Oral exam Flashcards
- Describe the different types of glial cells and their functional roles.
There are 3 Types:
Astrocytes
- found primarly in grey matter
- help maintain ionic balance
- take-up and process neurotransmitters
- Blood-brain barrier
- formation of scars following injury
Oligodendrocytes
- white matter
- form myelin (schwann cells make myelin in peripheral nerves)
- aids propogation of nerve signals
Mikroglia
- resides in the CNS
- derived from hematopoetic stem cells
- amoeboud and ramified
- ramified - dormant state
- amoeboid - activated, fagocytic
- cytokines tha modulate inflammatory response
- Describe the basis of the resting membrane potential and the function of the Na/K pump.
Resting membrane potential (approx. -65mV) determined by intra, extracellular ion concentrations.
- 2K+ in
- 3 Na+ out
- ATP -> ADP + Pi
Genom Na/K-ATPase som pumpar ut 3 Na+ och pumpar in 2 K+. Förbrukar ATP. Ger ca 5 mV. K+-läck-kanaler läcker tillbaka en del Kalium (finns även Na+-läckkanaler, men de är 20 ggr färre än K +-läck-kanalerna i antal) och ger det mesta av potentialen (85 mV).
- Describe the basis of the action potential – which are its different phases and which are the underlying ionic mechanisms.
- Ion channels open → depolarization of neuron (net infl ux of positive charge/excitatory postsynaptic potential)
- Depolarization to approx. -55mV → voltage-gated sodium channels open at axon hillock → sodium rushes into cell → action potential (neuron is positively charged to approx. +40mV
- Sodium channel becomes inactivated (absolute refractory period)
- Voltage-gated potassium channels then act → potassium flows out
- Sodium/potassium pump moves sodium out of cell, potassium in → hyperpolarization
- Sodium channels remain closed but can be activated (relative refractory period); hyperpolarization → stronger stimulus needed
JONPERMEABILITET: Under aktionspotentialen ändras PK/PNa drastiskt. Vad är bakgrunden? (1p)
AP sker genom att cellen depolariseras vilket öppnar spänningskänsliga Na+-kanaler. Dessa inaktiveras dock inom en kort tid efter öppnandet vilket gör att permeabiliteten för Na+ snabbt stiger till ett högt värde för att sedan snabbt sjunka tillbaka till ett lågt.
Depolariseringen öppnar även långsammare K+-kanaler (också de spänningskänsliga). Detta går dock långsammare varför cellen vid en AP initialt är mer permeabla för Na+ och cellen depolariseras. Snabbt inaktiveras dock dessa kanaler och permeabiliteten blir högre för K+-joner, vars kanaler inte inaktiveras. Detta leder till att K+ strömmar ut ur cellen som repolariseras (hyperpolariseras), vilket i sin tur leder till att de båda spänningskänsliga kanalerna återigen stängs.
- Compare excitatory and inhibitory synapses – what are the effects on the postsynaptic neuron and how do the two types of synapse interact.
excitatory postsynaptic potential (EPSP)
A neurotransmitter that causes depolarization of the postsynaptic membrane is excitatory because it brings the membrane closer to threshold. Although a single EPSP normally does not initi- ate a nerve impulse, the postsynaptic cell does become more excitable. Because it is partially depolarized, it is more likely to reach threshold when the next EPSP occurs.
inhibitory postsynaptic potential (IPSP)
A neurotransmitter that causes hyperpolarization of the post- synaptic membrane is inhibitory. During hyperpolarization, generation of an action potential is more difficult than usual because the membrane potential becomes inside more negative and thus even farther from threshold than in its resting state.
- Compare the process of release of ”small” neurotransmitters (such as glutamate and GABA) with that of ”large” neurotransmitters (such as neuropeptide Y and substance P) – similarities and differences.
- Small-molecule neurotransmitters (faster)
- Neuropeptides (slower)
- Describe the molecular machinery that mediates fusion of synaptic vesicles with the plasma membrane.
- action potential
- depolarization -> opening of voltage-gated Ca2+-chanels
- influx of Ca2+
- Ca2+ causes vesicles to fuse with presynaptic membrane
- transmittor realesed
- transmittor binds to postsynaptic receptor
- opening or closing of postsynapitc channels
- current
- removal of transmittor via glial uoptake och enzymatic degradation
- “Ca2+-binding protein, with bound Ca2+ indicated by spheres. (B) A model for Ca2+-triggered vesicle fusion. SNARE proteins on the synaptic vesicle and plasma membranes form a complex (as in A) that brings together the two membranes. Ca2+ then binds to synapto- tagmin, causing the cytoplasmic region of this protein to catalyze membrane fusion by binding to SNAREs and inserting into the plasma membrane.”
- Poisoning by Botulinum toxins and Tetanus toxin give rise to different symptoms. How do these toxins act? How do the symptoms produced by the two toxins differ and why?
Botulinum toxin causes paralysis by blocking release of acetylcholine from somatic motor neurons.
Tetanus neurotoxin (TeNT) binds to the presynaptic membrane of the neuromuscular junction, is internalized and transported retroaxonally to the spinal cord. The spastic paralysis induced by the toxin is due to the blockade of neurotransmitter release from spinal inhibitory interneurons.
“inhibit neurotransmitter release by cleaving the SNARE proteins involved in fusion of synaptic vesicles with the presynaptic plasma membrane (see Figure B). Tetanus toxin and botuli- num toxin types B, D, F, and G specifically cleave the vesicle SNARE protein synap- tobrevin. Other botulinum toxins cleave syntaxin (type C) and SNAP-25 (types A and E), SNARE proteins found on the pre- synaptic plasma membrane. Destruction of these presynaptic proteins is the basis for the inhibitory actions of clostridial tox- ins on neurotransmitter release.”
- Describe the mechanisms underlying the inactivation of neurotransmitters.
Glial uptake or enzymatic degration
- Describe the main structural and functional differences between ionotropic and metabotropic receptors.
Iontropic receptors
metabotropic receptors
10 Which are the main types of postsynaptic glutamate receptor and how do they differ?
Glutamate acts on two receptors:
- AMPA-receptor activates
- NMDA-receptor is inactivated at resting potential
AMPA- och kainatreceptorer är icke-selektiva katjonkanaler (permeabla för både Na+ och K+), som aktiveras av glutamat. Vid vilomembranpotentialen (ca -70 – -90 mV) ger bindningen av glutamat till AMPA- eller kainatreceptorer upphov till en inåtgående Na+-ström vilken genererar en EPSP.
NMDA-receptorn är en typ av glutamatbindande receptor som skiljer sig från AMPA- och kainatreceptorer, genom att den även regleras av membranpotentialen (voltage-gated). Denna egenskap beror på bindningen av Mg2+-joner till receptorn, vilket blockerar kanalen vid vilomembranpotentialnivån. Vid depolarisering släpper Mg2+-blockaden och kanalen kan aktiveras, vilket även kräver att glutamat är bundet till receptorn. NMDA-kanalen är även permeabel för Ca2+- joner.
- Describe the mechanisms underlying synaptic short-term plasticity
regulating calxium-levels?
Facilitation: increased probability of synaptic terminals releasing transmitters in response to pre-synaptic action potentials. Mechanism: Ca2+ is accumulated.
Depression: decreased probability of synaptic terminals releasing transmitters in response to pre-synaptic action potentials. Mechanism: depletion of vesicles, feedback, etc.
- Describe the mechanisms underlying synaptic long-term plasticity
(LTP, long-term potentiation) or depressing (LTD, long-term depression)
regulation of AMPA-, NMDA-recepttors
