Elements of cellular neuro| W2 Flashcards
(67 cards)
CNS consists of..
- brain
- Spinal cord
PNS consists of…
- sensory neurons
- motor neurons
- autonomic system
- nervous ganglia (cluster of nerve cell bodies located outside the CNS)
- enteric system (neurons in digestive system)
(spinal nerves,
(cranial nerves)
Retina
Basic NS functions
- Input (sensation/perception)
- Output (voluntary movement)
- Neuroendocrine function
- Autonomic function —> PNS branch + regulates involuntary bodily functions (e.g., heart rate, blood pressure, digestion, respiratory rate).
*Sympathetic (“fight or flight”)
*Parasympathetic (“rest and digest”)
*Enteric (largely independent network in the gut) - Visceral NS - connects your internal organs (like your heart, lungs, and stomach) to your brain and spinal cord + carries info from these organs
- e.g your stomach telling your brain it’s full) and sends signals to these organs
Higher NS function
- Thought
- Long term Memory
- Emotion
- Working Memory
Glial cells…
**ROLES:
**- glial cells wrap around neurons, forming a myelin sheath = insulating .
- maintain ionic balance,
- transmitter uptake,
- recovery from injury,
- modulate rate of AP propagation
EXAMPLES:
- Microglia (immune origin) = immune system of CNS + clean up debris, fight infections, and remove damaged cells.
* Astrocyte (neuronal origin)* = supporting neurons, controlling nutrients, + forms BBB to protect the brain.
-** Oligodendrocyte (central myelinating cell) **= myelinates cells in the CNS + insulation/faster ROT for nerve fibers
+ A single oligodendrocyte can wrap around multiple nerve fibers.
- **Schwann cell (peripheral myelinating cell) **= (PNS) + a single Schwann cell only wraps around one part of a nerve.
Neurons…..
Process information
* Sense changes in internal/external stimuli
* Communicate changes to other neurons
* Command body response
explain what happens during A- depolorisation, B repolorisation and C hyperpolorisation
A
1 Na+ / sodium, channels already open OR
Na+ has already entered neurone OR
no more Na+ channels to open OR
less Na+ outside to diffuse in OR
less steep Na+ concentration gradient ;
B – any one reason from:
2 sodium channels are, inactive / unresponsive OR
potassium channels are open OR
membrane is, impermeable / less permeable, to Na+ OR
membrane is more permeable to K+ ;
C – any one reason from:
3 harder to reach threshold OR
potassium channels are (still) open OR
sodium-potassium pumps need to restore the resting potential
4 hyperpolarisation at
role of acetylcholinestrase
breaks down ach to acetate and choline
so ach leaves binding site
depolraistion on post synaptic memb stops
stops continous action potentials
ach can be recyled
saltatory conduction
Na ion channels concentrated at nodes
action potential jumps from node to node
local circuits set up between nodes/longer
fast/increases speed of tranmisson
100ms-1 vs 0.5ms-1
- explain how a cholinergeic synapse fucntions (Ach)
- action potential/ depolarisation, reaches, synaptic knob ;
- Ca2+ ion VGC channels open (in pre-synaptic membrane) ;
- Ca2+ enters (synaptic knob/ pre-synaptic neurone) ;
- vesicles with acetylcholine, move towards /fuse with, pre-synaptic membrane;
- -(ACh) released I secreted I exocytosis ;
- ACh diffuses across synaptic cleft ;
- binds to receptors on post-synaptic membrane ;
- (ligand-gated) Na+ channels open and - Na+ enters post-synaptic neurone ;
- depolarisation I action potential I EPSP
- acetylcholinesterase, breaks down ACh / recycles Ach
why reducing temp reduces contraction efficeny in muscles
less ATP produced ;
-reduces movement of, Ca2+ / Na+ / ACh / neurotransmitter ;
no, Ach broken down
acetylcholine remains attached to receptors
acetylcholinesterase, less active /
fewer / no, Ca2+ bind to troponin
fewer / no, cross bridges formed
fewer / no, power stokes ;
-/ no, detachment of myosin heads (from actin)
no, cross bridges broken
reduced blood flow to muscle / energy diverted for thermoregulation (
Suggest how a tumour on the optic nerve could prevent the transmission of nerve impulses to the brain.
1) compresses nerve
2) damages myelin sheaths / Schwann cells
3) prevents the setting up of local circuits / saltatory conduction
4) stops Na+ / K+ pumps from working
5) blocks blood supply
6) oxygen supply / glucose supply / ATP production is reduced
describe role of ATP in muscle contraction
ATP hydrolysed. causing mysoin head to change shape + ATP binding frees mysoin from cross bridge
ATP used in AT of calcium ions back into SR
sliding filament model of muscle contraction
Nerve impulse reaches NMJ
Ca2+ channel gates open so Ca2+ ions enter synaptic bulb, vesicles w neurotransmitter fuse w presynaptic memb + releasing neuroT into synaptic cleft and binds to receptor on Post SM/sarcolemma so Na2+ ion channels open = depolorize memb of muscle fibres –> action potentail generated
depolorisation of sarcolemma spreads down t tubule
3) 1) Ca2+ is released from stores in SR and binds to troponin, changing it’s shape
2) troponin and tropomyosin move to different positions on thin filament, exposing myosin binding sites on the actin chain/filament
3) myosin head attactched to actin filament usuing ATP = binds to exposed binding sites, forming cross-bridges between thick and thin filaments/actomysoin cross brdidge
4) myosin changes shape + heads tilt, pulling/sliding actin filaments past myosin filaments usuing ATP, towards centre of sarcomere/shortens = power stroke
5) Free ATP binds to head so shape of myosin head change, binding of head to actin filament broken
6) ATPASE in mysoin head breaks ATP into Pi and ADP = recovery stroke
7) W continued stimulation calcium ions remain in sarcoplasm and cycle repeated IF NOT = calcium ions actively pumped into SR + T tubules
8) Troponin + Tropomyosin return to OG positions and contraction complete = MF relaxed
structure of thin filaments (actin
made of actin (a globular protein)
many actin molecules link to form a chain
2 chains twist to form an active filament
tropomyosin (fibrous): twisted around 2 chains/filament
troponin: attached to actin chain at regular intervals, Ca2+ binding site**
structure of thick filaments (myosin
made of myosin (a fibrous protein with a globular head)
fibrous protein anchors molecule to thick filament
globular heads point away from M-line
How do muscle contract
A band= actin + myosin
I band= only actin filaments
H zone= only myosin filaments
Z line= one sarcomere
When a muscle contracts, actin filaments slide over mysoin filaments:
- I band shorter
- Z lines closer tgt + sarcommere shortens
- H zone narrower
- A lines stay same length
- so everything shorter EXCEPT A bands
describe the roles of neuromuscular junctions, the T-tubule system
Sarcolemma/CSM infolds =T tubules help spread impulses through the sarcoplasm near SR
- muscles cells have myoglobin = so have higher affinity to O2 than Hb, accepting O2 from blood and stores O2 in muscles
- muscles attathed to skeleton
- small amounts of ATP in muscle fibres
role of synapses
1) one-way transmission beacuse receptors are only present on 1 side of synapse so impulses are unidrectional
2) interconnection of nerve pathways= 1 neuorne may have syanpses w/ many other nuerones
3) Summation: where 3 neurones tgt release small amounts of neurotranmsitter (not enough for Action potential to occur) at the same synapse
4) but tgt neuroT released WILL reach threshold level for action potential to occur
why do we need mitochondria in synaptic knob
produces ATP
ACh production
Vesicle fromation
Excoytosis
Functioining of ion pumps
explain using an example how sensory receptors in mammals convert energy into action potentials
baroreceptor in skin detect stimulus e.g pressure
stimulus causes sodium ion channels to open
potassium ion channels open
potassium ions leave axon cell
depolorisation
generator potential
if greater than threshold leads to action potential
less than threshold only localised epolorisation
increased stimulus leads to increased frequency of action potentials
size of action potential comapred to size of stimulus
- action potential only generated if stimulus reaches threshold level
-
below this threshold no action potential can be created
** the threshold for any nerve fibres is point at which sufficnet Na2+ ion channels open for Na2+ to move into axon FASTER than outflow of K+
Size of action potential always same
- bigger stimulus INCREASES the FREQUENCY of action potentials NOT STRENGTH e.g more action potentials fired!!!
- in a weak stimulus eg punched in stomach, many receptors in skin/baroreceptors detect stimuli and strong stimulu so reaches threshold potentia;, more action potentials generated
explain the importance of the refractory period in determining
the frequency of impulses
- ensures action potentials pass along as seperate signals + unidirectional
- length of refractory period determines max frequency of nerve impulses
- If a short refractory period allows high-frequency signals (many impulses per second).
- A long refractory period limits the frequency of signals.
-high-frequency signals allow neurons to comm more intense stimuli = bright light/immense pain
-W/O the refractory period = neuron overfire, causing confusion in signaling
Hyperpolorisation
- (K⁺) VGC channels stay open longer than needed during repolarization, causing extra K⁺ to leave.
- makes inside of axon more negative than the resting potential
- The charge inside becomes lower than -70mV
- Na⁺/K⁺ pump help balance the ions to return the membrane to the resting potential (-70mV).
- Happens right after an action potential.
- Na⁺ channels are inactivated, so no new action potential can occur, no matter the stimulus.
- Follows the absolute refractory period.
- K⁺ channels are still open, making the axon hyperpolarized.
