Zusammenfassung der Ressource
Basic
Neurophysiology
2
- cell types of the CNS
- Neurons
- 10%, extensively branched,
50% of CNS volume
- 3 basic parts:
dendrites & cell body,
Axon, Axon terminals
- dendrites receive signals from other
neurone. Cell body contains the
nucleus & controls growth & repair
- axon-single process extending
from cell body/collaterals-side
branches from the axon-transmit &
recieve signals from other neurone
- terminals-connect with
other neurons
- Axon length
varies: >1nm in
projection
neurons
connecting to
muscles/glands
& very short in
interneurons
forming local
circuits in spinal
cord
- Glial cells
- 90%, branch less extensively,
50% of CNS volume
- contribute to brain function by playing
supportive roles in support, nutrition,
insulation & repair
- astrocytes-fill spaces
between neurone, store
glycogen,regulate [K+] in
extracellular fluid
- Oligodendroglia (CNS), Schwann
cells (PNS)-wrap myelin sheaths
around axon
- Microglia-small
phagocytic immune
cells, repair &
inflammation
- Neuronal Communication
- presynaptic neuron conducts information
towards the synapse, synapse junction
between 2 neurone, postsynaptic
neurone-conducts info away from synapse
- 2 types
- electrical
- local currents from APs flow through gap
junctions between neurone-connexins form
pore so ions etc that convey electrical
signals can pass through
- Bi-directional currents
- No synaptic delay
- Reflex patheays for rapid transmission
- Embryonic tissue, inspiration
(coordinating breathing) & saccadic eye
movements (moving eyes side to side)
- chemical
- most common synapse in mammalian cells
- unidirectional
transmission of
signal pre- to
post-
- axodendritic-post onto pre
synapse/axosomatic-attatches to cell
body/axoaxonic-neuron forms synapse
with another pre-synaptic neurone
- Otto Loewi & 'Vagusstof'-removed neurons,added
fluid with chemical-heart rate slowed when no
neurone present-found the chemical to be Ach
- synaptic cleft-extracellular space between
the terminal bouton & the post synaptic
neuron mem.No direct transfer of current (via
neurotransmitter)
- synaptic vesicles dock at the active zone
of the presynaptic neurone. APs arrive &
depolarises the mem, Ca2+ channels
open,Ca2+ flows in=vesicles fuse
- chemicals released into cleft & bind receptors on
the postsynaptic men (QUANTAL RELEASE).
- chemicals actively re-uptaken back
into vesicles in the
presynaptic,degrade or diffuse
- synaptic delay-time from AP arriving at
synapse to AP in postsynaptic (~0.5ms)
- EPSP-neurontransmitter binding to receptor on
post causes the mem to DEPOLARISE (Na+
influx exceeds K+ efflux) CNS:glutamate
- single EPSP not sufficient to
generate AP. Graded
potential-summation required to
reach threshold
- 1000's synapses can simultaneously fire a
single neurone, activate different channels &
receptors in postsyn. Integration of all
EPSPs & IPSPs
- = NEURAL COMPUTATION (all or nothing decision-AP fired or not)
- spatial summation-signals
from pres to one post at the
same time, allows threshold
to be met & AP fired
- Temporal- single pre sends multiple
signals in succession-mem potential
doesnt have time to return to normal so
when second fired=increase & so on...
- shunting inhibition-if
inhibitory synapse activated
at same time as excitatory,
the depolarising current leaks
out before it reaches the
soma
- IPSP-neurotransmitter
binding causes
HYPERPOLARISATION
(Cl- influx or K+ efflux)
CNS:GABA
- Facilitation &
fatigue-with repeated
presyn stimulation,post
response is amplified
(EPSP/IPSP) OR
decreased.
- Facilitation=increase-
beneficial-learning or
detrimental-chronic pain
(signal bigger after continual
stimuli=greater pain)
- Fatigue-depletion of
neurotransmitter stores
at presynaptoc
terminal-cant produce
response as great as in
the past
- Muscle types (autonomic NS)
- smooth muscle (GI tract, blood vessels, uterus)
- striated muscle
- skeletal (movement, attatched
to bone-motor neurone)
- each muscle is enclosed in a sheath
of connective tissue. Within each
muscle are hundreds of muscle fibres
- each muscle fibre innervated by a
single axon from the CNS. Multiple
fibres innervated by branches of one
nerve-coordinated contraction of
many fibres
- somatic motor neurons-nerves that
innervate skeletal muscle fibres
- cell bodies in spinal cord or brainstem,
long branched dendrites which recieve
many synaptic connections
- myelinated axons & largest
diameter-fast conduction. Axon
terminates in NMJ-motor endplate
- NMJ
- presynaptic nerve,
postsynaptic mem of
muscle-plasma mem of
muscle cell highly folded
with many Ach receptors in
folds
- Ach channels-'all
or none'-single
channel secured
in a portion of
mem-either open
or closed so
always generated
same current
- but random duration
of opening for single
channel (mean=1ms)
- curent can depend on
other factors: no. of open
channels, Ach conc,
channel conductance &
mem potential
- 1. AP triggered in motor neuron 2.depolarisation of motor
terminal mem
- 3.depolarisation opens Ca2+, flows in-interferrs with docking
process between snaar proteins & vesicles=vesicles fuse with
mem=release Ach in cleft
- 4.Ach binds to ligand-gated nicotinic Ach
receptors=depolarisation of muscle cell mem
which causes voltage gated channels to open
- rapid removal of Ach=diffusion
away from receptor/breakdown
by acetylcholinesterase,reuptake
of choline into presynaptic via
Na+ co-transporter
- & recycling into vesicles via ATP
driven H+ counter-transport
- Ach is released in bursts /guanta. Single quantum
causes only a slight depolarization, called a
miniature end-plate potential (MEPP)
- 100-200quanta released simultaneously by a nerve
impulse, cause multiple MEPPs=summate to
produce an EPP=massive depolarisation (-20mv)=
- voltage gated Na+ channels open
- EPP's
different from
post synaptic
potentials
(IPSPs,
EPSPs)
- drugs & toxins that block NMJ transmission
- Fugu-sushi delicacy
(pufferfish)-tetrodotoxin-block
voltage-gated Na+ channels so no
AP in nerve-rapid decending
paralysis & cardiovascular collapse
- Black widow spider venom-binds receptors
on presynaptic mems=increases Ca2+
influx-excessive vesicle release rapidly
depletes stores=no neurotransmiss
- Cobra bite-a-bungarotoxin
binds Ach receptor-prevents
receptor activation=paralysis
of respiratory muscle
- Curare-arrow tip poison-south
american indians use to paralyse
prey-Ach receptor antagonist
- Organophosphates-compounds used
in insecticides-block breakdown of Ach
by acetylcholinesterases-were used in
medicated shampoo-linked to brain
damage
- botulinum toxin-from bacterium clostridium
botulinum-interferes with vesicle docking at synapse-blocks
neurotransmitter release=no contraction (BOTOX)
- Myasthenia
Gravis-autoimmune-body
produces Abs to Ach
receptors=reduced
mepps,smoothed endplate
folds,loss of
receptors,hypersensitivity
to blockers
- respond to
drugs that
inhibit
cholinesterase's
& prolong action
of Ach
- Cardiac (heart,
change in heart rate ,
contracting is
autonomous)