physiology-menti Flashcards
inwards
False
ganglion cell stimulation will be highest in dark
B
None of the above
-the direct innervation occurs in the lateral genicular nucleus
cyclic GMP activated Na influx
E
Enhances contrast (B)
E
D
middle ear
B
D
C
Option 4
False- scala media has endolymph
- False- its glutenate
D
Where do motor neurones that innervate skeletal muscle arise from?
ventral/ anterior horn of the spinal cord
what does the terminal portion of a motor neurone give rise to?
the terminal portion of a motor neurone gives rise to fine projections that run along the muscle cell
what is a motor end plate?
a synapse formed between the motor neurone and muscle
how many muscle cells can a single motor neurone control?
a single motor neurone can control multiple muscle cells but each muscle cell will only respond to a single motor neurone
Explain the physiology behind muscle contraction (at a action potential/ synaptic level)
- Action potential travels down the nerve
- AP triggers voltage gated Calcium channels to open, allowing an influx of Calcium
- ACh vesicles are released into synaptic cleft
- ACh diffuses across the synaptic cleft
- ACh receptors open and render membrane permeable to Na/K ions
- The depolarisation starts an action potential at the motor end plate
7.Transmission is stopped by acetylcholinesterase, which removed ACh in the synaptic gutter, turns it into acetate and cholinr and gets taken up by the presynaptic vesicles
which direction do Sodium and Potassium in regards to the cell and Sodium Potassium channel?
3 Sodium go out of the cell
2 Potassium come into the cell
Na- nah im leaving
K- okay ill come in
how and why does conduction differ in myelinated and unmyelinated axons?
it is faster in myelinated as the action potential can ‘jump’ from one node of Ranvier to the next
why is the nerve cell membrane described as leaky and what effect does it have on passive signals?
nerve cell membrane has can allow passive movement of potassium out of the cell and sodium into the cell (meaning it is not a perfect insulator)
-This means passive signals do not spread far from site of origin
(imagine a leaky garden hose as an analogy for an axon)
what can be done to increase the passive current spread (and this action potential velocity) of a neurone?
-decrease ri by increasing axon diameter
-increase rm by adding insulating material (myelin)
what are acetylcholine, amino acids and amines released from?
synaptic vesicles
what are peptides released from?
secretory vesicles
what can activate ionotropic ligand- gated ion channels (LGICs)?
Glutamate, GABA, glycine, acetylcholine and 5-HT
neurotransmitter may act directly or indirectly on ion channels
what receptors are involved in direct gating?
ionotropic receptors
neurotransmitter may act directly or indirectly on ion channels
what receptors are involved in indirect gating
Metabotropic receptors
fast EPSP is due to the activation of what type of receptors?
Ionotropic receptors (direct gating= gating of channels is rapid)
what type of gating is involved in ionotropic and metabotropic receptors?
ionotropic= ligand gated ion channels
metabotropic= G protein coupled receptors
is glutamate inhibitory or excitatory?
glutamate is excitatory
but has an inhibitory effect on metabotropic receptors
is gaba inhibitory or excitatory?
gaba is inhibitory
is potassium or sodium more permeable to the cell in neurones
Potassium is (so it ‘leaks’ more)
does sodium de or repolarise the post synaptic membrane?
Sodium depolarises it
what is the initial resting potential of post synaptic membrane?
-70 mV
what is the threshold action potential of the post synaptic membrane?
-10 mV
Give examples of excitatory neurotransmitters
Glutamate, acetylcholine and aspartate
explain how EPSP works (excitatory post synaptic potential)
- There is a release of excitatory neurotransmitter e.g. glutamate, acetylcholine, aspartate
- Glutamate attaches to the post synaptic membrane, allowing the post synaptic non selective (sodium and potassium) permeable channel to open
- 3 x Na+ influx dominates the 2 x k+ efflux, causing the post synaptic membrane potential to become depolarised by 10mv (this is the excitatory psp)
- EPSP summate, allowing the threshold (-10mV) to be reached, creating an action potential
what are examples of inhibitory neurotransmitters?
GABA (gaBa= Block)
Glycene
Glutamate (if bound to metabotropic receptor)
explain how IPSP works (inhibitory post synaptic potential)
- Pre synaptic membranes release inhibitory neurotransmitter e.g. GABA
- GABA binds to metabotropic receptor (indirect) on post synaptic membrane
- This causes opening of ligand gated chloride (Cl-) channel
- This causes an influx of Cl-, causing a hyperpolarisation (more negative)
- This hyperpolarisation causes the membrane potential to go from -70mV (it’s resting membrane potential) to -85mV, decreasing the excitability of the post synaptic neurone, making the neurone further from firing action potential
what are some clinical signs of decreased neuronal excitability/ conduction?
-weakness
-ataxia (balance, coordination + speech)
-hyporeflexia
-paralysis
-sensory deficit
what ion disturbances can lead to decreased neuronal excitability/ conduction?
-hypokalaemia
-chronic hyperkalaemia
-hypercalcaemia
Clinical signs of increased neuronal excitability/ conduction?
-hyper reflexia
-spasms
-fasciculations
-tetany
-tremors
-paraesthesias
-convulsions
examples of ion disturbances that may cause increased neuronal excitability/ conduction?
acute hyperkalaemia
hypocalcaemia
