Nervous tissue Flashcards

1
Q

neurology

A

study of nervous system

neurologist diagnoses/treats disorders of nervous system

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2
Q

nervous system 3 roles

A

1) sense, interpret, respond to stimuli

2) generate movement/gland secretion (“respond” to stimuli)

3) thought, emotion, memory

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3
Q

nervous system and homeostasis

A

contributes to maintaining homeostasis

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4
Q

3 functions/components of nervous system

A

sensory function

integrative function

motor function

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5
Q

1) sensory function

A

afferent neurons (sensory)

signal toward CNS

detects EXTERNAL & INTERNAL stimuli

E.g.
tapping shoulder (external)
heart-rate/GI-tract (internal)

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6
Q

2) integrative function

A

INTERNEURONS b/w afferent and efferent neurons

INTEGRATE feedback in CNS

“deciding” appropriate “response”

also involved in complex mental/psychological processes such as deliberating & consideration via memories

also involved in simple reflexes (E.g. patellar reflex – DTR)

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7
Q

3) motor function

A

“command” sent by CNS via EFFERENT neurons

activate EFFECTORS –> E.g. muscles/glands

Can be Somatic (voluntary) or Autonomic (involuntary)

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8
Q

two major divisions of nervous system

A

CNS –> brain and spinal cord

PNS –>
= cranial nerves (CN1-12),

= spinal nerves (dorsal/ventral roots/rami),

= peripheral nerves (e.g. via cervical/brachial and lumbosacral plexus)

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9
Q

number of neurons in different parts of nervous system

A

brain = 85-100 billion

spinal cord = 100 million

ENS (enteric nervous system) = 500 million

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10
Q

the brain (CNS)

A

within cranial cavity

structural areas (discussed in neurology) as follows:
= cerebral cortex, pons, medulla, cerebellum, hypothalamus, thalamus, basal ganglia, pituitary gland, etc.

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11
Q

3 layers of protection for brain

A

cranium

meninges (CT membranes)

CSF (Cerebrospinal fluid)
= Similar to Blood Plasma composition
= cushions brains
= keeps buoyant in cavities (reduces effective weight so brain not resting heavily against cranial cavity)

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12
Q

CSF & weight of brain (?)

A

CSF buoyancy plays a critical role in preventing the brain from being damaged by its own weight against the cranial cavity (???)

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13
Q

cerebrum

A

largest part of brain

TWO hemispheres

Generally, RIGHT side interacts with left side of body,
LEFT side interacts with right side of body
I.e.
Afferent/Efferent signalling

” Exceptions exist

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14
Q

brain weight/size vs ratio of brain to body weight

A

ratio of brain mass : body mass may be one of the variables indicating intelligence

other variables:
surface area
relative size of brain cortex

E.g.
mice/humans have similar ratio, but human brain is more complex

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15
Q

Spinal cord (CNS)

A

extending from brain

Within vertebral canal (of “ column)

protected via CSF & vertebral column

begins @ foramen Magnum

Ends @ L1/L2 Spinal level (to lumbar plexus & sacral plexus)

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16
Q

spinal cord structure (cross section)

A

internal GREY MATTER (nerve cell bodies)

external WHITE MATTER (nerve tracts, i.e. axons)
—-> ASCENDING & DESCENDING tracts (afferent & efferent)

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17
Q

PNS

A

nerves + sensory receptors

outside CNS

31 spinal nerves (C0 the coccygeal nerve)

12 cranial nerves

peripheral nerves (branches of spinal AND CRANIAL nerves)

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18
Q

spinal nerves

A

8 cervical spinal nerves

12 thoracic

5 lumbar

5 sacral

1 coccygeal

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19
Q

spinal nerves roots

A

ventral roots carry efferent fibres

dorsal roots carry afferent fibres

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20
Q

nerve plexus & spinal nerves

A

branching network of nerves

e.g. brachial plexus
via Ventral rami of C5-T1

(occurs via spinal nerves)

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21
Q

Cranial nerves

A

exit directly from brain or brain stem

CN 1-12 = 12 pairs

sensory & motor signals

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21
Q

somatic vs autonomic

A

see next slides

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22
Q

somatic

A

voluntary

motor control to skeletal muscles only

general/special sense

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23
Q

autonomic

A

involuntary

to smooth/cardiac muscles, & glands

sensory feedback from same areas that are innervated

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24
Q

SNS (somatic nervous system)

A

responsible for reflex arcs

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25
Q

ANS (autonomic) 2 (or 3) branches

A

Parasympathetic nervous system

sympathetic nervous system

enteric nervous system (part of parasympathetic nervous system)

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26
Q

sympathetic nervous system

A

“fight or flight” response

changes during perceived threat to survival

E.g.
increased heart rate (increase O2 supply to skeletal muscles for action)

dilation of pupils (see in dark, increase alertness/focus)

increase glucose from liver to brain/muscle (increased alertness, readiness of skeletal muscles

dilation of airways (O2 to brain/muscles via blood)

slowing of digestion (diverting blood supply & resources to musculoskeletal system)

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27
Q

parasympathetic

A

rest/digest

sexual activity

re-establish homeostasis

decreased heart rate
constriction of pupils
bronchoconstriction
increased blood flow – to GI tract & visceral organs

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28
Q

ENS

A

intrinsic to GI tract

functions independently but technically part of Parasympathetic nervous system (of ANS)

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29
Q

ENS includes…

A

sensory neurons (chemical/mechanical changes in GI tract)

motor neurons (smooth muscle contractions + gland secretion)

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30
Q

Enteric nervous system example

A

food enters stomach:

mechanoreceptors and chemoreceptors detect change (STRETCH & pH)

why?
food causes walls of stomach to stretch
food changes pH of gastric juices

In response?
stomach peristalsis
release of HCl

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31
Q

cells of nervous tissue

A

1) neurons

2) neuroglia

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32
Q

neurons

A

excitability

generate Action Potentials in response to stimuli

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33
Q

how fast do Action potentials travel?

A

1-100meters/second

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34
Q

neuroglia

A

supporting cells of nervous system

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35
Q

anatomy of neuron

A

cell body (aka PERIKARYON) – containing NUCLEUS + organelles

dendrites – projections from cell body – receive input

axon – long thin projection – conducts action potential away from cell body

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36
Q

perikaryon

A

cell body of neuron

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37
Q

axon hillock

A

where axon meets cell body

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38
Q

trigger zone

A

area within axon hillock

Action potentials generated here (begin here)

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39
Q

initial segment

A

segment of axon closest to axon hillock

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40
Q

note axon hillock and related terms

A

axon hillock + trigger zone

initial segment

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41
Q

axoplasm

A

cytoplasm of axon

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42
Q

axolemma

A

cell membrane in region of axon

axon membrane

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43
Q

axon terminals

A

axons and axon collaterals end @ AXON TERMINALS

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44
Q

synaptic end bulb

A

bulges @ end of axon terminal

END BULBS (@ axon terminal) joint w/ motor end plate of muscle fibre

I.e.
Neuromuscular junction

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45
Q

axon collateral

A

side branches

single neuron can communicate w/ many

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46
Q

Nissl bodies

A

granular bodies within cell body (perikaryon)

consist of Rough ER

make proteins

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47
Q

synapse

A

connection b/w two neurons

or b/w neuron & effector
E.g.
NMJ & synaptic cleft
note also:
presynaptic & post-synaptic membrane

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48
Q

Epineurium, perineurium, endoneurium (CT LAYERS)

A

epineurium surrounds entire peripheral nerve

perineurium surround nerve fascicles

endoneurium surrounds individual neuron

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49
Q

slow vs fast axonal transport

A

see following slides

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50
Q

slow axonal transport

A

materials in one direction:
Cell body to axon

supplies new AXOPLASM to developing/regenerating axons

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51
Q

slow axonal transport, rate of movement?

A

1-5 mm per day

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52
Q

fast axonal transport

A

materials in both directions
(to/from cell body)

including substances that are broken down / recycled

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53
Q

fast axonal transport, rate of movement

A

200-400 mm per day

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54
Q

structural (shape) classifications of neurons

A

1) pseudo-unipolar (unipolar)

2) bipolar

3) multipolar

4) Purkinje

5) pyramidal

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55
Q

unipolar neurons

A

tactile sensory neurons

dendrite and axon terminal with Axon in between – CONTINUOUS STRUCTURE

cell body connected to axon

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56
Q

bipolar neuron

A

found in retina, in olfactory area, & inner ear
(SPECIAL SENSES)

1 axon terminal and 1 dendrite on either end of cell body

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57
Q

multipolar

A

multiple dendrites @ cell body

single axon on other end

@ brain & spinal cord
@ motor neurons

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58
Q

Purkinje neurons

A

“massive, intricately branched, flat dendritic trees”

ONLY @ CEREBELLUM
—> Control motor mvmt

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59
Q

Purkinje fibres in heart (NOT SAME THING)

A

named after same scientist

role in cardiac function

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60
Q

pyramidal neurons

A

cell bodies shaped like pyramid

found @ cerebral cortex

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61
Q

neuroglia

A

support, nourish, protect neurons

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62
Q

neuroglia volume of CNS

A

about 1/2 volume of CNS

more numerous than neurons, but smaller

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63
Q

astrocytes

A

largest, most numerous neuroglia

FOUND IN CNS, not PNS (?)

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64
Q

astrocyte, major function

A

form Blood-brain barrier (BBB)

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65
Q

blood-brain barrier

A

tightly sealed lining

maintains selective permeability of capillaries

BBB prevents harmful substances entering CNS

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66
Q

other functions of astrocytes

A

regular blood flow

maintain chemical environment for neuronal signaling

help create Neurotransmitters

Assist neuron metabolism

phagocytosis of synapse

clear debris

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67
Q

oligodendrocytes

A

myelin sheath around CNS axons

facilitate speed of AP

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68
Q

microglia

A

phagocytes of CNS

remove…
–microbes
–cellular debris
–debris from damage

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69
Q

ependymal cells

A

single layer of cells

along VENTRICLES of brain
along CENTRAL CANAL (spinal cord)

Produce CSF (cerebrospinal fluid)

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70
Q

note about ependymal cells and ventricles of brain

A

FOUR major ventricles in brain (cavities)

they produce/store CSF

2 lateral ventricles –> INTERVENTRICULAR FORAMEN
–> 3rd ventricle
–> CEREBRAL AQUEDUCT
–> 4th ventricle
–> CENTRAL CANAL

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71
Q

Pathology: Gliomas

A

brain tumors arising from glial cells (neuroglia)

highly malignant/fatal

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72
Q

glial cells

A

neuroglia

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73
Q

examples of gliomas

A

astrocytomas

oligodendrogliomas

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74
Q

causes of gliomas

A

not fully understood

ionizing radiation
rare genetic conditions

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75
Q

satellite cells

A

surround cell bodies of neurons in PNS

function:
provide structural support

regulate exchange of substances b/w neuron & interstitial fluid

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76
Q

schwann cells

A

form myelin sheath of PNS neurons

similar function to Oligodendrocytes of CNS

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77
Q

myelination

A

insulation of axons via neuroglia

via oligodendrocytes in CNS
via schwann cells in PNS

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78
Q

why myelination

A

increase rate/efficiency of AP transmission

mechanism is via SALTATORY CONDUCTION via myelin sheaths

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79
Q

oligodendrocytes and CNS

A

single oligodendrocyte myelinates multiple neurons

cell body not on neuron

DOES NOT HAVE NEURILEMMA
I.e.
NO NEURILEMMA ON AXON OF CNS

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80
Q

schwann cells and PNS

A

Schwann cell found on single neuron

cell body attached to axon

has neurilemma

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81
Q

Neurilemma

A

outermost layer of axon

sheath of schwann cells

also covers nodes of ranvier

NO NEURILEMMA IN CNS axons

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82
Q

axolemma

A

underneath neurilemma

membrane of axon

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83
Q

nodes of ranvier

A

gaps in myelination

high concentration of ion channels

allows AP to “skip” along axon – increases speed of conduction
I.e.
SALTATORY CONDUCTION

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84
Q

unmyelinated neurons (axons)

A

found in a schwann cell that does not form myelin

neuron (axon) exposed to extra cellular environment

NO SALTATORY CONDUCTIONS
I.e.
Slower conduction of AP

(continuous, without jumping)

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85
Q

grey vs white matter

A

in brain & CNS

some regions lighter than others

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86
Q

grey matter contains

A

cell bodies

dendrites

axon terminals

unmyelinated axons

neuroglia cells

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87
Q

white matter contains

A

myelinated axons

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88
Q

white vs grey matter – location in brain vs spinal cord

A

brain –> grey is superficial, white is deep

spinal cord –> white is superficial, grey is deep

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89
Q

what is grey matter in cerebrum called?

A

cortex

*cerebral cortex

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90
Q

collections of nervous tissue

A

i.e.
how nervous tissue components are grouped together

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91
Q

e.g. of nervous tissue grouping

A

cell bodies typically grouped together

axons typically grouped together

the groups/collections have their own names

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92
Q

E.g. of clusters/groups of neuron structures

A

Ganglia (ganglion)
nuclei (nucleus)
nerve
tract

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93
Q

ganglia

A

neuronal cell bodies

located in PNS

E.g.
dorsal root ganglion

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94
Q

dorsal root ganglion

A

cell bodies of sensory neurons

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95
Q

note varicella zoster and dorsal root ganglion

A

varicella zoster virus remains dormant after initial infection

I.e.
in dorsal root ganglion

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96
Q

if dormant varicella zoster virus reactivates in dorsal root ganglion?

A

= herpes zoster

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97
Q

nuclei

A

neuronal cell bodies in CNS

E.g.
Lentiform nucleus
caudate nucleus

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98
Q

nerves

A

bundle of axons in PNS

either sensory or motor, or mixed

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99
Q

tracts

A

bundle of axons in CNS

E.g. (spinal cord)
ascending tracts (sensory UP)
descending tracts (motor DOWN)

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100
Q

tracts in brain

A

information/signals from one part of brain to another

E.g.
internal capsule
corpus callosum

101
Q

reflex

A

automatic nervous system reponse to certain kinds of stimuli

only in peripheral nerves & spinal cord

preserves homeostasis & protects organism through rapid adjustment

102
Q

E.g. of reflex

A

hand on stove

103
Q

5 components of reflex arc

A

1) stimulate receptor

2) activate sensory neuron

3) signal processing in CNS (via interneurons)

4) activation of motor neuron

5) response of peripheral effector

104
Q

e.g. Stretch reflex

A

“MONOSYNAPTIC” reflex

involves muscle spindles

why monosynaptic?
no interneuron
just motor/sensory neuron

regulates skeletal muscle length

105
Q

stretch reflex steps

A

increase muscle length

sensory neuron triggers motor response (contraction)

E.g.
patellar reflex (a DTR)

106
Q

E.g. postural reflex

A

maintains normal, upright posture

E.g.
calf/anterior leg muscles during standing

107
Q

withdrawal reflex

A

POLYSYNAPTIC

move away from stimulus

108
Q

strongest withdrawal reflex

A

painful stimuli

strength of response determined by location/intensity of stimulus

sometimes withdrawal reflex also triggered by touch/pressure receptors

E.g.
perceived danger

109
Q

flexor reflex

A

type of withdrawal reflex

affects muscles of limb

E.g.
pain when touching/grabbing hot pan

1) pain
2) sensory neuron to interneuron
3) motor neuron (anterior grey horn)
I.e.
contracts flexor muscles – withdraw hand
&
RECIPROCAL INHIBITION
= extensors relax

110
Q

crossed extensor reflex

A

contralateral reflex

coordinated with flexor reflex

flexion of affected side + extension of opposite side

E.g.
1) step on st sharp
2) extensor reflex prepares to receive/support body weight
3) flexor reflex lifts foot

111
Q

DTR

A

stretch reflexes

E.g.
biceps, triceps, ankle-jerk, patellar reflexes

reflex response provides info about specific segment of spinal cord via respective test

112
Q

note subjective response to a stimulus

(similar to but not technically same as withdrawal reflex?)

A

if a stimulus is subjectively seen as dangerous or threat – similar response may occur, even if touch is not painful

E.g.
abuse victim

E.g.
phobia of insects, regardless of presence of actual threat

113
Q

“conscious sensation” & subjective response to stimulus

A

E.g.
spider on arm

varying response depending on past experience with spiders

E.g.
someone with knowledge & interest in spiders might not have withdrawal reflex, especially if they are familiar with the species, and perceive minimal threat

114
Q

General sensation & Voluntary Efferent signals

A

in spider example –> voluntary efferent response mimics withdrawal reflex (?)

appears similar, but technically different (?)

however, the following activation of sympathetic nervous system response (fight/flight) is involuntary

115
Q

relevant pathology (multiple sclerosis)

A

autoimmune disease

progressive degeneration of myelin sheath of CNS axons

sheaths get replaced with scar tissue
fibrous/plaque
–> I.e. SCLEROSIS

116
Q

multiple sclerosis facts

A

idiopathic

genetic link

signs/symptoms:
fatigue
visual disturbance
paresthesia
progressive muscle weakness
“neurological deficits”

Prognosis:
5-10 years lower life expectancy
gap is steadily closing

117
Q

multiple sclerosis in Canada

A

one of the highest multiple sclerosis rates in the world

1/400 people
over 90,000 people

possible link to vitamin D deficiency

more common in AFAB (4x)
more common in people with a relative

118
Q

note upcoming terms, RMP, Graded Potential (GP), & AP (Action potentional)

A

see following slides

119
Q

rapidly changing membrane potential

A

creates electrical signal

120
Q

two things that create abiity to send electrical signals are…

A

1) (very) Negative resting membrane potential (RMP)

2) specific ion channels in cell membrane

121
Q

RMP

A

more naegative inside than outside

122
Q

RMP in neurons

A

-70mV in Neurons

-90mV in muscles

123
Q

why RMP?

A

buildup of positive ions outside cell

(sodium potassium pump (?))

124
Q

why RMP ? (2)

A

1) Na+/K+ pump
(AS WELL AS LEAK CHANNELS) (?)

2) INABILITY OF MOST ANIONS TO LEAVE CELL

125
Q

unequal distribution of ions =

A

inside cell mostly K+

outside cell mostly Cl- & Na+

126
Q

also inside cell

A

negatively charged proteins

127
Q

Na+/K+ pump

A

3 Na+ out

2 K+ in

one more cation pumped out than in = inside negative relative to outside

128
Q

ALSO NOTE LEAK CHANNELS

A

Sodium & Potassium leak channels

passive membrane channels always open

for Na+ & K+

129
Q

But how do leak channels establish RMP?

A

There are more K+ leak channels than there are Na+ leak channels

I.e.
more K+ leaves the cell than Na+ enters

= more relatively negative internal environment

130
Q

But what does Na+ /K+ pump do in response to leak channels?

A

Continues to work to reestablish chemical gradient

but ultimately once again, 2 K+ enters, and 3 Na+ leaves

131
Q

Why INABILITY OF ANIONS TO LEAVE CELL?

A

“anions can’t follow K+ out the cell”

they are attached to large molecules (E.g. ATP, or large proteins)

I.e.
Do not have appropriate channels?

I.e.
inside more negative

132
Q

How neurons generate AP?

A

reverse membrane potential via ion channels

133
Q

which ion channel types allow signal to be sent?

A

1) mechanically gated

2) ligand gated

3) voltage gated

134
Q

mechanically gated channels?

A

physical distortion of cell membrane

I.e.
SENSORY RECEPTORS INVOLVING TOUCH, STRETCH, PRESSURE, VIBRATION,
** & even hearing!!! **

135
Q

where are these mechanically gated channels found?

A

dendrites of neurons

136
Q

2) Ligand gated ion channels

A

AKA
chemically gated ion channels

Open when binding specific ligand (chemicals – NEUROTRANSMITTERS)

E.g.
ACh (acetylcholine) @ the NMJ

137
Q

where ligand gated ions channels mostly found?

A

mostly found on
a) DENDRITES
and b) CELL BODY of neuron

I.e.
where most synaptic communication takes place

138
Q

3) voltage gated ion channels

A

open or close in response to changes in MEMBRANE POTENTIAL

one of the classic characteristics of EXCITABLE MEMBRANE
–> I.e.
Membranes that generate/spread APs

139
Q

e.g. of Voltage gated ion channels

A

Na+, K+, Ca2+ channels

140
Q

Some notes about the SODIUM VOLTAGE GATED ION CHANNEL – what are the TWO independent gates of “ ?

A

sodium channels have 2 independent gates

ACTIVATION & INACTIVATION GATES

141
Q

Activation & Inactivation gates – functions

A

activation gate opens to let sodium in

inactivation gate closes to block sodium ions

142
Q

where are Na+ & K+ voltage gated ion channels?

A

they are on the AXON of a neuron

143
Q

where are Ca2+ voltage gated ion channels in the neuron?

A

on the synaptic end bulbs of the AXON TERMINAL

144
Q

review of where GATED CHANNEL TYPES ARE FOUND IN NEURON

A

chemically (ligand) gated channels are found on the NEURON CELL BODY & DENDRITES

Voltage gated channels are found on the AXON (Na+ & K+ ion channels)

Voltage gated Ca2+ channels are found at the AXON TERMINAL @ synaptic end bulbs

MECHANICALLY GATED ION CHANNELS are found on the DENDRITES of the neuron

LEAK CHANNELS found on cell body, dendrites, AND axon

145
Q

orientation/configuration of most gated ion channels @ RMP

A

closed

opening changes membrane potential

146
Q

where leak channels found?

A

axon, cell body, dendrites

147
Q

what are two electrical signals that neurons use to communicate?

A

1) Graded Potentials (GP)

2) Action Potentials (AP)

148
Q

what is GP

A

initial stimulation of neuron causes a Graded Potential (GP)

149
Q

where does GP occur?

A

in DENDRITES & Cell Body

150
Q

what are the 3 different types of outcomes when a GP occurs?

A

i) GP is strong enough and an AP is generated & goes down axon

ii) GP is not strong enough and an AP is not generated (GP dies out)

iii) GP INHIBITS the neuron by making the Membrane MORE NEGATIVE

151
Q

Graded potentials use which channels?

A

LIGAND GATED

& MECHANICALLY gated

152
Q

Graded potentials are _____

A

VARIABLE – inconsistent

I.e.
Vary in amplitude depending on strength of stimulus
I.e.
“graded”

They are small deviations from the membrane potential (-70mV)

153
Q

2 opposite effects of GP, depending on type

A

Can be depolarizing

or can be HYPERPOLARIZING

–> depolarizing = less negative / more positive

–> hyperpolarizing = make membrane more negative

154
Q

note EPSP & IPSP

A

excitatory & inhibitory POST-SYNAPTIC POTENTIALS

155
Q

GP are ____ized

A

localized

effects are limited to smaller areas of neuron – @ cell body &/or dendrites

156
Q

GP last a ____ time

A

they last a short time – unlike AP

157
Q

GP & Refractory period (?)

A

there is no REFRACTORY PERIOD for GPs

158
Q

can AP be generated without GP

A

no

They must occur

– AND they must adequately DEPOLARIZE the membrane @ “trigger zone”

159
Q

when GP sufficiently depolarizes the membrane @ trigger zone, what is it referred to as?

A

reaching threshold potential

160
Q

how is amplitude of GP determined?

A

stimulus strength

161
Q

EPSP which ion channel?

A

usually Na+ entering cell

162
Q

IPSP which ion channel?

A

usually Cl- entering cell

or K+ leaving cell

163
Q

summation of GP – and two types

A

GPs added together, adding to their strength, and ability to reach THRESHOLD POTENTIAL

1) Spatial summation
2) Temporal summation

164
Q

spatial summation of GPs

A

summation of GP

STIMULI OCCUR AT DIFFERENT PLACES @ SAME TIME

= more Na+ ligand/mech- gated channels = LARGER GP

165
Q

Temporal summation of GPs

A

stimuli ocurring @ same place @ different times (one after another) – in quick succession

I.e.
keeps sodium channels open –> Creates larger GP

166
Q

ACTION POTENTIALS

A

all or none

when THRESHOLD POTENTIAL REACHED
(AKA “AP threshold”)

I.e.
membrane sufficiently depolarized to activate VOLTAGE GATED ION CHANNELS @ axon

VIA the…
TRIGGER ZONE @ axon hillock

Moves towards…
axon terminals (One-directional)

167
Q

all or none

A

all channels open. Or none open.

(voltage gated ion channels)

168
Q

WHAT IS THE THRESHOLD POTENTIAL? (AP THRESHOLD) ? (in mV)

A

-55 mV

EPSP takes neuron closer to threshold
IPSP takes neuron farther from threshold

169
Q

what is the characteristic feature of SIZE & AMPLITUDE of AP?

A

always same same & amplitude

170
Q

the 3 phases of AP

A

1) depolarization

2) repolarization

3) hyperpolarization

171
Q

1) depolarization

A

GP causes membrane of AXON to reach THRESHOLD

@ -55mV voltage-gated Na+ channels open & Na+ rushes into cell

172
Q

2) repolarization

A

K+ channels open – K+ rushes out of cell

cell returns to -70mV standard RMP

173
Q

3) hyperpolarization

A

voltage gated K+ channels delayed in closing

I.e.
dip below -70mV standard RMP

eventually channels close & neuron reset to standard RMP

174
Q

list of steps in generating AP

A

1) RMP (-70mV) – both Na+ & K+ channels closed

2) depolarization to “threshold potential” –> -55mV (?) –> voltage gated ion channels open (Na+)

3) Rapid depolarization via voltage gated sodium channels –> goes from -55mV to positive value (E.g. +10)

4) @ +30mV membrane potential –> Na+ voltage gated channels close
(VIA INACTIVATION GATE**)
–> K+ voltage gated channels open

5) Repolarization via K+ channels
as RMP reaches -70mV again, voltage-gated K+ channels begin to close
—> TAKES some time to all close, so brief HYPERPOLARIZATION occurs

175
Q

what mV potential does INACTIVATION gate of Na+ voltage channels close?

A

@ +30mV

176
Q

when do K+ voltage gated channels open?

A

+30mV (?)

177
Q

when do K+ voltage gated channels begin to close?

A

-70mV

178
Q

why does hyperpolarization briefly occur?

A

takes while for K+ channels to fully close

179
Q

note about inactivation & activation gate of Na+ channels (voltage gated)

A

inactivation gate closes @ +30mV

later on activation gate closes again, and inactivation gate opens
–> @ RMP

180
Q

GP vs AP

A

duration, magnitude, decay?, location?

vary in duration, magnitude, and they decay, & occur @ dendrite & cell body
= GP

same duration, magnitude, long distance, only in axon
= AP

181
Q

refractory period types (2)

A

relative refractory period

absolute refractory period

182
Q

absolute refractory?

A

inactivation gate is closed – therefore no GP can let Na+ into cell

183
Q

relative refractory

A

inactivation gate open, and ACTIVATION gate is closed –> HOWEVER K+ channels still open

–> therefore a STRONGER GP than usual is required to bring cell back to THRESHOLD POTENTIAL (AP threshold)

184
Q

AP propagation

A

AP generated @ “initial segment” of axon (segment closest to “axon hillock” – where “trigger zone” is)

AP triggers adjacent units

only in one direction b/c of ABSOLUTE REFRACTORY PERIODS of voltage channels in opposite direction

185
Q

continuous vs saltatory AP propagation

A

continuous propagation occurs in UNMYELINATED axons
–> Slower –> 1m/s

saltatory propagation occurs in myelinated axons
–> only depolarization @ nodes is necessary
–> skips internodes b/c ions can’t cross myelinated region
–> faster than “CONTINUOUS” propagation

LARGER DIAMETER AXON = less resistance to ion movement = faster propagation

186
Q

axon diameter and propagation speed

A

LARGER DIAMETER AXON = less resistance to ion movement = faster propagation

187
Q

speed of propagation via 3 factors

A

1) myelination amt

2) axon diameter

3) temperature

188
Q

1) myelination

A

more myelination = faster

189
Q

2) axon diameter

A

more diameter = faster
(less resistance to ion movement)

190
Q

3) temperature

A

greater temperature = faster propagation

191
Q

nerve fibre types (3)

A

based on propagation speed

1) A fibres (very fast)

2) B fibres (moderately fast)

3) C fibres (slowest)

192
Q

A fibre types

A

alpha, beta, gamma, delta

193
Q

A fibres

A

largest diameter

myelinated

FASTEST

(up to 130m/s)

194
Q

A fibre speed

A

up to 130m/s

195
Q

where A fibres?

A

Axons for AP to to skeletal muscles

196
Q

what sensory impulses for A fibres?

A

touch, pressure, proprioception,

some pain/temperature

197
Q

B fibres

A

moderate size diameter

myelinated

moderately fast

(up to 15m/s AP)

198
Q

B fibre speed?

A

up to 15m/s

199
Q

where B fibres?

A

@ ANS

& visceral organs

200
Q

C fibres

A

smallest diameter

NO MYELIN

SLOWEST

201
Q

where C fibres?

A

reproductive, urinary, excretory, digestive, neurons

some pain receptors
(@ skin/viscera)

I.e.
NOCICEPTORS

202
Q

signal transmission b/w neurons

A

see following slides

203
Q

what is synapse

A

point of interaction

b/w two neurons

or b/w neuron & effector
(e.g. muscle/gland)

synapse = info filtered/integrated

204
Q

two synapse types

A

electrical

& chemical

205
Q

some synapse terminology

A

pre-synaptic neuron

post-synaptic neuron

axodendritic

axo somatic

206
Q

axo-dendritic synapse

A

synaptic end bulbs @ axon terminal

–> interact with DENDRITES

(of post-synaptic neuron)

I.e.
axodendritic SYNAPSE

207
Q

axo somatic synapse

A

synaptic end bulbs of axon terminal

–> interact with neuron cell body itself
(of post synaptic neuron)

208
Q

ELECTRICAL synapse

A

VIA GAP JUNCTIONS

209
Q

where electrical synapses?

A

neocortex

smooth & cardiac muscles (NEURONS OF “ ???)

210
Q

advantages of Electrical synapses

A

faster

synchronized
(large number of neurons / muscle fibres produce AP in unison)

coordinated
(contraction of heart muscle fibres, or visceral smooth muscle)

211
Q

chemical synapse

A

NT across synaptic cleft (Neurotransmitters)

MOST COMMON synapse type

MOST synapses b/w neurons

ALL synapses b/w neuron & effector

212
Q

speed of chemical synapse vs electrical

A

slight delay

213
Q

advantage of chemical synapse

A

more control over response (?)

CAN BE EXCITATORY OR INHIBITORY

214
Q

chemical synapse steps

A

AP arrives at synaptic end bulb of axon terminal

voltage-gated Ca2+ channel opens

Ca2+ stimulates exocytosis of synaptic vesicles containing NT (e.g. Acetylcholin)

Each vesicle containing several thousand NTs

NTs bind to LIGAND-gated ION channels on the POST-SYNAPTIC neuron (or on the effector)
I.e. “POST SYNAPTIC MEMBRANE”

ion flow generates GRADED POTENTIAL (Post-synaptic potential)

215
Q

recall: When do Ion channels @ post-synaptic membrane close?

A

signal ends when Neurotransmitter is…

1) broken down by enzyme (recycled)
E.g.
Acetylcholinesterase for ACh

2) “Diffuses out of synaptic cleft”

3) REUPTAKE by pre-synaptic neuron
(not for ACh)

216
Q

the complexity of POST-SYNAPTIC POTENTIALS

A

Note EPSP & IPSP

see following slides

217
Q

how many synapses (pre-synaptic neurons) can a single neuron receive signal from?

A

Net result of all signals (integration) @ AXON HILLOCK (trigger zone)

THOUSANDS

can be both excitatory or inhibitory

Determines rate of AP @ “INITIAL SEGMENT”

218
Q

synaptic fatigue

A

SYNAPTIC FATIGUE

E.g.
supply of NT not keeping up w/ demand (frequency of AP arriving @ Axon terminal)

Synapse unable to receive signal from Pre-synaptic neuron

–> Until NT (E.g. ACh) replenished

This inability to move AP from pre-synaptic neuron to post-synaptic neuron (b/c of NT activity)

219
Q

two types of Neurotransmitter receptor

A

1) Ionotropic receptors
(Ligand-gated receptors)

2) Metabotropic receptors
(G-protein coupled receptors)

220
Q

1) Ionotropic receptors

A

Ligand-gated receptors

Neurotransmitter connected DIRECTLY to ION CHANNEL

Excitatory or inhibitory

E.g.
ACh receptor @ NMJ is connected to Sodium Ion Channel

221
Q

2) metabotropic receptors

A

G-protein coupled receptors

via messenger protein (G protein) to open Ion channel

receptor not on ion channel

USUALLY INHIBITORY

ACh excitatory @Ionotropic receptors
inhibitory @Metabotropic receptors

222
Q

metabotropic receptors create ____ response usually (inhibitory or excitatory?)

A

usually inhibitory

223
Q

2 categories of Neurotransmitters

A

1) Small-molecule NTs

2) Peptide NTs (larger)

224
Q

E.g. of small molecule NTs

A

Acetylcholine

amino acids – Glutamate & Aspartate (excitatory)
GABA & Glycine (inhibitory)

Biogenic amines – Epinephrine & norepinephrine
Dopamine
Serotonin

Nitric oxide

225
Q

about ACh @ responses @ different locations

A

excitatory NT @ NMJ

“Excitatory between pre-ganglionic and post-ganglionic neurons of the ANS”

“Inhibitory NT in cardiac muscle in response to parasympathetic NS”

226
Q

about Amino Acids (as small-molecule NTs)

A

Glutamate & Aspartate
= excitatory AA small-molecule NTs

GABA & Glycine
= inhibitory AA small-molecule NTs

GABA = Gamma-aminobutyric Acid (CNS)
= GABA = stress-reducing, sleep enhancing

Glycine = inhibitory @ NMJ

227
Q

about BIOGENIC AMINES (as small-molecule NTs)

A

Epinephrine & Norepinephrine (adrenaline & noradrenaline)

= can act as HORMONE when released by ADRENAL glands
= also can act as NEUROTRANSMITTER in some neurons in brain & sympathetic nerves

Epinephrine & Norepinephrine contribute to
–> Fight/flight response
–> = increase in BP, heart rate, blood sugar, etc

228
Q

two other biogenic amines (as small-molecule NTs)

A

Dopamine (DA)
E.g.
mood & pleasure centres

Serotonin (5-HTP)
E.g.
sensory perception & mood

229
Q

last example of small-molecule NT

A

Nitric oxide

–> potent vasodilator
–> important excitatory NT in brain
–> role in erections in males

230
Q

2) PEPTIDE NEUROTRANSMITTERS

A

found in CNS/PNS

excitatory/inhibitory

USUALLY BIND TO METABOTROPIC RECEPTORS

many are also HORMONES (note larger size)

231
Q

Peptide NTs E.g.

A

ENDORPHINS & ENKEPHALINS
= neuropeptide
= act as painkiller
= 200x stronger than morphine

SUBTANCE P
= neuropeptide
= enhances pain perception

232
Q

discovery of first neuropeptides (i.e. peptide NTs)

A

neurons in brain w/ receptors for opiate drugs = discovery of first Neuropeptides

233
Q

what are the ways NT effects can be modified?

A

1) NT synthesis increased/decreased

2) NT release increased/decreased

3) NT receptors altered (activated/blocked)

4) NT removal increased/decrease

234
Q

1) NT synthesis increased/decreased

A

NT synthesis increased/reduced

E.g.
patient’s with Parkinson’s disease produce less dopamine

235
Q

2) NT release increased/decreased

A

NT release increased/reduced

E.g. amphetamines enhance release of dopamine & norepinephrine

e.g. botulinum toxin blocks release of ACh from somatic motor neurons

236
Q

3) NT receptors altered

A

NT receptors activated/blocked

E.g.
myasthenia gravis –
antibodies block ACh receptors @ NMJ
–> cause muscle weakness & fatigue

237
Q

4) NT removal increased/decrease

A

E.g.
cocaine delays reuptake of dopamine by blocking its “active transporters”
I.e.
prevents dopamine REUPTAKE by pre-synaptic terminal/neuron

238
Q

neural circuit types

A

neural circuits = functional groups of neurons

1) simple circuit
2) diverging circuit
3) converging circuit
4) reverberating circuit
5) parallel after-discharge circuit

239
Q

simple neural circuit

A

simplest

single presynaptic to single post-synaptic

1:1

VERY RARE

240
Q

diverging circuit

A

single neuron stimulates multiple neurons, which each stimulate multiple neurons

SIGNAL AMPLIFIES

E.g.
from brain to spinal cord to peripheral nerves to effector (for movement)

241
Q

converging neuronal circuit

A

multiple neurons stimulate single neuron

facilitates SUMMATION

E.g.
single motor neuron receiving numerous signals from brain

242
Q

reverberating neural circuit

A

similar to simple

however…
branches from later neurons synapse w/ earlier ones
(reverberate backwards)

E.g.
coordinated movements
short-term memory
breathing

243
Q

parallel after-discharge neural circuit

A

single pre-synaptic neuron stimulating post-synaptic neuron

same neuron also stimulates parallel neurons – which all synapse back to same post-synaptic neuron

E.g.
precise activities like solving math equations

244
Q

damage of nervous tissue and regenerative capabilities

A

see following slides

245
Q

neuroplasticity

A

adapt/change based on experience

physical changes =
= sprouting of new dendrites
= synthesis of new proteins
= changes in synaptic contact w/ other neurons

246
Q

neuroregeneration

A

mild-moderate damage of PNS is capable of being repaired

note role of protective sheath of NEUROLEMMA from Schwann Cells in PNS

PNS nerves have good chance of recovery

CNS nerves do NOT regenerate

247
Q

neurogenesis

A

birth of new neurons from undifferentiated STEM CELLS

occurs during embryological development

occurs in small/specific areas of brain throughout life

248
Q

processes during repair of peripheral nerve tissue

A

changes in cell body

also changes in axon distal to injury

CHROMATOLYSIS
= degranulation of Nissl bodies within the neuron (for repair process)

WALLERIAN DEGENERATION
= degeneration of distal portion of axon & myelin sheath
(also as a part of repair)

249
Q

process of PNS repair (continued)

A

Schwann cells multiply via mitosis

form REGENERATION TUBE

tube guides growth/repair of axon from proximal area

axons grow 1.5mm/day from proximal area

250
Q
A