November Exam Flashcards
(252 cards)
1
Q
Are cells a part of the internal environment?
A
no, they are maintained by it, but aren’t part of it
2
Q
Explain the breakdown of total body water
A
42L TBW
ICF = 28L
ECF = 14L (interstitial = 11L, plasma = 3L)
3
Q
Explain Na+, K+, Cl- and protein concentrations in body fluids
A
Na+ is highest in plasma and interstitial
K+ is highest in intracellular
Cl- is highest in plasma and interstitial
proteins are highest in intracellular, then plasma, then low in interstitial
4
Q
What is the equation relating diffusion distance to time?
A
t=x^2 / D
x is the distance, D is the diffusion coefficient
5
Q
How far are cells usually from capillaries?
A
25-50um
6
Q
What substances will diffuse through the cell membrane?
A
O2, CO2, fatty acids, steroids and alcohols with 5 or more carbons
7
Q
What is J in Fick’s law of diffusion? k? r?
A
J is the net RATE of diffusion
k is Boltzmann constant
r is the molecular radius
8
Q
What parts of Fick’s law of diffusion can be combined into D?
A
k, T, r and n
9
Q
Describe how the rate of diffusion is related to [ ] gradient, total surface area, temp, size and viscosity
A
proportional to [ ] gradient, surface area, temp
inversely proportional to size and viscosity
10
Q
What 5 things affect the rate of movement of molecules through protein channels?
A
size- smaller than 0.8nm charge electrochemical gradient pressure gradient hydration energy i.e. Na+ acts as a larger molecule than K+ with its H2O shell
11
Q
What are the relative permeabilities of the cell membrane to ions?
A
most permeable to Cl-
permeable to K+
least permeable to Na+
12
Q
What are the 3 characteristics of carrier-mediated transport?
A
chemical specificity
competitively inhibited
saturation
13
Q
What does facilitated diffusion use to move molecules across the membrane?
A
conformational change after binding
14
Q
What does the Na+/K+ ATPase move in each cycle?
A
3 Na+ out of the cell
2 K+ into the cell
15
Q
Explain how the Na+/K+ ATPase works
A
bind 3 Na+ hydrolyze ATP and release ADP get conformational change, now have low affinity for Na+ release Na+ high affinity for K+, bind 2 release Pi another conformational change new ATP binds conformational change, causes low affinity for K+ K+ is released
16
Q
What is oubain?
A
inhibits Na+/K+ pump
binds when K+ would normally bind
17
Q
What is digoxin?
A
inhibitor of the Na+/K+ pump
18
Q
What are the functions of the Na+/K+ pump?
A
helps maintain concentration gradients
cause slightly increased negativity outside the cell
keeps cell from swelling and bursting
19
Q
What determines osmotic pressure?
A
the # of molecules in solution (not size or type)
20
Q
What is an osmole?
A
the number of particles in one mole of an undissociated solute
21
Q
What are osmolality and osmolarity?
A
osmolality = Osmol / kg water osmolarity = Osmol / L solution
22
Q
What is the osmolality of body fluids?
A
300 mOsmol per kg water
23
Q
What happens in CF?
A
Cl- doesn’t leave the cell, Na+ will want to come in
H2O will move in
there won’t be as much periciliary liquid
cilia can’t clear the airway, mucus builds up
24
Q
What is hyponatremia?
A
water intoxication
drink too much water, ICF volume increases, brain swells, die
25
Where do changes to body fluids occur?
ALWAYS in ECF first
26
How large are slits in endothelial cells?
about 8nm
27
What is Kwashiorkor malnutrition?
severely malnourished, particularly in protein
decreased plasma proteins
decreases plasma colloid pressure
fluid doesn't move back into blood vessels as much
get edema
28
What is capillary hydrostatic pressure?
capillary blood pressure
| 25mmHg at the arterial end, 10mmHg at the venous end
29
What is interstitial hydrostatic pressure?
```
negative in subcutaneous tissue
positive in encapsulated organs i.e. brain, liver, kidney
+ moves into the plasma
- moves out of the plasma
-6mmHg to +6mmHg
```
30
What is interstitial colloid osmotic pressure?
osmotic pressure due to the proteins in the interstitium
| 5mmHg
31
What is plasma colloid osmotic pressure?
osmotic pressure due to the proteins in plasma
| about 28mmHg
32
What is the equation for net fluid movement across the endothelium?
NFM = Kf [(Pc-Pif) - (piP-piIF)]
33
What is the net fluid movement in capillaries?
+8mmHg at the arterial end = filtration
| -7mmHg at the venous end = reabsorption
34
What does Kf depend on? Where is it high and low?
permeability of capillary and surface area of endothelium
high in the kidneys
low in the brain
35
What causes fluid to move into the lymphatics?
pressure gradient
smooth muscle pumps
valves and contraction of skeletal muscles
36
What are 4 things that can cause edema?
decreased plasma proteins (decrease piP)
blockage of venous return (decrease Pc)
blockage of lymphatic system (can't remove excess)
tissue damage (increase Kf)
37
What generates RMP?
the selective permeability of the membrane to particular ions
K+ is allowed to leak out down its concentration gradient
38
What are the conditions for the Nerst equation?
membrane is only permeable to one ion
| there needs to a be concentration gradient for the ion
39
What are the equilibrium potentials for K+, Na+ and Cl-?
```
EK+ = -90mV
ENa+ = +60mV
ECl- = -70mV
```
40
What is an equilibrium potential?
the electrical potential which must be applied to the INSIDE of the cell to prevent the movement of an ion down its concentration gradient
41
What is the Goldman equation for?
finding membrane potential including K+, Na+ and Cl-
42
What is the formula for the Nerst equation?
61.5 log [outside]/[inside]
with valence of 1/-1
for Cl- is inside/outside (because valence is negative)
43
Why is the peak of an AP rounded?
because there is some overlap between Na+ and K+ channels being open
44
What is threshold? What does the AP usually depolarize to?
-55mV is threshold
| +45mV is where it goes to
45
How does membrane potential get back to RMP after hyper polarization?
chloride leaving the cell and Na+ leaking in
46
Explain tetrodotoxin poisoning
reversibly blocks the Na+ VG channels
can't depolarize the membrane, no APs
K+ channels will still open so you will get hyper polarization, but because Na+ can't come in there will only be a small depolarization
47
What is grayanotoxin?
block VG channels
48
What is tetraethyl ammonium (TEA)? Dendrotoxin?
block K+ VG channels
can't depolarize
muscles are constantly being activated
seizures
49
How long is an AP?
1-2ms in nerve cells
1.5-2ms in skeletal muscle
300ms in cardiac muscle
50
What causes the absolute refractory period in APs?
inactivated Na+ VG channels
51
What causes the relative refractory period in APs?
caused by hyper polarized membrane and because many Na+ channels are still inactivated
52
What are 3 things that happen as a result of refractory periods?
"all-or-none"
there is a max frequency of APs
AP is travels orthodramatically
53
What would happen to the AP if you increased the concentration of NaCl in the ECF?
ENa+ would increase and so the amplitude of the AP would increase (Na+ would come in more quickly)
54
What do local anesthetics do?
block Na+ VG channels, preventing APs
55
What are the "stabilizing forces" that try to maintain RMP?
Na+/K+ pump
K+ leaks out of the cell
Cl- leaks into the cell
56
What is happening when a cell hits -55mV?
the stabilizing forces can't stabilize enough anymore
57
What are 6 characteristics of sub-threshold responses?
they are local
decays/degrades very rapidly with distance
magnitude is proportional to magnitude of stimulus
can be depolarizing or hyperpolarizing
membrane isn't refractory
they can be summed
58
What is current? How is current carried?
it tis the rate of movement of positive ions
| from positive to negative potential
59
What cells produce the myelin sheath?
PNS- Schwann cells
| CNS- oligodendrocytes
60
Where are VG ion channels located in myelinated neurons?
Na+ are at the nodes
| K+ are at the paranodes
61
What are 2 advantages to saltatory conduction?
faster and conserves energy
62
How is axon diameter related to conduction speed?
unmyelinated- increases with square root of diameter
| myelinated- increases directly with diameter
63
Describe multiple sclerosis
myelin sheath gets damaged
APs can't propagate, muscles eventually can't contract
get paralysis
64
Are alpha motor neurons myelinated?
yes
65
Does the amount of Ach released at NMJ change?
no it is discreet
66
When Ach is released is there always enough to cause an AP?
yes
| i.e. the EPP generated will also be strong enough to reach threshold
67
Describe the receptors that respond to Ach at the NMJ
are called Ach-nicotinic (Ni) receptors
bind 2 Ach
are non-specific cation channels
they let in Na+ or K+
68
What is the RMP in muscle cells? What happens as a result of this?
-90mV
| when the non-specific cation channels open Na+ moves in because K+ is at EK+
69
How is an AP generated at the NMJ?
local currents (EPPs) open VG Na+ and K+ channels on the membrane adjacent to the endplate
70
What does botulin toxin do?
blocks the release of Ach at NMJ by breaking down proteins that are needed for vesicles to fuse to the membrane
stops muscles from moving (Botox)
can cause respiratory and musculoskeletal paralysis
71
What do nerve gases do?
block the action of acetylcholinesterase
get sustained depolarization of postsynaptic cell
seizures
can die of asphyxiation
72
What is myasthenia gravis?
antibodies bind to and block Ach receptors on the muscle cell end plate
can't open ligand-gated channels
no AP
73
Do muscle cells only have one nucleus? What else do they contain?
multinucleated
| contain glycogen, fat droplets and myoglobin
74
What is the lumen of the T-tubules in a muscle cell continuous with?
the ECF
75
Describe tropomyosin
rod-shaped protein with 2 alpha helical polypeptide chains wrapped in a supercoil
lies along actin
each one covers 6-7 myosin binding sites
76
Describe troponin
Troponin C- binds Ca2+
Troponin A- binds actin
Troponin T- binds tropomyosin
77
Describe myosin
2 polypeptides/molecule
| each head has 2 light protein chains, one binds actin, one binds ATP
78
What is the M line?
holds thick myofilaments together
79
What is the Z line?
holds thin myofilaments together
80
What does titin do?
helps hold thick and thin myofilaments in place and helps return to resting position after muscle contraction
81
What is a dihydropyridine (DHP) receptor?
voltage sensor on T-tubules that change conformation in response to APs
82
What is a ryanodine receptor?
are on SR
are opened by by DHP receptors
allow the release of Ca2+
83
Does one AP release enough Ca2+ to saturate all troponin molecules?
yes
84
Why does muscle contraction outlast the AP?
because Ca2+ flows out without saturation
| but pumping Ca2+ back into SR gets saturated and therefore takes longer
85
What is calsequestrin?
a Ca2+ binding protein found in the SR which can bind up to 50 Ca2+ molecules
86
What is the rate-limiting step in muscle contraction?
ATP hydrolysis
87
Explain the actin-myosin and ATP cycle
bind ATP
hydrolyze it, myosin has high affinity for actin
have AP, Ca2+ release etc
form crossbridge
Pi is released, get power stroke
ADP is released
new ATP binds and cross bridge is released
88
What are the 4 functions of ATP in muscle contraction/relaxation?
increasing the affinity of myosin heads for actin
energy for cross bridge movement
attaches to myosin allowing it to dissociate from actin
required to pump Ca2+ back into the lateral sacs
89
How do the axon diameters of alpha motor neurons differ with motor unit size?
small motor units have smaller diameter motor nerve
| large motor units have larger diameter motor nerve
90
How do you increase the force of contraction of a muscle?
frequency and motor recruitment
91
What is a muscle twitch?
the muscle contraction caused by a single AP in the motor nerve
92
What do muscle twitches have a period of latency?
AP needs to travel, neurotransmitter release etc before contraction starts
93
Why can you sum twitches but not APs?
APs are shorter and have refractory periods
94
What is complete titanic contraction?
when the twitches of a muscle sum to a smooth curve
95
Which motor units are recruited first in vivo?
small ones
because I is constant so the largest voltage comes from the neurons with the highest resistance
(first one to reach threshold fires first)
96
Which motor units are recruited first in vitro?
large ones
| V is constant so the largest I comes from smallest resistance
97
Which motor units fatigue first?
large ones
| small ones fatigue last even though they are recruited first in vivo
98
Describe slow-oxidative muscle fibers
```
Type I
red muscle
low myosin ATPase activity (~100ms)
innervated by small motor neurons (therefore early and last a while)
mainly use oxidative phosphorylation
resistant to fatigue
high content of myoglobin
dark
```
99
Describe fast-oxidative muscles fibers
```
Type IIa
high myosin ATPase activity
innervated by small motor neurons
use mainly oxidative phosphorylation
medium resistance to fatigue
high myoglobin content
```
100
Describe fast-glycolysis muscle fibers
```
Type IIb
white
high myosin ATPase activity
innervated by large motor neurons (recruited last and only for forceful movements)
use glycolysis
low myoglobin content
fatigue quickly
```
101
What are 5 functions of glial cells?
```
providing "back-up" glucose
removing neurotransmitters
removing ammonia
taking up K+
providing myelin sheath
```
102
Where can axons terminate on other axons?
dendrites, soma, axon terminals
103
What are Dr. Hore's equilibrium potentials for the ions in a representative neuron?
```
Na+= +60mV
K+= -90mV
Cl-= -80mV
Ca2+= +120mV
```
104
What are the characteristics of chemical synapses?
```
high electrical resistance
synaptic delay
enables integration
effects take ms to min
plasticity
```
105
What are the characteristics of electrical synapses?
low electrical resistance
cytoplasmic continuity
no synaptic delay
bi-directional
106
How big is an EPSP at a single synapse?
107
What is a difference between CNS synapses and NMJ?
CNS can be excitatory or inhibitory
| NMJ only excitatory
108
How does current flow at an inhibitory synapse?
in the opposite direction as an excitatory one i.e. make sit less positive near where you start an AP
109
What are 2 important characteristics of the axon hillock?
low electrical resistance
| high density of VG Na+ channels
110
How is an AP started on the post-synaptic neuron?
```
ligand-gated Na+/K+ channel opens
axon is high electrical resistance, axon hillock is low so current flows out of the axon hillock
causes depolarization
this will open Na+ VG channels
reach threshold then you get an AP
```
111
What are AMPA receptors?
ionotropic
open in response to glutamate and open Na+ channels and cause an EPSP
(normally what we think of with an AP)
112
What are NMDA receptors?
```
ionotropic
open in response to glutamate
open Ca2+ channels, very high conductance
usually open bc of strong activation
cause a cascade of secondary messengers
involved in plasticity
```
113
What are the 3 outcomes of NMDA receptors binding glutamate?
regulate existing AMPA channels ie phosphorylate them
insert new channels into the membrane
alter gene expression to make more channels
overall: change the excitability of the membrane
114
What are neuromodulators?
bind peptides
| activate GPCR to change excitability of the membrane in the same way NMDA receptors do
115
Name 5 classes of neurotransmitters or neuromodulators and examples of each
Ach
Biogenic amines
Dopamine, NE, E
Serotonin/5HT
Amino acids
glutamate
GABA, glycine
Neuropeptides
```
Miscellaneous
nitrous oxide (retrograde), CO, steroids
```
116
What is the main excitatory neurotransmitter in the brain?
glutamate
117
Name 2 widespread inhibitory neurotransmitters in the brain
GABA, glycine
| glyine is mainly at the spinal cord and brainstem
118
What is strychnine?
glycine antagonist
| gets rid of the inhibitory effect of glycine, causes painful muscles convulsions and eventually death through asphyxia
119
Describe long-term potentiation
use-dependent enhancement of synaptic response
increases size of EPSPs
in hippocampus and neocortex
long lasting
best cellular correlate of memory
pre- and post-synaptic mechanisms
occurs mainly at excitatory synapses with NMDA receptors
120
What are the mechanisms thought to contribute to LTP?
pre-synaptic
changing the Ca2+ channels to allow for more Ca2+ entry and thus more neurotransmitter release
post-synaptic
activation of secondary messengers resulting in the same changes as NMDA receptors have on AMPA channels
121
Where do presynaptic facilitation and inhibition come from? How do they work?
synaptic endings on the axon terminal on neurons
inhibition- decrease Ca2+ influx, less neurotransmitter released, smaller EPSPs
facilitation- increase Ca2+ influx, more neurotransmitter released, larger EPSPs
122
What is spatial summing?
the summing of synaptic potentials at different spatial locations on a neuron
123
What is temporal summing?
the summing of synaptic potentials at a single synapse due to repetitive firing of the presynaptic axon
124
What is longer, EPSPs/IPSPs or APs?
EPSPs and IPSPs, this is why they can summate
125
Where are the somas of sensory receptors found?
dorsal root ganglion
126
What is an adequate stimulus?
the particular form of energy that a receptor is most sensitive to
127
Can there be hyper polarization in the somatosensory system? (i.e. IPSPs, not referring to getting back to RMP)
no always depolarization
128
What are 4 characteristics of receptor/generator potentials?
depolarization is due to an increase in Na+/K+ conductance i.e. ion channel lets them both move, but Na+ is faster
local, not propagated
graded and proportional to the magnitude of the stimulus
can summate
129
Where is an AP generated in the somatosensory system?
at the first node
current flows out at the first node, get a current loop which causes depolarization and opens VG Na+ channels, AP if it reaches threshold
130
How do slowly adapting receptors signal intensity?
frequency and population coding
| respond to a static stimulus (position)
131
How do rapidly adapting receptors signal intensity?
population coding only
| signal movement of skin/hair (velocity)
132
What are 2 reasons why Pacinian corpuscles are rapidly adapting?
inner lamellae slip back in spite of maintained stimulus
| properties of ion channels in the axon membrane
133
What are the most sensitive mechanoreceptor?
Pacinian corpuscles
| detect vibration etc
134
Which receptors are rapidly adapting?
Pacinian corpuscles, Meissner's corpuscle
| hair receptors
135
Which receptors are slowly adapting?
Merkel's receptors, Ruffini's endings and free nerve endings
136
Are the axons of all receptors in the somatosensory system myelinated?
all except for free nerve endings (they also have small diameter axons and thus conduct slowly, C)
the other 5 are all A alpha or A beta
137
What is the difference between the 2 types of nociceptors?
one is A delta (myelinated, faster) and the other is C (unmyelinated)
138
What type of axons do the muscle spindle and GTO have?
muscle spindle
Ia afferent = A alpha
group II afferent = A beta
GTO = A alpha
139
Where do alpha motor neurons get classified?
they are A alpha, but aren't group I because the muscle nerve classification only includes afferents
140
What is an example of an A gamma axon? A delta? C?
A gamma- fusimotor neurons
A delta- fast pain, cold temp
C- slow pain, warm temp, crude touch
141
What is an example of Ia axon? Ib? II? III and IV?
Ia- annulo spiral from muscle spindle
Ib- GTO
II- flower spray from muscle spindle
III and IV- free nerve endings in muscle (IV is unmyelinated)
142
Describe the spinothalamic (anterolateral) pathway
contralateral
not as fast
used for pain, temp, crude touch and itch
large receptive fields
sometimes different modalities converge starting at 2nd order neuron
makes monosynaptic connection with a 2nd order afferent in spinal cord (cross over here) then travels up ventral part of spinal cord to the ventral posterior lateral nucleus of the thalamus
makes a 2nd connection here then goes to somatosensory cortex
143
Describe the dorsal column medial lemniscal system
only in mammals
contralateral
discriminative touch, proprioception, vibration
small receptive fields
neurons only respond to one modality (labelled line)
faithful transmission
fast conduction (A alpha, beta axons)
neurons travel all the way up to the brainstem to the dorsal column nuclei in the medulla before synapsing, cross over using medial lemniscus to the ventral posterior lateral nucleus of the thalamus, then synapse again and got to somatosensory cortex
144
How is the somatosensory cortex organized? Where is it located? Is this organization modifiable? How?
located on the post-central gyrus
goes medial to lateral, leg, trunk arm, face
it is modifiable, either through removal of GABA inhibition or an increase in Na+ ion channels on dormant pathways
145
What is a cortical column?
thousands of cortical neurons that are heavily interconnected in a vertical axis perpendicular to the cortical surface
each neutron in a particular cortical column responds to the same modality and has a similar receptive field
90% of them get info only from the DC/ML
146
Where is "body image" located in the brain? What happens if there are lesions to it?
posterior parietal cortex
right behind the somatosensory cortex
lesion effects are most obvious for the right side
result in disorder in appreciation of spatial aspects of sensory input from the left side of the body and left external space
147
What happens if you vibrate the triceps muscle as you try to touch your nose?
get increased discharge from muscle spindle Ia afferents resulting in the illusion that your hand passes through your head
148
What happens when you shine light on centre in a photoreceptor?
get hyper polarization of photoreceptor
causes a decrease in inhibitory neurotransmitter being released to bipolar cells
get graded depolarization of bipolar cells
depolarization and AP generation in retinal ganglion cells
149
What happens when you shine light off centre in a photoreceptor?
hyper polarize off-centre rod
releases horizontal cell from inhibition
depolarizes on-centre rod (like its in the dark)
makes the ganglion cells respond as though things are darker than they are
makes them particularly sensitive to contrast
150
Why are rods very sensitive to faint light?
more photopigment and converge ~100:1 on bipolar cells
151
How are photoreceptors acting in the dark?
Na+ channels are open, always have depolarization causing release of inhibitory neurotransmitter
152
Where does visual info go from the retinal ganglion cells?
to the lateral geniculate (thalamus) then to the visual cortex (simple cells)
153
Where are simple cells found?
in the visual cortex
154
Where does visual info from the right visual space go?
to the left visual cortex
155
What is an ocular dominance column?
series of orientation columns though 180 degrees
| one for each eye
156
What is a hyper column/hypercube?
ocular dominance columns for the right and left eye for one small patch of retina
ie analyses a small section of the visual field from the retina of both eyes
157
What results from a lesion to the higher areas of visual cortex?
prosopagnosia
| can't recognize familiar faces, maybe even their own
158
What are 4 ways that the visual system is related to the somatosensory system?
deconstruct and then reconstruct
retinotopic/somatotopic maps
columnar organization
lesions of higher areas lead to specific behavioural disorders
159
What range of hearing can be detect?
20-20 000Hz
160
How fast does the cochlea respond in contrast to the visual system?
1000 times faster
161
What sound do you lose first when you damage your cochlea?
high frequency
162
Where would a high frequency sound wave stimulate hairs cells?
short, stiff hairs by the base want to move at high frequency
the faster it is travelling the earlier it will reach its max
therefore it is near the base (narrow and stiff)
(short hairs= high frequency, long=low)
163
What are 3 ways our ears deal with impedance matching? By how much does this increase pressure at the cochlea?
outer ear acts as a funnel to concentrate sound
ossicles in the middle ear act as a lever system
area of the tympanic membrane is greater than that of the oval window
increases pressure 200-fold
164
Describe what happens when a hair cell gets moved in the ear
```
cation channels are mechanically opened
endolymph has high [K+] so K+ comes in
causes depolarization
VG Ca2+ channels open and Ca2+ comes in
neurotransmitter is released to cause AP on auditory nerve
```
165
Describe the sequence of events by which sound is relayed to the auditory cortex
```
air pressure variations
motion stapes
motion fluid in cochlea
motion basilar membrane
movement of hairs
increase permeability of hair cells to K+ (depolarization)
release of neurotransmitter
AP in auditory nerve
cochlea nucleus (brain stem)
medial and lateral superior olive
inferior colliculus
medial geniculate (thalamus)
auditory (temporal) cortex
```
166
Where does sound localization occur? How is this done?
medial and lateral superior olive
done using sound intensity and the time of sound arrival
dendrites go from each nerve to the same neuron in the medial and lateral superior olive, one produces excitation, one inhibition, this is how you tell which side the sound is on
167
How is the frequency of sound signalled?
place coding on basilar membrane
168
How is the intensity of sound coded for?
frequency of firing afferents
the number of afferents activated
(louder sound has a larger amplitude and so it activates more afferents)
**this is like SA touch receptor
169
How are high frequencies of sound signalled to be louder?
more firing of the neurons in the same place
170
What happens when there is a lesion in the auditory cortex?
deficits in locating sounds and recognizing sound patterns
| not deafness if only on one side because the info goes to both sides
171
What do the semi-circular canals do?
contain ampulla which has cupula inside
cupula is gelatinous, contains hair cells
when the head moves the whole structure moves, but the fluid lags behind so the hairs are depolarized
provide info about angular acceleration of head in any direction
(note: if you kept the fluid would catch up and there wouldn't be anymore signalling)
172
What do the otoliths do?
have a gelatinous mass with hair cells and CaCO3 crystals
when the body accelerates the crystals lag behind and depolarize the hair cells
signal linear acceleration
can continue to signal even with constant acceleration i.e. gravity
(both dynamic and static)
173
Does the vestibular system detect constant velocity?
no
174
What is benign positional vertigo?
crystals get into the semicircular canals
175
What is a utricle?
horizontal otolith
176
What is a saccule?
vertical otolith
177
What are kinocilium? How do they function?
they are long cilium that provide info about linear or angular acceleration
when hairs bend towards them ion channels open, K+ enters and receptor potential is depolarized
semicircular canals work in pairs so when hair cells on one side are depolarized, those on the other are hyper polarized
depolarized= increased firing of VIIIth nerve fibres
178
Where can info from the vestibular nuclei (in the brainstem) go?
thalamus-somatosensory cortex-posterior parietal cortex
or
spinal cord limb/ alpha MNs-limb muscles
brainstem/alpha MNs- eye muscles
cerebellum (can tune up limb and eye muscles info)
179
What are the 3 main functions of the vestibular system?
sense of equilibrium/orientation in space
vestibular postural reflexes (balance)
vestibular ocular reflex (keeping object of interest stationary on fovea in response to angular acceleration
180
What happens when you have vestibular damage?
cannot recognize a familiar faces when walking along the street
or read a book when sitting in bed
because head moves but you have no VOR
181
What 3 systems contribute to balance?
vestibular, leg proprioception and vision (optokinetic)
182
What is vestibular nystagmus?
can't keep eyes in one place
183
Is the vestibular ocular reflex guided by vision?
no it works when your eyes are closed
184
What are 4 types of eye movements?
saccades
smooth pursuit
vestibular ocular reflex
vergence
185
What are saccades?
fast, step-like voluntary and involuntary movements
| there is a fixed relationship between the amplitude and velocity of them
186
What is vergence?
eyes turn in for near objects
187
What are the 3 afferent feedback pathways used in the motor system?
to the spinal cord, thalamus and cerebellum
188
What are the 4 types of muscle receptors and what do they signal?
free nerve endings- pain, pressure, temp
GTO- tension
Ia afferent- length and velocity
group II afferent- length
189
How does the GTO work?
during contraction the tendon is pulled, stretches the capsule and compresses Ib nerve endings
190
What is the annulospiral sensory receptor?
Ia afferent muscle spindle receptor
191
How are the muscle spindle and GTO connected to muscle?
muscle spindle is in parallel
GTO is in series
(withe extrafusal fibres)
192
Where is intrafusal muscle found? Does it contribute to external force?
no external force
| is found at the poles of the muscle spindle
193
What happens when there is alpha-gamma co-activation?
there is an increase it Ia and group II muscle spindle discharge
194
How does Ia and group II muscle spindle discharge change when a movement doesn't go according to plan?
if its slower than expected, get increase in discharge
| if its faster than expected, get decrease in discharge
195
What is the latency of the stretch reflex? How does it compare to a voluntary reaction?
30ms to EMG onset vs >150ms
196
In what muscles does the stretch reflex occur?
extensor anti-gravity muscles
197
What is an EMG recording?
recording of extracellular current flow associated with APs in skeletal muscle
198
How come there is no stretch reflex in a relaxed person?
because only a tendon tap can generate EPSPs that summate fast enough to produce an AP
199
What is spasticity?
occurs with a lesion to the motor cortex or spinal cord
is a velocity-dependent increase in muscle tone
like an exaggerated stretch reflex (Ia afferent)
occurs bc of higher RMP
200
Which afferent neurons trigger the stretch reflex?
Ia and group II afferents
201
Is the spinal withdrawal reflex polysnaptic?
yes
202
Describe 4 characteristics of the spinal flexion withdrawal reflex
contraction and reciprocal inhibition
ipsilateral flexion, gives crossed extension (i.e. put other foot out)
has after discharge activity because of continuing discharge of nociceptors and reverberating activity
local sign- doesn't need to be flexion, can be whatever you need
203
Do all spinal reflexes have reciprocal inhibition?
yes
204
What are 2 characteristics of the scratch reflex?
programmed within the spinal cord
| has site specificity
205
Where are the neural circuits for locomotion?
spinal cord
| only fundamental i.e. won't know to step over something etc
206
Where is the motor cortex found? Is it contralateral?
precentral gyrus
| contralateral for the arm and leg, some contralateral sites for face
207
How does the somatotopic map on the percentile gyrus organized?
medial to lateral
| leg, trunk, shoulder, elbow, hand, face, tongue
208
Is the motor cortex muscle or movement representation?
movement
209
What ar the 3 main pathways of output from the motor cortex?
```
corticospinal/pyramidal tract
corticorubral tract (to the red nucleus)
corticoreticular tract (reticular formation in pons and medulla)
```
210
What output is the pyramidal tract for?
```
speed and agility
monosynaptic connections (10%) are used to move digits independently
```
211
What output from the motor cortex is for running, climbing and walking?
corticorubral and corticoreticular tracts
212
What happens if you have a lesion in the motor cortex?
weakness (or paralysis) and spasticity
213
What are 3 important characteristics of the pyramidal tract neurons?
have some discharge before movement
have some discharge preferentially for one direction of movement
have some discharge proportional to force or rate of change of force - frequency for code
(these are particularly in the monosynaptic neurons)
214
What are 5 factors that cause the time delay between onset of motor cortex discharge and movement?
conduction time from cortex to spinal cord
summation of EPSPs in alpha MNs
time from spine to NMJ
synaptic delay at NMJ
electrical mechanical coupling time (generating enough contractile activity)
215
What are granule cells?
excitatory cells in the cerebellar cortex that make connections with Purkinje cells
216
What kind of connections do Purkinje cells make in the cerebellar cortex?
always inhibitory
217
What happens if there is a lesion in the cerebellum?
no change in sensory or motor strength
| but movements are inaccurate and uncoordinated (ataxic)
218
What input goes to the medial cerebellum? Lateral?
medial- vestibular, auditory and visual
| lateral- cerebral cortex, motor cortex, proprio and cutaneous
219
What difference do primates have in their cerebellum?
increased size of lateral cerebellum
220
What is the only output of the cerebellar cortex to deep nuclei? Is it excitatory or inhibitory?
only output is the Purkinje cells
| it is always inhibitory
221
Do we have conscious awareness of our cerebellum?
no
222
Where does the lateral cerebellum project to?
frontal and motor cortex
223
Where does the medial cerebellum project to?
postural muscle MNs and eye MNs
224
What happens when you have a lesion to the medial cerebellar cortex?
dysmetric saccades
disordered smooth pursuit
disordered equilibrium, balance
gait ataxia
225
What happens when you have a lesion to the lateral cerebellar cortex?
dysmetric limb movements
intention tremor
arm ataxia
(more related to arm and legs)
226
What can mimix the effect of cerebellar lesions?
alcohol
227
What is the function of the cerebellar cortex?
subconscious, tunes up reflexes, motor programs and cognition
1) generation of accuracy
2) feedforward movement control
3) motor recalibration
4) cognition
228
What is feedforward movement control?
cerebellum sends out message to get muscle contracting anticipating what is going to happen
ie to catch a ball
229
How is motor recalibration thought to happen?
changing of the parallel fiber (from granule cell) to Purkinje cell synapse using input from climbing fibres (axons from the inferior olive)
ie is a modifiable synapse
230
What does the motor cortex send to the inferior olive? What else does the inferior olive receive?
motor cortex sends efferent copy of desired movement
| also get afferent feedback from muscle spindle etc and visual feedback
231
In what ways does the cerebellum contribute to cognition?
```
sensory discrimination (ie judging elapsed time)
spatial cognition (ie pegboard puzzles)
linguistic processing (ie noun-verb matching test)
```
232
What happens to the motor recalibration of cerebellar patients?
cannot recalibrate or do so slowly
233
What 3 areas of the cerebral cortex interact with the motor cortex?
supplementary motor area
premotor cortex
parietal cortex
234
Name the nuclei of the basal ganglia
caudate and putamen (neostriatum)
globus pallidus internal and external
subthalamic nucleus
substantia nigra pars compacta
235
What 4 areas of cortex have loops with the basal ganglia?
motor, oculomotor, limbic and cognitive (prefrontal)
236
What are the 2 inputs to the caudate/putamen?
cerebral cortex and substantia nigra pars compacta
237
What are the major transmitters in the caudate/putamen?
dopamine from substantial nigra, can be excit. or inhib.
glutamate from the cerebral cortex
Ach in the interneurons
238
What do neurologists try to balance in peoples brains with respect to the basal ganglia?
Ach and dopamine
239
What is the major output of the basal ganglia?
from the internal globes pallidus to the thalamus
| is INHIBITORY
240
What inhibitory neurtransmitter is used in the basal ganglia?
GABA
241
Are the pathways in the basal ganglia direct or indirect?
both
242
What are the functions associated with motor input to the basal ganglia?
limb and face movements
| disorders= Parkinsons and Huntingtons
243
What are the functions associated with oculomotor input to the basal ganglia?
eye movements
| disorders= fewer and slower saccades
244
What are the functions associated with limbic input to the basal ganglia?
emotion
| disorders= irritability, depression
245
What are the functions associated with cognitive input to the basal ganglia?
planning, working memory, attention
| disorders= absentminded, reasoning ability, dementia, tourettes, OCD
246
What is the function of the basal ganglia for motor loops?
exerts continuous inhibition which prevents unwanted movements
neural programs are selected by releasing them from inhibition
247
What are the features of Parkinsons disease?
```
rigidity
resting tremor
akinesia
bradykinesia
dementia
shuffling gait
mask-like face
flexed posture
```
248
What is thought to cause akinesia in Parkinsons?
increase in tonic discharge from the internal globus pallidus
gives increase in inhibition of thalamus
therefore decrease in the excitability of the motor cortex
249
What is are some characteristics of Huntingtons?
chorea- uncontrollable voluntary movement
slurred speech
is heritable
dementia
250
What is thought to cause the dyskinesia seen in Huntingtons Chorea?
decrease in tonic discharge from the internal globes pallidus
gives decrease in thalamus inhibition
this increase motor cortex excitability
251
What is hemiballismus? What causes it?
ballistic, involuntary movements caused by lesion in sub thalamic nucleus
252
What is thought to cause Tourette's?
excessive activity in the cognitive/prefrontal basal ganglia circuitry
