1
Q
CNS
A
brain + spinal cord (together = neuraxis)
2
Q
nerves in/out CNS
A
sensory/afferent = in
motor/efferent = out (incs glands etc)
3
Q
response to stimulus
A
4
Q
segmental reflex
A
just 2 neurons
possible w/o brain (so can be possible when dead)
e/g/ withdrawal reflex when grab toe
5
Q
patella reflex
A
tap patella + knee kicks out - useful diagnostically to see if sensory + motor + muscle all working
shows there can be multiple sensory pathways at once - patella reflex + to brain saying ‘touched’
6
Q
spinal cord structure
A
pathways in specific places in spinal cord - injury certain place will therefore cause certain symptoms, useful for diagnosis
7
Q
upper motor neurones
A
part CNS
corticospinal + corticonuclear motor pathways
8
Q
lower motor neurones
A
leave CNS + part PNS
2 types:
* alpha-motor
* gamma-motor
9
Q
cranial + spinal nerves
A
nerves in/out bottom of brain (not many) + nerves in/out spine
v similar
10
Q
neuron
nerve fibre
nerve
cell body
A
nerve cell
part neuron
‘trunking bunches axons + support cells
nucleus + G. app etc = soma = perikarion
11
Q
basic properties neurones
A
12
Q
effect of axon thickness
A
fatter axons conduct faster as less resistance electrical signal, e.g. evolved in squid
13
Q
main fibre types
A
- A
- Aa (A delta)
- C
defined by characteristics neyronal axon
14
Q
A fibres
A
- large, fast, myelinated
- carry touch + press sensations
- also many motor neurons this type
15
Q
Aa fibres
A
- small, lightly myelinated - bet A + C anatomically
- important in transmission of pain
16
Q
C fibres
A
- smallest, slowest, unmyelinated
- sensory + autonomic motor neurons
- inflammatory pain, e.g. heat takes longer feel
17
Q
saltatory conduction
A
elec current jumps from node to node along myelinated axon
18
Q
why do myelinated neurons conduct faster
A
myelin insulates = conduction not disspated in tissues = faster
neurons cont salty sol bc salty sols conduct elec
19
Q
effect cooling on neuronal conduction
A
decreases conduction velocity = decreased speed at which a pots gened + travel to brain = less a pots through = increased refractory periods = less pain
20
Q
main factors affecting conduction velocity
A
- fibre diameter
- myelination
- temp
21
Q
refractory period
A
period in which can’t fire a pot
1. absolute = a pot impossible as Na+ channels inactivated
2. relative = stim not big enough cause a pot
* after a pot harder gen another as mem more neg + polarised + some Na+ channs inactivated
22
Q
types neurones
A
- multipolar
- pseudo-unipolar
- bipolar
23
Q
multipolar neurone
A
- standard found most places
- loads of ways off
24
Q
pseudo-unipolar neuron
A
- comes out 1 place but immediately splits
- sensory neurone - spinal reflex
25
bipolar neurone
* 2 routes out cell body
* seen least often
* sensory neurone - retina
26
synapse
* junction bet 2 neurones, generally mediated chems
* give graded excitation post-syn neurone - deviation RMP big enough = a pot gened
causing excitatory (depolarising)/inhibitory (hyperpolarising) postsynaptic pot = EPSP/IPSP
| expect 1 neurone to many
27
electrical synapse
ionic current directly 1 cell to another for fast communication + to synch activity grp neurons/muscle cells
* v important in heart to spread contraction
28
pre-synaptic Ca2+ channel types
1. L-type
2. N-type
3. T-type
blocked by several types toxins
| structurally sim Na+ v-gated w few aas diff
29
L-type Ca2+ channel
* main type
* act for **L**ong time
* cardiovascular drugs target these
30
N-type Ca2+ channels
**N**either long not transient = open middle amount time
31
T-type Ca2+ channels
**T**ransient = briefly opening
32
how chem synapse works
arrival a pot at pre-synaptic = change mem pot = v-gated Ca2+ channs open = influx Ca2+ = exocytosis NT as vesicles move + fuse presyn mem, NT moves across synaptic cleft + fuses postsyn mem = a pot stimmed + gened next neuron
33
a pot feedback type
all or nothing = reach threshold + all Na+ channs open = pos feedback
| pos feedback usually pathological
34
acetylcholine recycling
Removed synaptic cleft 3 ways:
1. diffusion
2. enz degradation
3. uptake into cells (neurons + glia)
enz acetylcholinesterase (ACHE) breaks down -> choline + acetate - choline taken up into presyn neuron on Na+-choline cotransporter, reformed by enz (AcCoA) + repackaged vesicles to go again
| breakdown Ach = end response
## Footnote
small mol NTs (like Ach) packages terminal. large peptide NTs packaged cell body + transported via microtubules
35
how receptors in post-sym mem work
ligand-gated ion channels = receptors in post-syn mem
* have central pore whose diameter is altered when transmitter binds receptor
36
hyperkalaemia
causes depolarisation = RMP close threshold = neurons more excitable = muscle twitching
| K disorder
37
hypokalaemia
causes hyperpolarisation = RMP further from threshold = sk muscle weakness
| K disorder
38
synaptic summation
several presyn end bulbs release NT same time = more likely gen nerve impulse
* consider effects canceling out inhibitory vs excitatory etc
* spatial + temporal
39
drugs involving NTs
1. antagonists = NTs blocked binding
2. agonists = mimic NT as chemically similar to cause false response
3. block enzs that degrade NT to prolong action
40
neuromuscular junction is?
| NMJ
special type synapse bet neuron + sk muscle cell not 2 neurons
41
what is terminal button
small knob @ end axon that releases NTs
42
how does NMJ work
* a pot in motor neuron propogated to terminal button
* presence a pot triggers opening v-gated Ca2+ channs = entry Ca2+ terminal button
* triggers release Ach by exocytosis
* Ach diffs across space sepping nerve + muscle cells
* Ach binds specific receptor sites on motor end plate muscle cell mem (= cholinergic receptors)
* opens ion channs in mem
* relatively large movement Na+ into muscle cell vs small K+ out = end-plate pot
* small EPSPs add up + cause local current flow bet depolarised endplate + adjacent mem
* = v-gated Na+ channs mem open
* mem pot depolarises to threshold
* = a pot gened, propagated through muscle cell
| NMJ = always nicotinic receptor
43
diff sk muscle + nerve responses post-syn
* sk muscle RMP tends more neg (~90)
* a pot sk muscle slower
* a pot along surface nerve vs down T tubules penetrating muscle (= slower)
* diff ion channs but analogous
44
v rough how a pot causes contraction in sk muscle
a pot running along + into muscle causes tension = Ca2+ released muscle centre
45
sims bet synapse + NMJ
* both consist excitable cells sepped synaptic cleft, preventing direct transmission elec activity
* axon terminals of both store chem messenger
* binding NT w receptor sites postsyn mem opens specific channs, allowing ion movement to alter mem pot cell
* resultant change of both graded pot
46
diffs bet synapse + NMJ
1. neuron-neuron vs motor neuron-sk muscle fibre
2. NMJ = 1-1 transmission a pot; synapse = summation EPSPs
3. NMJ always excitatory; synapse excit or inhib
* sk muscle only inhibited in CNS, not at NMJ
47
what is ANS
autonomic nervous sys
* involuntary, often unconscious
* maintains homeostasis
* consistingautonomic sensory neurons, integrating centres CNS, autonomic motor neurons, effector organs in periphery (e.g. smooth muscle, heart, glands)
| incs central + peripheral nerve components
48
where is ANS regulated
centres in brain - mainly hypothalamus + medulla oblongata (receives input other parts cerebrum)
49
most famous autonomic nerve
vagus - sensory + motor components from many systems + controls much parasympathetic sys
50
sensory receptor types
1. chemoreceptors - monitor blood CO2 levels
2. mechanoreceptors - detect degree stretch walls organs, blood vessels...
3. baroreceptors - type mech to detect blood press
51
ANS peripheral components
pre + post ganglionic motor neurones w nuclei in CNS + ganglia
1 sensory neuron, cell body in dorsal root ganglion
| not in somatic
52
ganglion
collection cell bodies outside CNS
53
pre vs post gang neurons
post unmyelinated = bunch together appear grey.
bunch myelinated pre together appear white (myelin whiteish)
54
junction postgang neuron on effector organ vs NMJ
postgang:
* can inhibit or excite target
* branched w varicosities
* longer latency - synapse in middle = slower response (fast but direct elec transmission faster)
* greater spatial activation
55
what are varicosities
swellings that can all release neurotransmitter - dropping it from number places along, not just at end
56
which muscle type which sys
ANS = smooth
SNS = skeletal
57
sympathetic vs parasympathetic
| w/in ANS
sym = fight or flight
parasym = rest + digest
| not mutually exclusive
58
sympathetic general
controlled + processing in brain cortex - hypothalamus
59
parasympathetic general
**S**alivation
**L**acrimation - keep eye good cond + lubricated
**U**rination
**D**igestion
**D**efecation
| panic response, e.g. peeing yourself asw
60
where does parasympathetic response originate from in neuraxis
brainstem cranial nerves + sacral (bottom) spinal cord = craniosacral sys
| not from segments spinal cord in between
61
parasympathetic pre + post gang neuron structure
long pre, v short post - ganglion often in wall target tissue, e.g. in gut wall/heart
more local as not loads post gang neurons (1:2 pre:post)
62
viscera
organs in main body cavity, esp in abdomen
63
balance bet symp + parasymp sys
when at rest parasymp more dominant + symp acting low level to maintain homeostasis, then in response fear/excitement symp more dominant w widespread response
64
diff bet somatic + autonomic
65
structure neurons sympathetic sys
short pre, long post
ganglion far from tissue, often in sympathetic trunk (v close spinal cord + most nerves symp sys pass through)
66
adrenal medulla
| structure + function
* centre adrenal gland on end sympathetic nerve
* chromaffin cells secrete mostly adrenaline (lil bit noradrenaline) directly into bloodstream for generalised symp response
* ganglion + post-gang neuron all in one in tissue (=technically no postgang)
67
4 options motor pathway autonomic reflex
1. lots together, synapse together, form loop in trunk, leave together, then to extremities - blood vessels, sweat glands, hair erector muscles
2. straight on to tissue - sep to heart/thoracic viscera (white as lots myelinated postgang neurones)
3. spinal nerve through symp chain to own ganglion (prevertebral)
4. synapse in adrenal medulla - special case
68
fight or flight response
in anticipation - immediate increase heart rate, mostly due adrenaline + noradrenaline
stress set up to have O2, heart rate etc ready prior to needing to run so get set off straight at max. otherwise would pass out too much activity from sprinting as not enough time build up O2, cardiovascular sys etc
| mediated hypothalamus + medulla in brainstem
69
sympathetic ANS NTs
short, myelinated pregang releases Ach (bc synapse)
longer, unmyelinated postgang releases noradrenaline
70
parasymp ANS NTs
long myelinated pregang releases Ach that binds nicotinic receptors
shorter unmyelinated postgang releases Ach that binds muscarinic receptors
71
nicotinic vs muscarinic
both receptor prots Ach acts on
N fast, M slow so ganglions (synapse bet 2 neurons has be) + somatic all fast
* smooth muscle + glands slow = M
72
summary NTs + receptors
73
muscarinic receptor details
typical G prot coupled receptors
* 5 molecular subtypes known
* most pharmalogical agents non-selective
* M2 + M3 most important
74
G prot coupled as opposed ion channs
response slower to start + lasts longer
75
catecholamine postsyn receptors
* alpha1 - typically on blood vessels, e.g. vasoconstriction arterioles
* alpha2
* beta1 - typically on heart, e.g. increase heart rate
* beta2 - in airway for bronchodilation, e.g. ventolin in inhaler B2 agonist
| = adrenoreceptors to adrenaline + noradrenaline
76
anaphylactic shock
massive drop blood press due allergies, severe injury, etc
NSF
flashcards
Decks in class (22)
# Cards
-
Histology198
-
Membranes56
-
Embryology42
-
Proteins42
-
Nervous system76
-
carbs47
-
skeletal + smooth muscle66
-
nitrogen27
-
anatomy15
-
lipids23
-
cardiovascular343
-
Gastrointestinal499
-
forelimb302
-
urinary145
-
respiratory152
-
head374
-
cns354
-
hindlimb184
-
skin68
-
repro235
-
endocrine112
-
pharmacology115
