Lectures 4-5 : Synapse Flashcards
where does an electrical synapse occur?
gap junction
what proteins form a gap junction channel? what are they made of?
- 2 connexons
- 6 connexins for a connexon
what flows through a gap junction?
materials such as small molecules, or ions
there is a current that passes equally well on both sides
what does an AP become in a gap junction?
PSP - postsynaptic potential
what is unique about gap junction synapses?
they are bi directional
where are gap junctions most commonly located? what are the cells that form gap junctions called?
glial cells or areas where synchronization is important
electrically coupled
how could a PSP trigger an action potential?
PSPs are small about 1mV, therefore several PSPs are needed to strongly excite a cell
where does a chemical synapse occur?
the synaptic cleft
what are membrane differentiations?
dense accumulation of proteins on wither side of the synaptic cleft
what are the types of membrane differentiations?
- active zones
- postsynaptic density
what is the active zone?
area on presynaptic cell at which neurotransmitter is released
what is the post synaptic density?
contains receptors which turn the chemical signal to electrical signals
NT –> AP
what is the synaptic vesicle?
membrane delineated vesicles that contain NT
signal conversation pathway?
types of synapses axons can have?
what is a specialized synapse?
neuromuscular junction
what occurs at a neuromuscular junction synapse?
neuron terminates on motor end-plate of muscle fiber - very reliable and fast transmission
they are large
acronym for NT release pathway?
S - synthesis
R - release
A - action
T - termination
what happens to vesicles when NT are released?
vesicles fuse with membrane and release contents into the cleft
what are the two types of vesicles? what do they store?
clear = small molecules
dark = large molecules
what is dales principle?
for neurotransmitter synthesis pathways, neuron only contains the enzymes necessary to synthesize that neurotransmitter but none of the subsequent enzymes needed to convert it into later products
what is the exception to dales prinicple?
many peptide-containing neurons can release a neurotransmitter along with a peptide
co transmitters
- can release 2 or more neurotransmitters simontaneaously
what are the 3 types of NT? what are the NTs they produce?
1) Amino acids
- GABA, Glycine
2) Amines
- monoamines: serotonin/5- HT, acetylcholine
- Catecholines: dopamine - norepinephrine
epinephrine
3) Peptides
how does the release of a peptide differ?
- cells needs to be stimulates more – it takes more Ca to
trigger the release - Ca channels are much closer to vesicles
what did otto loewi’s experiment do?
confirmed the existence of chemical (NTs)
both frog hearts slowed, when gate was opened
what is vagussstoff?
ACh
vSNARES vs tSNARES
vSNARES = proteins in the vesicle involved in docking
tSNARES = on the presynaptic membrane (terminal axon), helps anchor vesicle.
what is synaptotagmin?
protein found in SNARE complex, Ca2+
sensing protein
what do NT when they are released from synapse?
bind to receptors on the other side
cause depolarization or hyperpolarization
what ions move when the cell hyper-polarizes? depolarizes?
what are the kinetics of how fast a change in the charge of a membrane occurs?
overall NT release pathway?
1) action potential travels down the axon
2) arrives at terminal button
3) terminal button depolarizes
4) Vesicles fuse with membrane, release contents into
synaptic cleft
what does the speed and direction of a change in charge depend on?
Ion
Type of receptor`
What are the 3 known NT receptor types?
Ligand- gated
Auto recpetors
G- protein couples receptors
what is an EPSP?
depolarization of the postsynaptic membrane potential by the action of a synaptically released neurotransmitter
what are ways of generating ESPS?
increasing Na+ conductance
what are NTs that are excitatory?
glutamate
what is an IPSP?
a change in the postsynaptic membrane potential by the action of a synaptically released neurotransmitter, making the postsynaptic neuron less likely to fire action potentials.
what NTs are inhibitory?
GABA and glycine
what is a method of generating IPSPs?
increasing Cl- conductance
what are the neuropharmacology of receptors
antagonists
- binds to receptor and inhibits NT from binding
receptor agonist
- binds to the receptors, mimics its normal activity
inhibitor
- inhibits the normal function of specific proteins involved in synaptic transmission
what are agonist examples?
- nicotine
what is a ligand?
the NT that binds to a receptor
what are the parts of a ligand gated receptor? what are they made of–how can they differ?
subunits that go through the membrane
single polypeptide chain
subunits have different amino acid subunits that come together to make different subtypes
what are examples of the subunits and subtypes of receptor?
Glutamate
- AMPA (Na, K+)
- NMDA (Na, K, Ca)
- kainate (Na, K)
ligand gated channel pathway?
selectivity : ligand vs. VG channels?
ligand is less selective
speed : ligand vs. G-protein?
ligand are faster but G-proteins have longer
what are autoreceptors?
on presynaptic cell
activated by the NT they release
generally are GPCRs which then go on to regulate some aspect of the cell
phosphorylation definition and agent?
- adds phosphate group to protein
- carried out by protein kinase
dephosphorilization
- remove phosphate from protein
- carried out by protein phosphatase
what are g proteins made of? specifics?
a single polypeptide chain that passes through the membrane 7 times
what are G protein effetcs like?
slower, stronger, longer lasting, with more diverse effects on the postsynaptic cell
what are the subunits of a gprotein?
alpha
gamma
beta
ionotropic receptors 3 facts and example?
metabotropic receptors?
what are two receptors that bind ACh?
components of g- protein activation?
Neurotransmitter
Receptor
G- protein
Alpha, gamma & beta subunits
Effector protein
GDP & GTP
components of cAMP signaling?
Receptor – GPCR
G- protein – Gs
Effector enzyme – Adenylyl cyclase (AC)
Substrate of effector enzyme – ATP
Second messenger – cAMP
Protein kinase – Protein kinase A (cAMP dependent protein kinase)
components of Phosphoinositide or DAG?
What are the components?
Receptor – GPCR
G-protein – Gq
Effector enzyme – PLC
Substrate of effector enzyme – PIP2
Second messengers
- DAG
- IP3
- CA2+
Intermediaries
- IP3-R
- ER
- CaM
Protein kinases
- PKC
- Ca/CaM kinase
what ions correlate with glutamate, ACh, GABA and glycine?
excitatory vs. inhibitory?
EPSP - IPSP
stimulatory vs. inhibitory
excite post synaptic - inhibit post synaptic
how much energy does a little packet of neurotransmitter have? what are these small energies called?
about .5mV - miniature endplate potentials
what is synaptic intergration?
the process by which multiple synaptic potentials combine in one post synaptic neuron
what is quantal analysis?
the smallest unit of neurotransmission is the release of the contents in one vesicle
- mini
- all ESPs are multiple of the mini
how can synaptic integration happen?
spatial summation
temporal summation
what is spatial summation?
adding together of many ESPS generated at the same time on multiple synapses of a dendrite
what is temporal summation?
adding together of ESPs that occur close together in time
what is the length constant?
quantifies the length that depolarization travels before decaying to 37% of its original strength
- further away from the spike trigger zone on the axon, the less likely it is that an AP will be generated
- longer the length constant = neuron is better at preventing dissipation of depolarization
- longer the length constant = more likley that EPSP at a distant synapse will cause an AP
what are the kinds of dendrites?
passive
excitable
how do passive dendrites function?
- depolarization decreases along axon, loosing charge
how do excitable dendrites function?
- voltage gated sodium channels are on the dendrite, depolarization spreads and opens channels
- lets in more depolarization
- depolarization spreads
- oscillations of Vm due to activation of voltage gated ion channels
how do G proteins increase length constant?
- protein kinases can function by either opening of closing channels
internal resistance & membrane resistant concerning :
def, what resistance depends on, results when inc, results when dec
shunting Inhibition
when an inhibitory synapse is activated close to the soma, the resultant IPSP can work to cancel out the incoming EPSP
this is called shunting inhibition because this inhibitory synapse near the soma can “shunt” away excitation and prevent the neuron from firing
the neuron is held at a membrane potential below threshold
what are the ways that a signal can be terminated?
diffusion
re uptake
degradation
desensitization
continued exposure to high concentration of NT makes channels stop responding
diffusion process?
neurotransmitter simply diffuses out of the synaptic cleft down its concentration gradient
e. NO - nitric oxide
re uptake process?
NT is retrieved from the synaptic cleft for processing and re-use –> can be degraded by enzymes or transported into vesicles
Ex. 5-HT reuptake transporters
degradation process?
enzymatic inactivation of the NT
Ex. acetylcholinesterase destroys ACh
Removal of specific NT’s (ACh, Catecholines, serotonin, amino acids)
Termination of events in Postsynaptic Cell
