabotropic (second messenger)
  • may be on the dendrite but cell body and axon hillock is common too
258
Q

Describe release of NT

A
  • depolarization of terminal by AP causes the voltage gated calcium channels to open
  • influx Ca
  • Ca binds to docking proteins
  • docking proteins have vesicles associated with them-the calcium binding triggers a conformational change that brings the vesicle into contact with the membrane
  • fusion of vesicular with cell membrane creates opening
  • NT released in synaptic trough
  • NT diffuses to post synaptic cell and binds to this receptor
  • triggers some AP in post synaptic cell
259
Q

Inotropic Ca Na

A

Cell depolarized and an EPSP

260
Q

Inotropic Cl K

A

Cell hyperpolarized and an IPSP occurs

261
Q

Metabotropic

A

Gs (AC)
Gi (inhibit AC)
Gq (activate IP3/DAG)

262
Q

How is NT removed from the synapse

A

Reuptake

Enzymatic destruction in the trough

263
Q

Monoamines from tyrosine

A

Dopamine-clinical relevance relevance: parkinson disease/mood/affect/emotional experience
Two metabotropic receptors

Cetecholamines
-epinephrine (adrenalin)-sympathetic ANS
-NE (noradrenalin)-sympathetic AMS
Receptors-both alpha and beta adrenergic

Removed via reuptake enzymes and enzymatic destruction

264
Q

Monoamine NT from histidine

A

Histamine
Waking up
H1 and H2 receptors

265
Q

Monoamine NT from tryptamine

A

Serotonin (5HT)-clinical relevance mood/affect/arousal
-multiple receptor subtypes
1 inotropic-triggers vomiting (found in area postrema)
-rest metabotropic

266
Q

Acetylcholine NT

A

chloride entrance into he cell
Two receptor
GABA-a ionotropic (chloride)
GABAb-metabotropic

Higher in CNS

Clinical relevance-general anesthesia and activation to reduce speciality

267
Q

Excitatory aa

A

Glutamate and/or aspartate

Non-nmda receptors and NMDA receptors

268
Q

Non NMDA receptors

A

Na influx

Typical ionotropic response

269
Q

NMDA receptor: calcium influx

A

With excess activation after seizure/stroke/TBI

Influx of calcium excessive

270
Q

Two divisions of the PNS

A

Somatic and autonomic

271
Q

Somatic nervous system

A

Motor efferent to skeletal muscle

Sensory fibers going to the spinal cord or brain (includes the sensory fibers from the viscera as well as cutaneous and muscle afferent

272
Q

Autonomic nervous system

A

Efferent fibers to the viscera, glands

273
Q

What makes CSF

A

Choriod plexus and membranes lining the ventricles

274
Q

Describe CDF

A

Starts as filtrate of plasma, but modified

Low protein, glucose, and K compared to blood

Mg is higher than plasma

275
Q

Clinical relevance of CSF

A

Hydrocephalus

276
Q

BBB two components

A

Tight junctions between capillary endothelial cells

Podocytes from glial cells cover the capillaries to reduce surface area

277
Q

What does BBB do

A

Prevent or reduce movement from blood to CSF

278
Q

Glucose transport across BBB

A

Need ransporter insulin INDEPENDENT

279
Q

NaK2Cl BBB

A

Moves all four ions out of the CSF

Activation tied to K levels

280
Q

P-glycoproteins -(permeability or pump glycoproteins):

A

Moves many drugs/other substances from CSF to blood

281
Q

What can damage BBB

A

High bp

282
Q

Clinical relevance of BBB

A

Ability of drugs to penetrate CNS; hydrocephalus

283
Q

What circumventricular organs

A

Regions BBB not complete

Tight junctions between capillary endothelial cells are not present.

284
Q

What regions are CVO

A

Area postrema-at opening of 4th ventricle
OVLT and dubfornical organ-around the third ventricle (AV3V)
Posterior pituitary

285
Q

Purpose of CVO

A

Require exposure to plasma constituents to do their job

286
Q

Area postrema

A

Elicits vomiting in response to certain chemicals in the blood

287
Q

OVLT/SFO

A

Uses plasma osmolarity to trigger thirst/ADH release

288
Q

Posterior pituitary

A

ADH and ocytocin release when triggered

289
Q

Consequence of CVO

A

More sensitive to damage due to toxins int he blood

Drugs will cross the BBB in these regions

290
Q

Cerebral blood flow is under __ control

A

Local

291
Q

Cerebral blood flow has more blood flow under what conditions

A

More active neurons
More metabolites
More blood flow due to vasodilation

292
Q

What conditions cause less cerebral blood flow

A

Less activity
Less metabolites
Less blood flow

293
Q

__ is a potent vasodilator of cerebral blood flow

A

NO

294
Q

__ dilates and cerebral blood vessel directly and indirectly

A

Hypoxia

295
Q

If system blood pressure goes too high what happens

A

Activation of alpha adrenergic receptors on cerebral vasculature

Vasoconstriction

Prevents the high blood pressure from damaging the capillaries

The capillaries are where the BBB is-so this effect protects the BBB as much as possible

296
Q

What happens if brain blood flow is compromised

A

Brain will activate pressor regions in medulla

Drive systemic pressure up to force blood through to the brain

297
Q

The vasculature in the brain is innervated with ___ (pretty much the only place in the body)

A

Nociceptors

298
Q

When is pain perceived from vasculature in the brain

A

Distended
Torqued/twisted/equilivent
Headache

299
Q

Clinical relevance of cerebral blood flow

A

Intracranial bleeds can have dramatic effect on bp

Increased intracranial pressure CNA lead to tremendous increases in systemic bp as the brain tries to maintain perfusion

300
Q

Awake

A

Sleep/wake cycles are apparent

Volition/consciousness may not be present

301
Q

Aware

A

Different levels

Minimally conscious->full consciousness

302
Q

Core of system

A

To get to awake requires two components
Medullary reticular activating system and parabrachial nuclei
-glutamate
-both through the thalamus (dorsal path) and bypassing the thalamus (ventral path0

Pedunculopontine tegmental nucleus and laterodorsal nerve (Ach, ditto-dorsal and ventral path)

303
Q

Serotonergic, noradrenergic, and dopaminergic are required for full awareness/consciousness

A

Ok

304
Q

Clinical relevance of brain arousal mechanisms

A

Coma vs. persistent vegetative state vs. minimally conscious vs conscious

305
Q

Cutaneous senses

A

Receptors(specialized, bare nerve endings, generally bare nerve endings have the highest threshold)

Paths to the brain
Dorsal columns (generally fine touch)
-spinothalamic tract

306
Q

Processing in the brain

A

Regardless of pathway-synapses allow the signal to be refined or lost

  • both related to strength of stimulus-strong stimulus=lots of AP=high probability of getting through
  • prior to the cortex, most of what happens is related to making the signal as clean as possible
307
Q

Once in the cortex what happens to the signal

A

S1 for initial processing-identify the characteristics of what activated the receptors
S2-stereognosis (ability t recognize an unseen object by touch, compare two. Objects, ties to memory)

308
Q

PTO

A

Association complex

Naming objects

309
Q

Clinical relevance of brain processing

A

Strokes can produce disruptions in sensory processing leading to numbness

310
Q

Nociceptors

A

Peripheral mechanisms

Spinal processing is different for the C fibers

Central processing of painful inputs

311
Q

Peripheral mechanisms nociceptors

A 
Bare nerve endings
Slightly myelinated (a delta fibers) or unmyelinated (C fibers)

The peripheral ending can be activated by numerous chemicals, including bradykinin and substance P

312
Q

Importance of peripheral mechanisms

A

Leads to sensitization of the nociceptors and increased activation with similar stimulus-the pain perceived increases

313
Q

Spinothalamic path

A

Likely for fast/sharp pain (a delta)

314
Q

Spinoreticulothalamic path

A

Likely for slow/dull pain (C fibers)

315
Q

Why is the spinoreticular path important

A

Bc there is a synapse in the spinal cord at the level where the afferent enters the spinal cord

316
Q

Synapse in spiral cord at the level where the afferent enters the spinal cord

A
  • gating mecahnism (gate theory of pain)-non nociceptive input from abeta fibers (cutaneous) inhibits painful inputs via presynaptic inhibition
  • descending opoid inputs via the raphe nuclei also act to decrease transmission at this synapse
  • prescribed opoids work to reduce pain transmission by activating this circuit
317
Q

Central processing of painful inputs

A

Widespread distribution-lesioning in the brain will not block the perception of pain, although it will change it (it may be less well localized )

Insular cortex

318
Q

Why is the insular cortex important

A

Coordinates autonomic responses

Damage produces pain asymbolia-painful inputs are recognized as painful, but not perceived as unpleasant

319
Q

Chronic neuropathic pain

A

Results from changes in periphery

  • sensitization of the nociceptors themselves
  • changes in spinal cord sensitivity to nociceptive input
320
Q

Cornea

A

Most refraction of light, but constant

321
Q

Lens

A

Variable refraction

322
Q

Round lens

A

More bending, required for something close to us

323
Q

Flatter lens

A

Less bending far vision

324
Q

Cataract

A

Cloudiness in lens interferes with light passages

325
Q

Presbyopia

A

Inability to change shape of the lens (stiff)

326
Q

Retina

A

Rods and cones

327
Q

MOA photoreceptors

A

Light hitting photoreceptor causes it to hyperpolarized

Reduces glutamate relase

328
Q

Bipolar cells

A

ON center (light hitting the center of the receptive field turns the cell on)

OFF center (light hitting the center of the receptive field turns the cell of)

The difference is due to different glutamate receptors not he different cells

329
Q

Ganglion cells

A

On and off centers

Dictated by bipolar cells

330
Q

Pathway to the brain

A

Optic nerve->optic chiasm->lateral geniculate body->primary visual cortex->V2, V4, dorsal and ventral visual pathway

331
Q

Optic chiasm

A

The fibers fromt he nasal retina on either side cross

Thus information from either the left of the right visual field goes to the appropriate side of the brain

332
Q

Lateral geniculate body

A

Eye movements-so disruptions in the lateral geniculate body disrupt the ability of the eyes to move together

  • also focus
  • in addition-detectionof motion and initial processing (what’s the interesting stuff here_
333
Q

Primary visual cortex

A

Initial processing
Columns devoted to orientation of the lines in the visual field
Job:create a contour map of the visual field
Blobs:initial color processing

334
Q

V2

A

Depth perception

335
Q

V4

A

Color perception

336
Q

Dorsal visual pathway

A

Use of visual information in motion

337
Q

Ventral visual pathway

A

Higher cognitive processing using visual information

338
Q

Consequence of having a dorsal and ventral visual pathway

A

The ability to name an object can be divorced fromt he ability to copy the object

339
Q

Cochlea endolymph

A

Surrounds the hair cells

High K low Na

340
Q

Cochlea perilymph

A

Similar to plasma/ECF

High Na low K

341
Q

Basilar membrane

A

Hair cells arise from the organ of corti

342
Q

Tectorial membrane

A

Top of hair cells insert into this

343
Q

Basilar membrane

A

Bends based on wavelength of sound

  • high pitched sounds (short wavelength) cause maximal bending close to the oval window
  • low pitched sounds (low wavelength/low frequency) cause maximal bending at the helicotrema (away from the oval window
344
Q

Pathway to brain auditory

A

Superior olive->inferior colliculus_.primary auditory cortex->auditory association cortex

345
Q

Superior olive

A

Localization of the source of the sound

  • medial detect intra-aural time differences
  • lateral detects intra-aural volume differences
346
Q

Inferior colliculus

A

Suppresses information from echoes

347
Q

Superior colliculus

A

Creates 3D map of where the sound is

348
Q

Primary auditory cortex

A

Tonotopic map of the sound, loudness

349
Q

Auditory association cortex

A

Complex map of sound, including harmonies

350
Q

Vestibular (vertigo/dizziness)

A

Detection of linear and angular acceleration

351
Q

Linear acceleration (straight paths in either the horizontal or vertical dimension)

A

Utricle-horizontal

Saccule-vertical

352
Q

Angular acceleration (curved lines)

A

Semicircular canals
-horizontal aka lateral-turning in circles
Anterior canals-falling forward
Posterior canals-falling backward

353
Q

As with hearing, the binding of the hair cells creates __

A

AP

354
Q

Reflexes controlling eye movement when we fall/rotate are major actions

A

Central processing is related to suppressing the reflexes

355
Q

Motor control clinical relevance

A

Spacicity, parkinson, Huntington

356
Q

Myotactic reflex

A

Muscle spindles-sensitive to length of the muscle

Stretching muscle=stretching muscle spindle-> contraction of stretched muscle

357
Q

Parts of the muscle spindle

A

Middle (sensory portion)
-nuclear bag, nuclear chain fiber, afferent neurons (1a length and rate of change, II length)

End

  • contractile (myosin and actin)
  • efferent neuron (gamma motoneuron-behaves just like alpha motoneuron, but only influences the muscle spindle)
  • role: control the sensitivity of the muscle spindle to stretch (more activity=more sensitivity, less activity=less sensitivity)
  • activity of the gamma-motoneuron is controlled via the brainstem(brainstem facilitatory region-activates the gamma motoneurons, is spontaneously active)
  • brainstem inhibitory region(inhibits gamma amotoneurons, requires activation by cortex, spasticity results from damage to the cortical regions that activate the brainstem inhibitory area)
358
Q

Golgi tendon organ reflex (inverse myotatic, auto genie inhibition reflex)

A

Too munch force in contracting muscle could tear the tendon

  • golgi tendon organ detects the force being developed
  • causes strong inhibition of contracting muscle that stops the contraction
359
Q

What works in voluntary motion

A

Primary motor cortex
Supplementary and premotor cortex
Cerebellum
Vestibulocerebellum

360
Q

Primary motor cortex

A

Relat the desired action to the lower motoneurons to activate the muscles

361
Q

Supplementary and premotor cortex

A

Planning of motions, postural control

362
Q

Cerebellum

A

Spinocerebellum (medial-postural control, lateral-correct ongoing motion)

Cerebrocerebellum(planning of complex motion; motor memory

Vestibulocerebellum (eye movements/postural movements for future motions)

Basal ganglia (mother may I)

363
Q

Direct pathway basal ganglia

A
  • dopamine from substantia nigra
  • binds to striatum neurons expressing the D1 receptos
  • activates them
  • dopamine allows motion (activation of the direct pathway allows motion)
  • clinical relevance-Parkinsonism results from loss of dopaminergic inputs and is characterized by bradykinesia
364
Q

Indirect pathway basal ganglia to activate

A

Ach activates GABAergic input

When active, the indirect pathway inhibits motion

365
Q

Indirect pathway basal ganglia to allow motion,

A

Must be inhibited at the same time the direct pathway is activated

  • dopamine from nigrostriatal neurons
  • binds to striatum neurons that express the D2 receptos
  • D2 inhibits the neuron
  • leads to inhibition of the indirect pathway
366
Q

Huntington disease

A

Loss of indirect pathway results in excess motion

Physiology (7 decks)

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