Nervous system Flashcards
CNS
brain + spinal cord (together = neuraxis)
nerves in/out CNS
sensory/afferent = in
motor/efferent = out (incs glands etc)
response to stimulus
segmental reflex
just 2 neurons
possible w/o brain (so can be possible when dead)
e/g/ withdrawal reflex when grab toe
patella reflex
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’
spinal cord structure
pathways in specific places in spinal cord - injury certain place will therefore cause certain symptoms, useful for diagnosis
upper motor neurones
part CNS
corticospinal + corticonuclear motor pathways
lower motor neurones
leave CNS + part PNS
2 types:
* alpha-motor
* gamma-motor
cranial + spinal nerves
nerves in/out bottom of brain (not many) + nerves in/out spine
v similar
neuron
nerve fibre
nerve
cell body
nerve cell
part neuron
‘trunking bunches axons + support cells
nucleus + G. app etc = soma = perikarion
basic properties neurones
effect of axon thickness
fatter axons conduct faster as less resistance electrical signal, e.g. evolved in squid
main fibre types
- A
- Aa (A delta)
- C
defined by characteristics neyronal axon
A fibres
- large, fast, myelinated
- carry touch + press sensations
- also many motor neurons this type
Aa fibres
- small, lightly myelinated - bet A + C anatomically
- important in transmission of pain
C fibres
- smallest, slowest, unmyelinated
- sensory + autonomic motor neurons
- inflammatory pain, e.g. heat takes longer feel
saltatory conduction
elec current jumps from node to node along myelinated axon
why do myelinated neurons conduct faster
myelin insulates = conduction not disspated in tissues = faster
neurons cont salty sol bc salty sols conduct elec
effect cooling on neuronal conduction
decreases conduction velocity = decreased speed at which a pots gened + travel to brain = less a pots through = increased refractory periods = less pain
main factors affecting conduction velocity
- fibre diameter
- myelination
- temp
refractory period
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
types neurones
- multipolar
- pseudo-unipolar
- bipolar
multipolar neurone
- standard found most places
- loads of ways off
pseudo-unipolar neuron
- comes out 1 place but immediately splits
- sensory neurone - spinal reflex
bipolar neurone
- 2 routes out cell body
- seen least often
- sensory neurone - retina
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
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
pre-synaptic Ca2+ channel types
- L-type
- N-type
- T-type
blocked by several types toxins
structurally sim Na+ v-gated w few aas diff
L-type Ca2+ channel
- main type
- act for Long time
- cardiovascular drugs target these
N-type Ca2+ channels
Neither long not transient = open middle amount time
T-type Ca2+ channels
Transient = briefly opening
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
a pot feedback type
all or nothing = reach threshold + all Na+ channs open = pos feedback
pos feedback usually pathological
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
small mol NTs (like Ach) packages terminal. large peptide NTs packaged cell body + transported via microtubules
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
hyperkalaemia
causes depolarisation = RMP close threshold = neurons more excitable = muscle twitching
K disorder
hypokalaemia
causes hyperpolarisation = RMP further from threshold = sk muscle weakness
K disorder
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
drugs involving NTs
- antagonists = NTs blocked binding
- agonists = mimic NT as chemically similar to cause false response
- block enzs that degrade NT to prolong action
neuromuscular junction is?
NMJ
special type synapse bet neuron + sk muscle cell not 2 neurons
what is terminal button
small knob @ end axon that releases NTs
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
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
v rough how a pot causes contraction in sk muscle
a pot running along + into muscle causes tension = Ca2+ released muscle centre
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
diffs bet synapse + NMJ
- neuron-neuron vs motor neuron-sk muscle fibre
- NMJ = 1-1 transmission a pot; synapse = summation EPSPs
- NMJ always excitatory; synapse excit or inhib
* sk muscle only inhibited in CNS, not at NMJ
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
where is ANS regulated
centres in brain - mainly hypothalamus + medulla oblongata (receives input other parts cerebrum)
most famous autonomic nerve
vagus - sensory + motor components from many systems + controls much parasympathetic sys
sensory receptor types
- chemoreceptors - monitor blood CO2 levels
- mechanoreceptors - detect degree stretch walls organs, blood vessels…
- baroreceptors - type mech to detect blood press
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
ganglion
collection cell bodies outside CNS
pre vs post gang neurons
post unmyelinated = bunch together appear grey.
bunch myelinated pre together appear white (myelin whiteish)
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
what are varicosities
swellings that can all release neurotransmitter - dropping it from number places along, not just at end
which muscle type which sys
ANS = smooth
SNS = skeletal
sympathetic vs parasympathetic
w/in ANS
sym = fight or flight
parasym = rest + digest
not mutually exclusive
sympathetic general
controlled + processing in brain cortex - hypothalamus
parasympathetic general
Salivation
Lacrimation - keep eye good cond + lubricated
Urination
Digestion
Defecation
panic response, e.g. peeing yourself asw
where does parasympathetic response originate from in neuraxis
brainstem cranial nerves + sacral (bottom) spinal cord = craniosacral sys
not from segments spinal cord in between
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)
viscera
organs in main body cavity, esp in abdomen
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
diff bet somatic + autonomic
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)
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)
4 options motor pathway autonomic reflex
- lots together, synapse together, form loop in trunk, leave together, then to extremities - blood vessels, sweat glands, hair erector muscles
- straight on to tissue - sep to heart/thoracic viscera (white as lots myelinated postgang neurones)
- spinal nerve through symp chain to own ganglion (prevertebral)
- synapse in adrenal medulla - special case
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
sympathetic ANS NTs
short, myelinated pregang releases Ach (bc synapse)
longer, unmyelinated postgang releases noradrenaline
parasymp ANS NTs
long myelinated pregang releases Ach that binds nicotinic receptors
shorter unmyelinated postgang releases Ach that binds muscarinic receptors
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
summary NTs + receptors
muscarinic receptor details
typical G prot coupled receptors
* 5 molecular subtypes known
* most pharmalogical agents non-selective
* M2 + M3 most important
G prot coupled as opposed ion channs
response slower to start + lasts longer
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
anaphylactic shock
massive drop blood press due allergies, severe injury, etc
