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reception starts when photons hit
retinal, inside opsin
Opsin activates transducin, which activates phoshodiesterase, which
reduce [cAMP], which closes ion channels
In light, photoreceptors are
hyperpolarized
Blocking BMP at end of gastrulation means cells can become
neural plate
IF a cell's notch receptors get bound, it cannot be a
neurons
If notch does not get bound, cell becomes a
neuron
Sonic hedgehog signalling determines
dorsal/ventral positioning in neural tube
Hox genes determine
segmentation
Developing axons can travel by
contact, ECM, CAMS, and cadherins
Developing axons can also follow
tropic signals
Axonal growth cones extend with
f-actin then microtubules
Sea slugs can be
trained by poking them
electric fish can teach us about
sensorimotor integration
Mice learn mazes with
place cells
What determines the resting potential of a neuron?
The permeability of the membrane
During an action potential, which of the following statements is true
the influx of Na+ ions causes the cell to depolarize
In the voltage-clamp experiments of Hodkin and Huxley, they treated the squid axon with a pufferfish toxin called tetrodotoxin (TTX). What did this treatment prove about potential changes?
sodium channels were responsible for the early inward current
As you hold your pencil to fill out this scantron, your touch receptors are getting activated and sending a voltage change along their axon to a postsynaptic neuron. This must mean the touch receptor is
mechanically-gated
What is the role of ATPase pumps in a neuron after repeated stimulation?
They remove sodium ion in exchange for potassium to reset concentrations
All of the following are involved with synaptic transmission at electrical synapses except:
synaptic vesicles
Which of the following is true about restraint of neurotransmitter vesicles at the axonterminal?
The vesicles are released by phosphorylation of synapsin.
Which of the following is not an accepted criterion for defining a molecule to be a neurotransmitter?
It must be synthesized in the presynaptic terminal
For your honours research project you create a mutant mouse that has defective synaptotagmin proteins in its axon terminals. What most likely happens in the terminal after excitation?
Vesicles would dock at the terminal but not fuse to the membrane
Assume synapse A represents a GABAergic synapse, synapse B a nicotinic cholinergic synapse, and synapse C a glutaminergic synapse with postsynaptic AMPA receptors. How would neuron#2 respond to cholinergic stimulation in the presence of intense GABAergic stimulation
Neuron #2 would not respond because GABA activation would inhibit the release of glutamate at C.
If an excitatory muscarinic receptor is bound, what sequence of events would happen in the postsynaptic neuron?
1. Phospholipase C (PLC) cleaves PIP2
2. Calcium ions are released
3. G-protein is activated
4. IP3 channels are activated
b. 3,1,4,2
Upon graduation you get hired by a pharmaceutical company investigating new drugs to treat anxiety. The one you are tasked with acts as an agonist on a GABAA receptor. What role could this drug play in reducing anxiety?
c. It would gate a chloride channel, allowing Cl- to flow in
13. Dopaminergic synapses can function as a negative feedback loop. Which of the following best explains this statement?
Excess dopamine in the synapse binds to presynaptic receptors to stop dopamine release.
14. Drugs known as SSRI can be an effective treatment for depression because
They slow the reuptake of serotonin, increasing its excitatory effect
In a signalling cascade using G-proteins and cAMP, which is not a signal amplification step?
activation of adenylyl cyclase by a G-protein
16. If you are studying the effects of a lipophilic steroid on postsynaptic signalling, which of the following should be true?
c. It can bind to an intracellular receptor for effects on the nucleus
17. What does a ryanodine receptor do?
It binds calcium in cytoplasm to release calcium from intracellular stores
Which of the following would be activated by cAMP inside of a neuron?
PKA
If you treat a neuron with a growth factor and notice a kinase that is activated in a cellularcascade that targets transcription factors to enhance cell growth, what type of kinase is mostlikely involved?
MAPK
20. Why is thyroid hormone such an important developmental regulator?
Because it goes straight to the nucleus where it binds to receptors that trigger transcription
How do AMPA and NMDA receptors differ?
AMPA open directly upon glutamate (or could say ligand or receptor) binding, NMDA need the presence of other cofactors (or could say glycine) or that cell must first be depolarized for receptor binding
According to the Goldman equation, what would happen to the membrane potential if the permeability to sodium ions increased in a neuron at rest? What would cause the permeability to change
part 1 increase. Part 2 sodium ion channels open.
What does a patch-clamp experiment using inside-recording measure?
movement of ions through a single channel after treatment with intracellular ligand (have to have both single channel and intracellular part. Could say movement of current instead of movement of ions)
What does the RAB3A/GTP complex do in an activated presynaptic neuron?
directs synaptic vesicles to the active zone
What specific peptide causes Ca2+-dependent fusion to a presynaptic membrane?
synaptotagmin
What steps are involved in an inhibitory muscarinic receptor slowing down heart rate?
acetylcholine binds receptor, adenylyl cyclase activity is reduced, making more cAMP, increasing flow of K+ out of pacemakers
When a cyclic nucleotide signalling cascade starts, it will keep having effects until an enzyme in the neuron stops the cyclic nucleotide. What enzyme does this?
phosphodiesterase
If a growth factor binds a receptor, causing dimerization and autophosphorylation on thecatalytic domain of the receptor, it likely bound to what type of receptor?
receptor tyrosine kinase
What role does calcium play in catecholamine synthesis?
calcium enters through voltage-gated channels (not necessary for credit) and activates kinases, which activates tyrosine hydroxylase, which make catecholamines
What kinase is activated by diacylglycerol (DAG) and plays an important role in neural cell growth?
PKC
Compare and contrast passive versus active conduction in a neuron. Where does each occur and how does each propagate. Be sure to consider all portions of the neuron. How and why does myelin affect each type of conduction.
Passive occurs in dendrite and in axon terminal between sodium gates (or within nodes of Ranvier) (1 point). Propagates by diffusion of ions along a concentration gradient.(1 pt) Active occurs only in axon(1 pt). Propagates by sequential opening of sodium channels (at Nodes of Ranvier or at sodium gates) (1 pt). Myelin makes both propagate faster. Reduces diffusion loss of ions for passive, making it possible to have wider spaced gates and speeding active propagation.(1 pt for both Myelin clauses)
Passive occurs in dendrite and in axon terminal between
sodium gates (or within nodes of Ranvier)
Propagates by diffusion of ions along a
concentration gradient.
Active occurs only in
axon
Propagates by sequential opening of sodium channels (a
Nodes of Ranvier or at sodium gates
Myelin makes both propagate
faster
Reduces diffusion loss of ions for passive, making it possible to have
wider spacedgates and speeding active propagation
During neural development and growth, neurons must receive growth factors as signals to continue to survive and change. If the growth factor binds to a receptor tyrosine kinase, describe the pathway of activation that might happen to result in genes transcribing new proteins to influence cell growth. You don't need to identify every step in the pathway, just in general how activated receptor turns on transcription
should say receptor tyrosine kinase is active and forms a dimer; catalytic part (orintracellular part) is activated and undergoes self-phosphorylation. This activates g-protein(could also say RAS) which activates kinases to turn on CREB (as transcription factor).Could also say activates PLC which activates kinases to turn on CREB.
receptor tyrosine kinase is active and forms
dime
catalytic part (or intracellular part) is activated and undergoes
self-phosphorylation
This activates g-protein(could also say RAS) which activates kinases to turn on
CREB (as transcription factor).
Could also say activates PLC which activates
kinases to turn on CREB
Your mother is curious about what you are learning in school and asks you, "once an action potential reaches the end of an axon, how does that cause neurotransmitter-filled vesicles to dock
with and fuse to the axon terminal?" (Mom is smart and knows the answer. She is testing you to make sure you are studying rather than drinking with your friends). Explain to your mother all the relevant steps involved in this process. Make sure you ONLY cover the parts mom is asking about.
Has to have synaptotaxin and SNAP-25 on membrane fusing with synaptobrevinon vesicle for docking. Ca2+ comes in causing synaptotagmin to bind pulling vesicle to fuse
Has to have synaptotaxin and SNAP-25 on membrane fusing with
synaptobrevinon vesicle for docking.
Ca2+ comes in causing synaptotagmin to bind pulling
vesicle to fuse
If you are studying a network of neurons that form an oscillatory circuit to control a repetitive behaviour without conscious input, you are most likely studying a(n):
central pattern generator
Prairie voles form monogamous mating pairs while meadow voles do not show social bonding despite being very closely related evolutionarily. What major difference exists in the brains of these two species that may help explain the evolution of social bonding?
prairie voles have higher levels of vasopression receptor expression
Which of the following statements is true concerning place cells in mice?
They are complex spike cells that change firing rate depending on location of the animal
To what does the concept of "adaptive cancellation" in sensorimotor systems refer?
The ability to differentiate environmental cues from self-generated cues.
In the beginning stages of neurogenesis some cells are fated to become ectoderm while neigbouring cells become fated to become neural plate. Which statement below is TRUE concerning the determinants of cell fate?
Areas with chordin/noggin/follostatin expression will form neural plate.
How are a cortical neuron's birthday and cortical layer organization related?
cells that originate at around the same time are organized in the same layers.
Fetal retinoid syndrome is a collection of birth defects caused by disruption in retinoic acid signalling and can disrupt segmentation of hindbrain formation if it occurs early in development. Which of the following signalling factors would most likely explain this association between retinoic acid levels and hindbrain segmentation?
Hox
What is one role of the Wnt signalling pathway in neural development?
It controls lengthening of the neural tube
Which of the following is TRUE regarding fibroblast growth factor (FGF) in developing neural tissues?
It is inducible factor that binds to receptors to influence neural motility
A signaling molecule released by the notochord that cause neuronal systems to form is best described as a(n):
inducible factor
Which of the following cell types will NOT form from neural crest cells?
cortical neurons
Proneurons adopt a non-neural fate through activation of __________ by ____________.
d. notch: delta
For your honours thesis project your supervisor asks you to put developing neurons in petri plates coated with lines of extracellular matrix to direct axon outgrowth. What makes your supervisor think the axons will follow the pathway laid down?
Because integrins will be activated by extracellular matrix proteins.
Semaphorins bound to the cell surface of extracellular matrix
cause growth cones to collapse and axons to stop growing
Neurotrophic factors
play a role in adjusting the size of neuronal populations to an appropriate number
Some developing tectal neurons start on one side of the brain but send axons to the opposite side, crossing the midline as they go. Which of the following statements accurately explains how the growth cone is first attracted to and then repelled from the midline?
Towards the midline netrin encourages actin polymerization but after the midline slit and netrin combine to cause actin breakdown
If one followed a growth cone through a "decision point" at which a choice about direction was made, one would observe the growth cone
extending numerous filopodia in different directions as it searches for guidance cues
At the developing neuromuscular junction, what is the role of agrin in synaptogenesis?
it causes existing acetycholine receptors on the muscle to aggregate
For neurotrophin receptors what is the fundamental difference between tyrosine kinase (trk) and p75 receptor responses?
Activation of trk can lead to cell survival while activation of p75 can lead to cell death
Why don't CNS axons regenerate?
Because the mature CNS does not have as much laminin
It is important to study neuroscience in many different vertebrates because many brain structures share ____________________ across group
homology
In the sea slug model of learning and memory, what is the importance of spike broadening to neural sensitization?
spike broadening refers to the enhanced response of the presynaptic neuron after sensory activation. Could also say spike broadening is a mechanisms of presynaptic facilitation
The main inducible factor responsible for dorsal-ventral patterning early in neural tube development is called ______________________________.
Sonic hedgehog (okay if they just say hedgehog or shh).
The three early stages of embryonic development that we covered in class were
blastulation, gastrulation, neuralation
Cortical neuroblasts differentiate in the ventricles and migrate to their final position by crawling along what cell types (be specific).
should say radial glia.
During neurogenesis, an ectodermal cell gets exposed to the following series of signalling factors: Chordin, a medium dose of sonic hedgehog, activated delta, and bHLH. What does that cell ultimately become (be as specific as possible)?
a ventral motor neuron
What mediates fasciculation in the context of axon pathfinding?
NCAM or cell adhesion molecules
During axon growth in a developing neurites, microfilaments are formed when______________ gets polymerized into ___________________.
g-actin; f-actin (could also say globular actin and filamentous actin
As new synapses form on a muscle fiber many more synapses initially form than are needed. The ones that survive will win the competition for neurotrophic support and show coordination of
electrical activity
What is the difference between anterograde and retrograde transport in a neuron?
anterograde is from cell body (or nucleus) to axon (or to dendrite); retrograde is from axon to cell body
Your father refuses to buy you a dog as a pet so in desperation you adopt a sea hare (Aplysia)and bring it home to be your new friend, naming it Gertrude. You decide to teach Gertrude anew trick. As you poke her siphon, Gertrude withdraws her gill so, to reinforce this, you poke her tail along with the siphon. Gertude quickly learns so that only a brief touch is now needed to withdraw her gill. What is the general term for this neurological trained response? How would this work at the synaptic level to increase this motor behaviour, making sure to provide details on the neurons involved at this synapse (there are 3 to worry about). What cellular mechanism can cause the enhanced response of siphon withdrawal?
response is associative learning/sensitization (presynaptic facilitation also okay) (1pt). Neurons involved are interneuron, sensory neuron and motor neuron (1 pt).Mechanism has to have serotonin binding to a g-protein-coupled receptor (1 pt) then it has to activate cAMP and then PKA to cause K+ channels to stay closed (1 pt) for longer presynaptic activation and thus more motor neuron response (1 pt here)
response is associative learning/sensitization (presynaptic facilitation also okay) (1pt). Neurons involved are
interneuron, sensory neuron and motor neuron
Mechanism has to have serotonin binding to a
g-protein-coupled receptor
then it has to activate cAMP and then PKA to cause
K+ channels to stay closed for longer presynaptic activation and thus more motor neuron response
At the end of gastrulation a developing embryo has 3 cell layers. Which of these adopts a neural fate and what determines which cells can become of neural origin? Made sure to include all relevant signaling factors and where they come from to make these cells follow a neural path.
ectoderm becomes neural plate (1 pt). BMP released by mesoderm (1 pt) turns cells into epidermis, chordin/noggin/follastatin (only have to say one of these; 1 pt) released from organizer/blastopore block BMP (1 pt) so cells that don't get BMP turn into neural plate (1 pt)
ectoderm becomes neural plate (1 pt). BMP released by mesoderm (1 pt) turns cells into
epidermis,
ectoderm becomes neural plate (1 pt). BMP released by mesoderm (1 pt) turns cells into epidermis, chordin/noggin/follastatin (only have to say one of these; 1 pt) released from organizer/blastopore block
BMP (1 pt) so cells that don't get BMP turn into neural plate (1 pt).
As a neurite sends out a growth cone it can use 6 different cues to guide its path along the developing central nervous system. Name 5 of these cues and for each state one receptor that is activated to affect growth cone direction.
1. extracellular matrix (ECM okay) adhesion activates integrin receptors
2. cell surface adhesion (or cadherins or NCAMS). Receptor will be either other cadherins (but not catenin) or other NCAMs (just CAMS okay)
3. fasciculation. Receptors are again NCAMS
4. Chemoattraction/netrin. Receptors should be DCC/UNC5 (having one is fine)
5. Chemorepulsion. Semophorin receptor (didn't give them a name) or Slit/Robo activation along with netrin
6. Contact inhibition. Semaphorins here bind to plexin or Ephrins bind to Eph receptors.
1. extracellular matrix (ECM okay) adhesion activates
integrin receptors
2. cell surface adhesion (or cadherins or NCAMS). Receptor will be either
other cadherins (but not catenin) or other NCAMs (just CAMS okay)
3. fasciculation. Receptors are again
NCAMS