Flashcards in Lecture 6 Deck (91):
These increase neuronal surface for synaptic contact:
Where do afferent axons synapse in CNS?
nerve cell bodies and dendrites
T or F? Input to neurons in the CNS is always excitatory.
Small protrusions off of dendrites:
Is the shaft synapse excitatory, inhibitory, or either?
Is the spine synapse excitatory, inhibitory, or either?
Is the somatic synapse excitatory, inhibitory, or either?
Is the axoaxonic synapse excitatory, inhibitory, or either?
This type of synapse is prevalent in CNS during development - less so in adult CNS:
This type of synapse is the only mode of transmission bw cardia and smooth muscle cells:
What are electrical synapses found in mature neurons?
in interneuronal connections
The synaptic efficacy of this/these type(s) of synapse can be modulated;
A molecule must be under ____ Daltons to pass through a GAP jucntion:
Coupling bw cell connected via GAP junctions is both:
electrical and metabolic
T or F? The CNS ECM in the synaptic clefts.
F. No ECM
Which are narrower, clefts of the NMJ or clefts of the CNS synapse?
CNS synapse (no ECM)
Which has a greater postsynaptic density, excitatory or inhibitor bouton?
What anchors transmitter receptor and intracellular signaling machinery in excitatory synapse?
prominent postsynaptic density
This type of vesicle recycling is involved in high frequency firing:
2 types of vesicle recycling:
Kiss-and-run and fusion and collapse
Step in competence maturation of fusion vesicles:
docked, primed, cocked, armed
What is required for vesicle docking?
Ca binds to receptor and changes conformation
What is the fusion event mediated by?
This snare protein is on the vesicle membrane:
This snare protein is on the target membrane:
These are targets of botulinum:
syntaxin and SNAP-25
T or F? Once a vesicle is armed it can go either pathway, Kiss-and-run or fusion and collapse.
This type of vesicle recycling has a readily releasable pool:
What happens if SNARE proteins encounter botulin toxin?
fusion and exocytosis is prevented, blocking transmission
T or F? The whole vesicle is collapsed in both Kiss-and-run and fusion and collapse.
F. Not in Kiss-and-run
2 major classes of ion channels:
voltage and ion gated
Where does neurotransmitter bind in order for a channel to open?
to a receptor on the ion channel
Are "fast neurotransmitters" used with ligand-gated channels, voltage-gated channels, or either?
Are "slow neurotransmitters" used with ligand-gated channels, voltage-gated channels, or either?
This type of neurotransmitter mediates synaptic transmission:
This type of neurotransmitter modulates synaptic transmission:
Do GPCRs act with "slow neurotransmitters" or "fast neurotransmitters?"
T or F? Ligand-gated ion channels are metabotropic.
Are GPCRs ionotropic or metabotropic?
What does the G-protein bind to once activated?
This type of neurotransmitter can trigger a 2nd msg pathway and regulate phosphorylation:
2 major families of ligand-gated channels:
1. Glutamate receptors
2. GABA (inhibitory - CNS), ACh, Glycine (check)
Where are both the ligand binding domain and the C terminal located with ACh, GABA, and glycine receptors?
Where is the C terminal located in glutamate receptors?
How many subunits do GABA, ACh, and Glycine have?
5 subunits, each w/ 4 trans domains
How many subunits do glutamate receptors have?
4 subunits, each w/ 3 transmembrane domains
How many binding sites does the glutamate receptors have?
2, N terminal and 3rd and 4th exc loop
Where is the C terminal of the glutamate channel located?
What helps anchor the glutamate receptor, providing stability and mobility of the receptors?
proteins at postsynaptic site
Major NT in the CNS for excitation:
Major NT at the NMJ:
What ends the action of NT(glutamate) in the CNS?
reuptake by terminals glial cells
Glutamatergic receptor types:
AMPA and NMDA (agonists)
T or F? AMPA and NMDA are both antagonists.
1. permeable to Na and K
- permeable to Na, K and Ca
- complicated IC signaling
- blocked by Mg
- presynaptic activation (release T)
- postsynaptic activation (remove Mg)
- ionotropic: AMPAR and NMDAR, have intrinsic channels
- metabotropic: g-coupled
- coincidence detector
- regulate synaptic plasticity
- key player in learning
- co-agonist for NMDA to open channel fully
- increase conductance
- antagonist for NMDA receptor
- binding site
learning and memory depend on neurons modifications
excessive inflow of Ca through NMDAR channels
released -> bind at postsynaptic -> channels activated -> Na/K flux -> uptaken by excitatory AA transporters on glial cells -> becomes glutamine -> back to nerve terminal -> conversion
uptakes 90% of glutamate
inhibitory in CNS
termination reuptake by terminals and glial cells
- postsynaptic in spinal cord and brain
- postsynaptic in brain
block inhibitory signal -> potential very - -> hyperpolarization
GABA receptors binding sites
- for GABA
- for steroids: modulators
- for barbiturates: anesthetics
glutamate receptors location (AMPAR, NMDAR)
- postsynaptic densities
- dendritic spines and shafts (distal)
GABA receptors location
- soma (AP trigger zone)
- proximal dendrites
- limited inhibitory transmission so better location
due to Na influx
due to Cl influx
- 1 cell body with many dendrites
- dendrites serve as input segments
- 1 axon = 1 output
motoneuron synapse distribution
- 80% on dendrites
- 20% on cell body
divergence of motoneuron axon branches
governed by size of motor unit
- control of contraction
Patella tendon reflex pathway
- stretch stimulus -> stretch receptor in extensor muscle -> afferent activated -> excitatory monosynaptic and inhibitory disynaptic activated
- extensor contraction stimulated
- release glutamate
- EPSP, stimulate dorsal root
- flexor contraction prevented
- interneuron innervates motorneuron
- release glycine
- IPSP, stimulate posterior root
5 subunit ligand-gated channel
- NAChR, GABA R
- inhibitory in CNS
- each subunit = 4 TM
- C terminal is EC