Studied by 612 people
metabotropic (GPCRs are metabotropic)
are odorant receptors ionotropic or metabotropic?
g-protein coupled receptors (GPCRs, largest subfamily of them)
are odorant receptors ion channels or GPCRs?
the cilia
on what part of the ORN are odorant receptors expressed specifically?
another part of the cell
are odorant receptors densely expressed in the axonal terminal or in another part of the cell?
excitatory (glutamatergic)
are ORNs inhibitory or excitatory?
glutamate
what neurotransmitter do ORNs utilize?
yes (neurogenesis every 4-8 weeks)
do ORNs regenerate?
olfactory epithelium
where are the cell bodies of ORNs located?
cilia
thin protrusions from the dendrites of ORNs containing odorant receptors
dendrites of ORNs (mucus layer)
where are cilia located?
broad tuning curves
do odorant receptors have broad or narrow tuning curves?
receptors bind to multiple odorants/ligands (overlap of odorant expression)
what does having a broad turning curve mean in terms of ligand-to-receptor binding?
yes (mammals: human = 10cm², cat = 20cm², dog = 170cm²)
does the size of the olfactory epithelium vary amongst species?
no, variable % of pseudogenes (inactive)
are all odorant receptor genes in the human genome functional?
one gene
each olfactory receptor neuron expresses the products (proteins) of how many odorant receptor genes?
broad tuning curve (overlap of odorant expression)
why can a single ORN be activated/depolarized by multiple odorant molecules?
no (only one kind)
does a single ORN express multiple kinds of odorant receptors on its cilia membrane?
receptor cilia
on what part of the neuron should I apply an odorant if I wanted to stimulate that neuron in a laboratory under experimental conditions?
CNG and Ca2+ activated Cl- channels
opening of what types of membrane channels causes membrane depolarization (in olfactory cilia)?
adenylyl cyclase (AC)
what does the g-protein activate (what is the enzyme)?
glomeruli
where axons of olfactory receptor cells expressing the same gene meet in the olfactory bulb
yes
do the axons from olfactory receptor neurons end in the glomeruli?
ORNs expressing the same gene
do glomeruli receive input from random ORNs or from ORNs expressing the products of the same odorant receptor genes?
olfactory cortex
olfactory bulbs project to the ______ directly
olfactory tract
the olfactory bulbs project to the olfactory cortex via the…
only one
each mitral cell receives information from only one/many glomerulus
periglomerular (PG), tufted, mitral (MT), granule (GC), other interneurons
what kinds of cells lie in the olfactory bulb?
reciprocal connections
mitral and tufted cells make __________ with periglomerular and granule cells
one cell excites another cell, which in turn, inhibits the first cell
reciprocal connections are when…
laminar (layered)
olfactory bulbs have a _______ structure
mitral cells and tufted cells
which are the only cells which project out of olfactory bulbs and into the primary olfactory cortex?
granule cells & periglomerular cells
which are some main inhibitory cells that are thought to mediate lateral inhibition in the olfactory bulbs?
granule cells
inhibitory cells (that release GABA) in the olfactory bulb and make reciprocal connections with mitral cells
lateral inhibition
what phenomenon seen in sensory systems are granule cells thought to mediate in the olfactory bulbs?
signal discrimination / contrast enhancement
lateral inhibition is…
yes
is olfactory adaptation calcium-mediated (is calcium required for both proposed intracellular pathways of adaptation)?
(odor fatigue/adaptation) pathway one
Ca2+ entry via activated CNG channels
Ca2+ binds Ca2+ binding protein (calmodulin)
Ca2+ calmodulin/protein complex modulates CNG channel, reduces cAMP affinity
decreased olfactory transduction
(odor fatigue/adaptation) pathway two
Ca2+ entry via activated CNG channels
Ca2+ activated CaMK II (Ca2+/calmodulin-dependent protein kinase II)
CaMK II reduces Adenylyl cyclase (AC) activity via AC phosphorylation
less cAMP produced
decreased olfactory transduction
primary olfactory cortices: piriform cortex, amygdala, entorhinal cortex,& olfactory tubercle
what brain areas do bulbar projection neurons directly send their axons to (what are their direct targets)?
no
does olfactory information require thalamic relay (going to thalamus before primary olfactory cortex) just like every other sensory modality?
secondary olfactory cortices: insula (area of proposed flavor reception), orbitofrontal cortex (OFC)
hippocampus (object association), thalamus
hypothalamus
secondary/indirect targets of bulbar projection neurons
where Schaffer collaterals (axons of CA3 pyramidal neurons) synapse onto CA1 pyramidal neurons
where exactly is plasticity heavily studied in the hippocampus that we discussed in class?
axons/processes from CA3 pyramidal neurons
what are Schaffer collaterals?
yes
are CA3 neurons glutamatergic (excitatory synapses)?
AMPA and NMDA receptors
what postsynaptic receptors mediate plasticity?
NMDARs - AMPA receptors must allow enough Na+ in to repel the Mg2+ blocking the NMDA receptor (from allowing Na+ and Ca2+ in for further depolarization)
which postsynaptic receptors are considered coincidence receptors and why?
Ca2+
what is the ion of importance that NMDA/coincidence receptors are permeable to which participates in signaling intracellular pathways?
yes
does activity of postsynaptic NMDARs correlate with changes in synaptic strength in general?
yes (less Ca2+ influx = LTD, more = LTP)
does activity of NMDARs correlate with levels of intracellular calcium?
both
is calcium signaling important for LTP, LTD, or both?
protein phosphatases
small increases in intracellular Ca2+ activate…
protein kinases
large increases in intracellular calcium activate…
both
when glutamate is released presynaptically by the axons of CA3 neurons and diffuses down the cleft to the postsynaptic membrane, does it bind both AMPARs and NMDARs or only one of those?
no
do NMDARs open as soon as glutamate binds?
Mg2+ blocks pore
why don’t NMDARs open as soon as glutamate binds?
AMPARs to allow enough Na+ influx to repel Mg2+ block
what do NMDARs require in order to open?
NMDARs
what receptors have to be activated/opened in order for LTP to take place?
post-synaptically
are NMDA receptors expressed pre- or post-synaptically at the CA3 to CA 1 synapse?
ligand-gated ion channels
what kind of receptors are AMPA and NMDA receptors in the first place?
no
are AMPARs and NMDARs GPCRs?
yes
are AMPARs and NMDARs ionotropic receptors?
yes
are AMPARs and NMDARs ligand-gated ion channels?
no (NMDARs are voltage-dependent but do not require voltage to open)
are AMPARs and NMDARs voltage-gated ion channels?
Mg2+ expulsion from NMDARs, Ca2+ influx (depolarization), increase in activity
what postsynaptic changes lead to a potentiated postsynaptic response?
yes
Does the phosphorylation of existing and the addition of new AMPARs both lead to a higher postsynaptic depolarization in response to presynaptic glutamate release?
yes
Is higher postsynaptic depolarization mediated by the calcium-dependent activation of certain kinases (enzymes)?
yes
Can structural changes also potentiate the postsynaptic response?
formation of additional postsynaptic sites (dendritic spine morphogenesis) and growth of postsynapse sites
how can structural changes potentiate the postsynaptic response?
dendritic spine morphogenesis
activity dependent formation, growth and maturation of new spines→ increased connectivity between axon and dendrites→ more contacts, larger overall contact area→ increased probability for synaptic release
yes (through phosphorylation)
can we grow existing synapses?
yes
can we grow new synapses between two cells?
only synapses receiving strong inputs and not all synaptic connections will be strengthened
what does input specificity mean in the context of LTP?
only synapses receiving a prolonged low-intensity stimulus input will be depressed/weakened
what does input specificity mean in the context of LTD?
dependent on local activity
is LTP dependent on local activity only at synapses at which it occurs or is LTP happening at one synapse dependent on what is happening at all other synapses the neuron makes?
yes
is plasticity in the hippocampus dependent on intracellular calcium signaling in the postsynaptic neuron?
yes - protein kinases
does calcium activate a specific set of enzymes in LTP?
phosphorylate AMPARs (leading to increased activity)
what do protein kinases do in order to potentiate the post-synaptic response?
protein phosphatases
What enzymes are activated by calcium in LTD?
HFS —> high Ca2+ influx —> [Ca2+] > 5 micromolar —> protein kinase —> phosphorylated synaptic protein yields LTP
LTP pathway
LFS —> [Ca2+] 1 micromolar —> protein phosphatase —> unphosphorylated protein yields LTD
LTD pathway
insertion of more AMPARs into the post-synaptic membrane
does not require new protein synthesis
short-lasting - one to a few hours
what are the events that happen in the postsynaptic dendritic spine during early LTP?
synthesis of new proteins/RNA
what is the one event only associated with late LTP and not early?
submerged platform (morris maze) = mutants slower in finding… don’t learn shape-location associations
mazes + food = never learn correct direction of food’s location, always guessing
are there any experiments (ephys or behavior) in mice that show the importance of NMDARs in the conduction and maintenance of LTP in the hippocampus?
habituation
decrease in the strength of a behavioral response to a repeated application of a mild stimulus
organism/circuit learns to ignore stimuli that are no longer novel to free ability to respond to novel/important stimuli
decrease
is habituation an increase/decrease of a response with repetitive stimulation?
non-associative learning
is habituation a form of conditioning or non-associative learning?
repeated touching of siphon = decreased gill retraction
habituation in aplysia
motor neuron
does the activity in the sensory or the motor neuron change in order for the gill withdrawal behavior to be observed?
decreased neuronal activity
how does the activity of motor neurons change in habituating aplysia?
medial temporal lobe
We learned from the case of H.M. that structures in what lobe are very important for the formation of declarative memories?
no
Are those structures also vital for the formation and retention of motor/procedural memories based on studying patient H.M.?
anterograde amnesia (unable to form new memories / retain new info)
What were H.M.’s most severe symptoms after the surgery?
cannot form new declarative memories
Was H.M. incapable of forming new declarative memories or new procedural/motor memories, or recalling previously learned skills?
improve (stopped)
Did the seizures improve or did they get worse?
b. an increase in synaptic strength will occur only at synapses receiving strong inputs and not at other synapses that are not receiving strong inputs
What does “input specificity” refer to in the context of LTP in hippocampus?
a. an increase in synaptic strength will occur at all synapses including the ones which do not receive strong inputs (such as high-frequency stimulation) as long as they are on the same cell as the ones receiving strong inputs
b. an increase in synaptic strength will occur only at synapses receiving strong inputs and not at other synapses that are not receiving strong inputs
c. input specificity means that LTP is specific to a single brain area
d. input specificity means that LTP is specific to inhibitory synapses only
e. input specificity means that if some synapses a cell makes strengthen, other synapses that cell makes have to weaken regardless of activity
a. insertion of additional AMPA receptors into the plasma membrane
During hippocampal LTP, increased postsynaptic responses in the CA1 neuron can result from:
a. insertion of additional AMPA receptors into the plasma membrane
b. dephosphorylation of existing membrane AMPA receptors
c. decreases in intracellular calcium
d. activation of voltage-gated potassium channels
e. decreased activity of NMDA receptors
e. none of the above: all the above events are associated with early phase LTP
What event is NOT associated with the early phase of LTP?
a. phosphorylation of existing AMPA receptors
b. insertion of more AMPA receptors into the membrane
c. increases in intracellular calcium concentrations
d. activation of protein kinases
e. none of the above: all the above events are associated with early phase LTP
e. none of the above – the best area to apply the odorant is not listed
If you wanted to evoke a response in an olfactory receptor neuron, the best area on the neuron to apply the odorant will be:
a. the base of the soma
b. along the length of the axon
c. at the axonal terminal
d. b and c
e. none of the above – the best area to apply the odorant is not listed
c. any one given olfactory receptor neuron expresses the products (proteins) of multiple odorant receptor genes
Which of the following statements about the olfactory system is INCORRECT?
a. the size of the olfactory epithelium varies amongst species
b. the number of total odorant receptor genes in the human (and other mammals) genome is higher than that of functional receptor genes because some are pseudogenes
c. any one given olfactory receptor neuron expresses the products (proteins) of multiple odorant receptor genes
d. olfactory receptor genes encode for G-protein-coupled receptors
e. pseudogenes do not produce the expression of functional odorant receptors
b. postsynaptic cytosolic calcium increases correlate with activity of postsynaptic NMDA receptors
Which of the following statements about synaptic plasticity in the hippocampus is correct?
a. changes in synaptic strength are dependent only on AMPA receptors
b. postsynaptic cytosolic calcium increases correlate with activity of postsynaptic NMDA receptors
c. activation of protein kinases is independent of calcium levels in the postsynapse
d. activation of protein phosphatases requires very high levels of cytosolic calcium
e. a and d
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