Karteikarten
Action potential
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- 1Glial cells: - Four main functions:: non-neuron cells that support neurons and do not produce electrical impulses
(1) to surround neurons and hold them in
place
(2) to supply nutrients and oxygen to neurons; (3) to insulate one neuron from another
(4) to destroy pathogens and remove dead neurons - 2Microglial cells:o Have phagocytic function
- 3Macroglia:astrocytes, oligodendrocytes, ependym
- 4Oligodendrocytesimportant for myelination of neurons in CNS
- 5Schwann cellsimportant for myelination for PNS neurons
- 6Astrocytes:star-shaped glial cells in the brain and spinal cord
- Maintains extracellular ion balance
- Forms tight junctions in blood-brain barrier to protect from toxins in blood
- Fibrous astrocytes present in cerebellum
- Protoplasmic astrocytes present in grey matter - 7Nernst Equation:predicts membrane potential for single ion
(E = emf in volts, R = gas constant, T = absolute temp, F = Faraday constant, z = charge of ion)
ZX would be +1 for sodium ion and -1 for chloride ion, so ® − $% = -61 at about 37 Celsius - 8Threshold voltage:voltage needed to open voltage-gated Na channels (around -55mV)
- 9Resting Membrane Potential:potential difference across membrane of living cell in resting
condition
- For neurons, RMP is -70mv (inside more negative than outside) for 3 main reasons
o Na/K pumps: 3Na out, 2K in ® slightly negative charge in cell
o Abundant K+ channels ® K+ leaves, anions stuck inside ® super negative inside cell - 10Cell ismuch more permeable to K+ than Na+
o Small amount of Na channels ® Na enters ® cell slightly less negative - 11Potential exists due todifferent composition (specific ion concentration) of ICF and ECF
- 12Inside cell,K+, phosphate (PO43-) is high, and protein (anions) is high
- 13Outside cell,Na+ is high, Cl- is high, and Ca2+ is high
- 14Cell membrane’sselective permeability affects this (role of Na+ / K+ pump)
- 15Sodium concentrationis much higher outside the cell
- 16Potassium concentrationis much higher inside
- 17During resting state,cell becomes selectively permeable to K+ ® starts to move out of the cell via leaky channels ® outside of the cell becomes even more positive
- Unlike Nernst equation, Goldman-Hodges equation takes into account permeability of multiple ions - 18Electrochemical gradient:Electrochemical gradient: ions diffuse across membrane due to
- Electrical gradient: like charges repel, opposites attract
- Concentration gradient: high to low
-When concentration gradient (chemical force) = electrical gradient (electrical force), cell is at equilibrium (no net movement). Equilibrium potential calculated by Nernst equation: - 19Ions move across membranevia (1) leaky channels (2) voltage-gated ion channels (3) ligand- gated ion channels
Na+/K+ pump maintains resting potential
- Pushes out 3 Na+, pulls in 2 K+
- If inhibited (e.g., by digitalis for heart failure), the concentration gradient is los - 20Depolarization:Na+ in
- 21Polarization:K+ out
- 22Voltage-gatedpotassium channels open and close very slowly
- 23Depolarization of a membranecauses opening of a voltage-gated potassium channel
But because it’s slow, it actually opens during repolarization (even though opening starts during depolarization)
Brings action potential to an end - 24Tedrodotoxin (TTX):powerful neurotoxin found in puffer fish
- Inhibits voltage-gated Na+ channels (can’t depolarize, no action potentials)
- Leads to paralysis - 25Lidocaine:same mechanism ® local anesthetic
- 26Hyperkalemia:Potassium increase in ECF > cell becomes highly excitable
- Clinical: Hyperkalemic period paralysis
- Autosomal dominant disease with mutation in the voltage-gated sodium channel of muscle - 27Hypokalemia:Low potassium concentration in ECF
- 28Hypercalcemia:High calcium concentration in ECF
- Blocks voltage-gated Na channels ® decreases excitability - 29Hypocalcemia:Low calcium concentration in ECF > cell becomes highly excitable
- Removes gating in voltage-gated sodium channel ® Na conductance increases (more Na
comes into cell) - 30Channelopathies:caused by misfunction of ion channel subunits or its regulatory proteins
o May be either congenital or acquired (from autoimmune attack on ion channel) - 31Paralysis:In hyperkalemic periodic paralysis, high levels of K+ in blood interact with genetically caused abnormalities in sodium channels (pores that allow the passage of sodium molecules) in muscle cells, resulting in temporary muscle weakness and, when severe, in temporary paralysis.
- 32Ataxia:Channelopathies resulting directly from mutations in ion channels underlie some forms of cerebellar ataxia. In addition, alterations in ion channel localization or availability in the absence of any channel mutation, can profoundly alter cerebellar neuronal excitability, resulting in ataxia.
- 33Night Blindness:The incomplete form of X-linked congenital stationary night blindness (CSNB2) is caused by mutations in the CACNA1F gene, which encodes the voltage-gated calcium channel CaV1.4 expressed heavily in retina. One of the important properties of this channel is that it inactivates at an extremely low rate.
- 34Myelinated neurons:myelin promotes saltatory conduction
- CNS Myelin: Oligodendrocytes
- PNS Myelin: Schwann Cells - 35Myelin insulatesagainst ion escape, so that action potential can be preserved
- 36Larger axon diameterLarger axon diameter > faster conduction
o Less resistance (just like electrical wires have lower R for big d)
Conduction velocity increases
- No myelination at Node of Ranvier, so this is where efflux/influx of ions can occur
- Decreases capacitance, How?
- Clinical: demyelination disorders (multiple sclerosis, Guillon-Barre)
o Current leaks out without insulation, not enough for action potential - 37Time constant:8 = 9 : where 9 is membrane resistance (inverse of permeability) and : is ''''
membrane capacitance (charge stored in axon) - 38Smaller tau - Larger tauSmaller tau > more rapid change in response
- Larger tau > extended repolarization (more time to send the next stimulus) - 39Length constant:= <9 /9 = index of how well a sub-threshold potential will spread across '"
axon as a function of distance
- rm is membrane resistance and ri is internal resistance of axon
- Remember that resistance is inversely proportional to diameter - 40Conduction velocityincreases for myelinated neurons
- thickness of the membrane (increase in separation of cations and anions) and by decreasing
the amount of charge stored on both sides of the membrane. - 41Multiple sclerosis-demyelinating disorder of CNS. Thus membrane resistance decreases (current leaks out) thus faster decay of currents, insufficient to produce an AP. Multiple sclerosis: progressive demyelination of axons in the CNS leading to loss of motor control and sensory deficits. Common in severe diabetes mellitus due to demyelination of peripheral axons.
- GBS damages the peripheral nervous system (PNS). - 42Smaller diameterSmaller diameter > higher resistance > lower conduction velocity
- 43Electrical synapsesmore common in cardiac / smooth muscle cells
- 44Chemical synapsecommunication pattern: one-way conduction
- 45Steps1. Action potential travels along presynaptic neurons
2. This opens voltage-gated calcium channels (Ca2+ moves from ECF to ICF)
3. Calcium triggers exocytosis of synaptic vesicle containing neurotransmitter
4. Neurotransmitters bind to receptors on the postsynaptic membrane (ligand-gated ion channels)
5. As long as neurotransmitter is bound, ions move inside cell and trigger response
6. Response terminated by removing neurotransmitter from synaptic cleft (degradation, reuptake, or diffusion - 46Excitatory Postsynaptic Potential (EPSP): on potential)generated at postsynaptic membrane due to excitatory neurotransmitters (e.g., glutamate)
- Results in excited neuron (Na+ influx ® depolarization ® spread of action potential) - 47Inhibitory Postsynaptic Potential (IPSP):generated at postsynaptic membrane due to
inhibitory neurotransmitters (e.g., GABA)
- Results in inhibited neuron (K+ efflux, Cl- influx ® hyperpolarized ® no action potential)
- In brain, IPSPs mediated by GABA-A receptor
o Clinical: Activated by several drugs (benzodiazepine and barbiturates)
o Binding sites for these drugs exist on chloride ion channel
o Causes activation of Cl channel causing more Cl- to come inside cell ® inhibition
§ Aka hyperpolarization potential (sever with barbiturates) § Vm near ECl, makes it harder for depolarization - 48End Plate Potential (EPP):produced at junction of motor neuron and muscle (aka motor end plate)
- Multiple end-plate potentials add up ® produces action potential ® travels down rest of muscle fib - 49Temporal:: one synapse through time (stimulated back-to-back again and again)
- 50Spatial:several synapses stimulated at same time
Location: dendrites, cell body, sensory receptors - 51Action potentials are all-or-none:if threshold is not reached in one go, you do not get action potential
- Short-term and rapid changes in resting membrane potential, propagated
- Axon hillock is the trigger point - 52Once you hit threshold (-55mV),activation gate of voltage-gated Na channels triggered >Na channel open > Na rushes in > cell voltage increases
- 53Once you hit a positive voltage ((say +30mv) , it triggers inactivation gate ® closes
- 54Positive voltage opens Ca channel,which connects snare proteins > release
neurotransmitter vesicle - 55Release of neurotransmitteris at axon terminal (synapse), specifically presynaptic terminal
- 56Positive voltageslowly opens voltage-gated potassium channel > potassium leaves much faster > negative voltage (-90 mv) → closes Ca channel > stops neurotransmitter release
- 57Negative voltageslowly closes voltage-gated K+ channel > resting membrane potential reached
- 58Graded potentials can be summed until threshold is reached - Temporal: - Spatial:- Temporal: one synapse through time (stimulated back-to-back again and again)
- Spatial: several synapses stimulated at same time - 59Excitatory (EPSP), EPP (neuromuscular junction)- More likely to produce an action potential
- Depolarization - 60Inhibitory (IPSP)- Less likely to produce an action potential
- Hyperpolarization
- Membrane stabilization
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- Karteikarten am Action potential , erstellt von Shan Ali am 27/08/2022.
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