Fysiologie Spier/Zenuw
64 important questions on Fysiologie Spier/Zenuw
Membrane Protein Carrier
e.g. includes carriers that do facilitated diffusion
Process Carrier Protein
2. X enters from the outside & binds @binding site
3. Outer gate closes and X becomes occluded (still bound)
4. Inner gate opens (still bound)
5. X exits and enters the inside of the cell
6. Inner gate closes
Cycle can go in reverse order
Functional Components of Gated Channels
2. Sensor(s)
3. Selectivity Filter
4. Open channel pore
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Gate of Gated channels function
Sensor(s) of Gated channels
1. changes in membrane voltage
2. 2nd messenger proteins acting on cytoplasmic face of membrane protein
3. ligands (neurohumeral agonists) binding to extracellular face of membrane protein
Selectivity filter of Gated Channels
Primary Active Transport
Secondary Active Transport
Subunits Na-K pump
beta: essential for proper assembly & membrane targeting
Electrophysiology of cell membrane
Vm skeletal, smooth & cardiac muscle
smooth: -55mV
erythrocyte: -9mV
Planar Lipid Bilayer
Model Assumptions of Electrodiffusion
2. constant electric field
3. ions moving independently of one another
4. constant permeability coefficient of P
Permeability Ions in Cell types
- high permeability to K
- low permeability to Na, Ca
Vertebral skeletal muscle fibers: high permeability to Cl
Ionic current & Ohm's law
Vm more -ve than Ex --> current negative/in
Vm more +ve than Ex --> current positive/out
Overshoot/Undershoot Definitions
undershoot: more negative than Vrest = afterhyperpolarization
Threshold, amplitude, Time course & Duration depend on:
2. intracellular & extracellular concentrations of Na, K, Ca and Cl
3. membrane properties (capitance, resistance, geometry)
Size of graded voltage change
Depolarization (short process)
Two Phases of Refractory Period
P2: relative refractory period = the minimal stimulus necessary for activation is stronger or longer than predicted by strength-duration curve for the 1st AP
These phases arrive from gating properties of Na and K
Local circuit loops
always flow in complete circuit, along paths of least resistance.
The higher the membrane resistance and cable radius
The higher the resistance of internal conductor
Electrical (2 types of synapses)
2. rectifying synapse: allows depolarizing current to pass readily only in 1 direction.
Neurotransmitters that can activate ianotropic/metabotropic receptors
Neurotransmitter Receptors Transduce info by:
=ianotropic receptors -> rapid opening channels
2. G-protein coupled receptors
=metabotrophic receptors (involves GTP)
- interact with ion proteins or 2nd msg effector proteins
ACh activates - muscle but inhibits - muscle
Process Nicotinic Ach channel activation
Process Muscarinic Ach receptor activation
Neuromuscular junction/end plate
Synaptic Basal Lamina
AChe (synthesis and function)
- moves into synaptic vesicle via Ach-H exchanger (ACh influx, H+ efflux)
- fueled by ATP produced by mitochondria in nerve terminal
Where does release Ach occur?
Permeability to Ions AChR channel
impermeable to Cl
Toxins/Drugs Affecting Pre-synaptic Membrane Channels
- Tetrodotoxin (-)
- Saxitoxin (-)
2. K channel:
- Dendrotoxin (-)
3. Ca Channel
w-conotoxin (-)
ALL ANTAGONISTS
Toxins/Drugs Affecting Post-synaptic Membrane Channels
- Tetrodotoxin (-)
- Saxitoxin (-)
- u-conotoxin (-)
2. AChR channel
- acetylcholine (+)
- nicotine (+)
- d-tubocurarine (-)
- a-bungarotoxin (-)
3. Acetylcholinesterase
- physostigmine (-)
- DFP (-)
Agonists of AChr preventing transmission
- activate opening channels
e.g. succinylcholine, carbamylcholine
Muscle Types & Properties
Cardiac: specific to heart
Smooth: mechanical control of organ systems, blood vessels, airway passages
Cycle of Mechanical Work
Trigger for Contraction for All Muscle Types
Myofiber of Skeletal muscle
Neuromuscular Junction (Muscle)
When Ach:Nicotinic Receptor Process
2. rises to threshold
3. activates voltage gated Na channels near end plate
4. triggers AP along surface membrane
5. penetrate into T-tubules
6. surround myofibrils at junctions of A&I bands in each sarcomere
7. each T-tubule associates with 2 terminal cisternae of the SR
Excitation-Contraction (EC) Coupling
- Beginning depolarization of T-tubule initiates cross-bridge contraction cycle
L-type Channels consist of:
Depolarization of Tetrad (2 effects)
1. Open Cav1.1 pore -> allows electrodiffusive Ca entry
2. Mechanically activates each of 4 directly coupled subunits of another channel: SR Ca release channel (in terminal cisternae and faces t-tubule)
Cav1.1 interacts with RYR1
Cav1.1 in closed state
therefore: EC-coupling in skeletal muscle is an electrochemical process involving voltage-induced Ca release mechanism
Mechanism 1 Modulating RYR1 activity
1. cytoplasmic Ca
2. Mg
3. ATP
4. Calmodulin (CaM)
5. protein kinase A (PKA)
6. Ca-calmodulin-dependent Kinase II (CaMII)
Mechanism 2 Modulating RYR1 Activity
sympathetic ANS activates B-adrenergic receptors
--> PKA mediated phosphorylation of RYR1 results in faster and larger increase in cytoplasmic Ca (stronger skeletal muscle contraction)
EC-Coupling Skeletal Muscle Process
2. Mechanical coupling between l-type Ca channel and Ca-release channel causes release channel to open.
3. Ca exits the SR via Ca release channel activating troponin C and causing muscle contraction.
4. Ca entering the cell via l-type ca channels can also activate the release channels
Thin Filaments (characteristics)
attach to opposite faces of Z disk, cross-linked by a-actinin proteins
Thick Filaments (Characteristics)
partially interdigitate, results in light/dark bands
I bands & A bands
A bands: dark, myosin filaments, anisotropic
During contraction: I bands shorten, A bands stay --> "sliding filament model"
Thin Filament: F-actin
F-actin: association of tropomyosin & troponin complex
2 Myosin Light Chains
2. 1 regulatory light chain (RLC/MLC-2)
Myosin Heavy Chain (MHC)
2 wrap around eachother (form dimer)
each MHC has:
1. at tip: several loops that bind actin
2. at middle: nucleotide site for binding/hydrolyzing ATP
Cross-Bridge Cycle Start
-Absence ATP/ADP
- Myosin attached to actin
Cross-Bridge Cycle Step 1
- reduces affinity of myosin for actin
- myosin head releases from actin
Cross-Bridge Cycle Step 2
- products retained within myosin active site
- myosin head in cocked position
Cross-Bridge Cycle Step 3
- cocked myosin loosely bound to new position actin filament
- 6 actin filaments surround 1 thick
Cross-Bridge Cycle Step 4
- triggers increased affinity of myosin-ADP complex for actin
- strong cross-bridge state
- = RATE LIMITING STEP
Cross-Bridge Cycle Step 5
- conformational change causes neck to rotate around head
- bending causes actin/myosin filament to pass each other
- pulls Z-lines closer together shortening sarcomere and generates force
Cross-Bridge Cycle Step 6
- dissociation of ADP from myosin
- leaves actomyosin complex in rigid attached state
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