Exam 1 material Flashcards

1
Q

What are the three main divisions of the brain? Excluding the spinal cord.

A

Prosencephalon (forebrain)
Mesencephalon (midbrain)
Rhombencephalon (hindbrain)

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2
Q

What makes up the prosencephalon (forebrain)?

A

Telencephalon

Diencephalon

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3
Q

What falls under the telencephalon?

A
cerebral hemispheres
cerebral cortex
subcoritical white matter
basal ganglia
basal forebrain nuclei
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4
Q

What falls under the Diencephalon?

A

hypothalamus
thalamus
epithalamus

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5
Q

What makes up the mesencephalon (midbrain)?

A

Cerebral peduncles
midbrain tectum
midbrain tegmentum

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6
Q

What are the 2 branches of the Rhombencephalon (hindbrain) and what falls under each?

A

Metencephalon (pons and cerebellum)

Myelencephalon (medulla)

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7
Q

Directions in brain. Flip at midbrain. what are they above and below the midbrain?

A

Below: for ease going in order of North East South West …Rostral (nose), Dorsal (back), Caudal (tail), Ventral (front)

Above: rotate the below 90 degrees counterclockwise.

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8
Q

directions of planes

A
Horzontal plane (axial)
sagittal plane
coronal plane (frontal)
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9
Q

Classical neuron anatomy arrangement

A

Dendrites -> cell body -> axon -> synapse to other dendrites

multiple orientations and configurations

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10
Q

Main functions of Glia cells (4)

A
  1. supportive of neurons
  2. maintain nutrition
  3. manage waste
  4. balance ions

*they interact on different levels to form synaptic connections.

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11
Q

Types of Glia cells

A

Astrocytes
oligodendrocytes / schwann cells
Ependymal cells
microglia

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12
Q

Astrocytes (functions)

A

encase synapse, regulate chemical environment

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13
Q

Oligodendrocytes vs Schwann cells (functions)

A

Oligo: CNS myelin. have multiple arms

Schwann: PNS myelin

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14
Q

Ependymal cells (functions)

A

Cerebral spinal fluid, lines central canal and spinal cord

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15
Q

Microglia (functions)

A

just like macrophages, but in the brain.

immune stuff.

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16
Q

Glutamate (excite or inhibit?)

A

Excitatory neurotransmitter

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17
Q

GABA (excite or inhibit?)

A

Inhibitory neurotransmitter

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18
Q

Acetylcholine

A

Muscles / Autonomic

receptor types: Nicotinic and Muscarinic

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19
Q

Norepinephrine

A

Sympathetic

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20
Q

Neuromodulation: What 2 neurotransmitters?

A

Dopamine (motor system…)

Seratonin (mood)

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21
Q

Cord segmentation

A
  • segmented from development
  • four groups
  • Cord ends around L1, then caudal equina
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22
Q

Ventral vs dorsal roots

A

Ventral (front) roots - motor

Dorsal (back) roots - sensory

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23
Q

White and gray matter in regards to brain and spinal cord.

A

in brain, white is on the inside.

flips in spinal cord (white on outside)

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24
Q

White vs gray matter

A
White = mostly fat , myelin
gray = mostly cell bodies
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25
Q

Frontal lobe (functions)

A
  • primary motor cortex
  • “expressive” language (left-side)
  • “executive function”
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26
Q

Parietal lobe (functions)

A
  • primary sensory cortex
  • spatial processing
  • multimodal (all the senses?) integration
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27
Q

Circle of Willis

A

Allows the blood supply of the brain to “communicate with each other”
- connects various areas. front to back. side to side.

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28
Q

CT scans (goods, bads, etc.)

A
  • Fast.
  • no big contraindications
  • LOT of radiation

Good: blood, bone (bright white!), general outlines
Bad: soft tissue resolution

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29
Q

MRI scans (good, bad, etc.)

A

-No radiation
-very high resolution
several contraindications, and slow

Good at: soft tissue, weird things
Bad at: bone (invisible), blood (confusing)

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30
Q

contrast in imaging

A

used to detect leaks/tears/highlighting

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31
Q

Membrane potentials: Electrical currents

A

current has to be caused by a flow of ions.
no flow = no current.

Need: ion gradient, permeable membrane.
I = V/R

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32
Q

Nernst equation conceptual

A

E = …
it calculates the resting membrane potential required to maintain ion gradient

  • only considers one ion!
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33
Q

Goldman-Hodgkin-Katz equation (conceptual)

A

similar to nernst but includes multiple ions!

adds a term in the equation for every ion in the system.

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34
Q

Mammalian neuron. Is the concentration higher on the inside or outside?

Potassium
Sodium
Calcium

A

Potassium - inside conc higher

Sodium - outside conc higher
Calcium - outside conc higher

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35
Q

Action potential (what order of channels)

A

initially due to sodium channels opening (3 NA). then they close. potassium channels open (2 K) and it under shoots (hyperpolarization)

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36
Q

Passive conduction vs active

A

passive - decays over distance

active - is constant over distance

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37
Q

What channel has a “trap door”

A

sodium. causes a refractory period.

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38
Q

Why is it important to have different receptor types?

A

to eliminate cross-talk. make it more specific

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39
Q

Myasthenia Gravis

A

autoimmune disease

-destroys ACh receptors

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40
Q

Ionotropic vs metabotropic receptors

A

ionotropic: paired to an ion channel
metabotropic: paired to a G-protein

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41
Q

Acteylcholin: Nicotinic receptor

A
inotropic excitatory (non-selective)
-found in brain, autonomic ganglia (sympathetic/parasympathetic) and motor endplate
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42
Q

Acetylcholin: Muscarinic receptor

A
  • Metabotropic excitatory

- found in brain, parasympathetic end-organs

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43
Q

ACh: clinical apps

  • Succinylcholine
  • Nicotine
  • Muscarin:
A
  • Succinylcholine: Director nicotinic ACh activator (paralytic drug. contract until no ACh to contract)
  • Nicotine: Mild nicotinic ACh activator (jitters)
  • Muscarin: Mild muscarinic ACh activator (massive parasympathetic response)
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44
Q

Glutamate

A

Excitatory found in brain. (physical trauma can cause release -> lead to seizures)

  • ionotropic receptors: NMDA (main..big bro)**,AMPA (lil bro), Kainate
  • metabotropic receptors: mGluRs
45
Q

GABA

A

Inhibitory found in brain. Alcohol in low dose GABAa agonist. High dose also glutamate antagonist.

  • ionotropic receptors: GABAa,GABAc, chloride channels.
  • metabotropic receptors: GABAb
46
Q

Glycine

A

GABA’s lil bro

  • similar as GABAa receptors
  • inhibitory, inotropic, chloride channels
  • found in spinal cord
47
Q

Dopamine

A

Metabotropic…found in brain: 2 paths.

Mesolimbic pathway: linked to mood.
Nigrostraital pathway: initiation of movement. (motor control)

*also active peripherally as a vasoconstrictor.

48
Q

Dopamine applications. one for each pathway

A

Nigrostriatal path: loss of output leads to Parkinson’s

Mesolimbic path: observed in Schizophrenics. drugs can fix but can cause hallucinations.

49
Q

Norepinephrine (central and peripheral functions)

A

Excitatory metabotropic receptors: alpha and beta adrenergic

Centrally: wakefulness (wake cycles)
Peripherally: sympathetic response (maintains vascular tone)

50
Q

Where is norepinephrine produced?

A

Locus coeruleus

51
Q

Epinephrine

A

norepinephrine lil bro (same receptors)

- found less in CNS

52
Q

Histamine (central and peripheral function)

A

-Metabotropic receptor

Centrally: arousal, nausea (vestibular funct?)
peripherally: immune reactions, gastric acid secretion

53
Q

Serotonin

A

found in brain.
mood regulator

*SSRI antidepressants increase serotonin

54
Q

electrical synapses

A

direct flow of ions through gap junctions

55
Q

chemical synapses

A

electrical signal transduced through a chemical diffusing across a gap

56
Q

Axonal transport

A

nucleus - DNA - RNA - ER - RER - Golgi apparatus -> microtubules transport down

57
Q

Lambert Eaton

A

similar to myasthenia gravis, but antibodies are to calcium channels

58
Q

Early development main steps (6)

A

1) zygote
2) Morula
3) Blastocyst
4) Bilaminar embryo
5) Gastrulation
6) Neurulation

59
Q

zygote

A

initial fertilized cell

60
Q

Morula

A

zygote dives several times (16-32 cells total)

  • same overall volume
  • happens over several days
61
Q

Blastocyst

A
  • Morula cavitates, forming Yolk sac
  • clump of cells inside blastocyst: Inner cell mass
  • forms around time of implantation, about a week old
62
Q

Bilaminar embryo

A

A second cavity forms (the Amnion) on the other side of the inner cell mass

-composed of two layers (hypoblast and epiblast)

63
Q

Hypoblast layer

A

next to yolk sac. does NOT contribute to final embryo

64
Q

Epiblast layer

A

next to amnion. ALL cells from the final embryo derive from these cells

65
Q

Gstrulation

A
  • formation of 3-layer embryo by folding into itslf
  • hypoblast cells (next to yolk sac) are obliterated

-converts the epiblast cells (next to amnion) to: Ectoderm, Mesoderm, and Endoderm

66
Q

Ectoderm

A

during gastrulation epiblast cells converted to this.

***source of skin/nervous system

67
Q

Mesoderm

A

during gastrulation epiblast cells converted to this.

***source of muscle/bone/connective tissue

68
Q

Endoderm

A

during gastrulation epiblast cells converted to this.

***Source of GI and GU system

69
Q

Neurulation

A

Folding of Ectoderm in onto itself to form the neural tube

-Mediated/signaled by the notocord (which turns into intervertebral discs)

  • Floorplate
  • Roofplate
  • Neural crest
70
Q

Floorplate (formed during Neurulation)

A
  • Anterior-most part of neural tube

- Forms motor neurons

71
Q

Roofplate (formed during Neurulation)

A
  • Posterior-most part of neural tube

- forms sensory neurons

72
Q

Neural crest (formed during Neurulation)

A
  • forms from edge of neural tube before it seals
  • migrate away from neural tube and forms 4 things

4 things: peripheral ganglion, facial bones, melanocytes (skin pigment), parts of heart (valves/septums)

73
Q

What are the four parts formed when the neural crest moves away from the neural tube?

A

1) peripheral ganglion
2) facial bones
3) melanocytes (skin pigment)
4) parts of heart (valves/septums)

74
Q

Nerve anatomy (3 layers/parts)

A

Epineurium
Fascicle
Perineurium

75
Q

Epineurium

A

connective tissue covering of nerve

76
Q

Fascicle

A

collections of axons within nerves

77
Q

Perineurium

A

connective tissue covering of fascicles

78
Q

3 main types of injury

A

Neurapraxia
Axonotmesis
Neurotmesis

79
Q

Neurapraxia

A
  • loss of conduction, without any physical disruption
  • frequently compression-type injury
  • leads to disruption of myelin, microtubules, edema, or some other easily repairable block to action potential conduction
  • usually returns to function in several days
80
Q

Axonotmesis

A
  • disruption of axons, with intact connect tissue
  • can repair through Wallerian degeneration and regrowth
  • Wallerian degeneration takes 2-3 weeks
  • nerve regrows at 1mm/day or about 1 inch/month
81
Q

Neurotmesis

A
  • Disruption of entire nerve
  • will NOT regrow properly unless epineurium is surgically repaired
  • if repaired, injury repairs as in axonotmesis
82
Q

Location/mechanism of injury

A

-most common nerves injured are in extremeties

mech:
compression (mechanical/ischemic; usually neurapraxic)
laceration (usually neurotmesis)
traction (usually axonotmesis)
uncommon causes (chemical, heat, radiation)

83
Q

Wallerian degeneration

A
  • takes 2-3 weeks
  • nerve distal to injury site degenerates and is phagocytized.
  • proximal axon regresses, forms growth cone
  • process coordinated by Schwann cells
84
Q

Axon regrowth requires what 4 things?

A

1) clearing of old neuron (Wallerian degeneration)
2) a conducive environment (from the Schwann cells)
3) a physical conduit (intact epineurium)
4) no physical obstruction (ABSENCE of glial scar)

85
Q

Is the final repaired axon/synapse pattern exactly the same as pre-injury?

A

No. is similar to the original but never reconstitutes the original complexity

86
Q

Nerve repair in CNS

A

1) wallerian degeneration similar to in PNS
2) No Schwann cells, debri cleared by microglia and astrocytes
3) instead of creating conducive envir., glia overproliferates and forms glial scar that are a physical barrier to axon regrowth ***

87
Q

Neurogenesis in CNS

A

1) very little if any
2) neurogenesis observed in olfactory bulb (smell) and hippocampus (memory) in lower animals
3) neurogenesis only observed in hippocampus in humans

88
Q

Hebb’s postulate

A

Basically if input and output correlate it stays and strengthens.

if different it weakens and changes.

89
Q

Long-term potentiation

A

synapses with synchronous or high-frequency firing are strengthened.

*can be modulated by chemical channels

90
Q

Long-term depression

A

synapses associated with excessive stimulation are down-regulated.

*can be modulated by chemical channels

91
Q

General principles of plastiity (based on what, limited resources, limited to what?)

A
  • develops based on feedback from experience
  • limited resources so all specialization comes at a cost to other cortex
  • plasticity is limited to “nearby” cortex (horizontal connections)
92
Q

Neuromuscular junction

A
  • nerves synapsing directly on muscles

- affected by diseases to muscles, proteins, neurotransmitters

93
Q

Peripheral nerves

A
  • relatively consistent in their location and innervation
  • innervate specific areas of body
  • little overlap
94
Q

Peripheral plexuses

A
  • “reorients” nerves

- because it mixes multiple nerves together, can caused deficits

95
Q

Spinal roots

A
  • collect all sensory/motor input from a level

- sensitive to pathology around bony spine

96
Q

Lower vs upper motor neuron

A

Lower motor neuron synapses on the muscle
upper motor neuron from descending pathways

*injury to each produces classic syndromes

97
Q

Motor unit organization

A
  • each motor neuron innervates multiple muscle fibers
  • usually all contained within one muscle
  • each muscle fiber only innervated by one motor neuron
  • motor units vary in size and number of contacts
  • depolarizing neuron generally activates all connected fibers
98
Q

Fiber types

A

Type 1: slow twitch
-low force, non-fatiguable, oxidative metabolism
Type IIa: fast fatigue-resistant
-intermediate
Type IIb: fast twitch (fast fatiguable)
- strong force, high fatiguable, energy from ATPase

99
Q

Size principle

A
  • slow twitch activated first

- increasing force requires larger unit recruitment

100
Q

motor unit response to stimulation

A

after injury: motor unit organization degenerates

after chronic stim: fiber types can adapt

101
Q

spinal cord organization: White matter

A
  • descending tracts

- inter-level connections

102
Q

spinal cord organization: Grey matter

A
  • alph-motor neurons
    a) medial: axial
    b) lateral: appendicular
    c) span across multiple spinal levels
  • interneurons
103
Q

spinal cord organization: Ventral roots

A
  • exiting motor nerve fibers
  • combine with posterior sensory fibers to form spinal root
  • exit through bony foramina
104
Q

Lower motor neuron syndromes

A
  • flaccid paralysis
  • hyporeflexia
  • atrophy (use it or lose it)
  • fibrillations
  • fasciculations
105
Q

fibrillations vs fasciculations

A

Fibrillations: spontaneous electrical activity in muscles (seen on EMG)

Fasciculations: Spontaneous gross muscle contraction (occur in unorganized pattern)

106
Q

Muscle spindle (what are the parts sensitive to?)

A

Group 1a: sensitive to dynamic stretch
Group II: sensitive to static stretch
Gamma-motor neurons - spindle gain
** responsible to stretch reflex

107
Q

Golgi tendon organ GTO (sensitive to what? and prevents what?)

A

Group Ib sensory fibers - sensitive to muscle contraction

***prevents overexertion of muscles

108
Q

Flexion/Crossed-extension reflex (what happens?)

A

1) input from nociceptive pathway (pain)
2) ipsilateral flexion (withdrawal)
3) contralateral extension (support)