lecture 10b synapse Flashcards
synapse
Information is transmitted either electrically or chemically at a junction between two neurons known as a
electrical vs chemical response
electrical is much faster and interacts with most to all, and has synchromous firing, bidirectional, no neurotransmitters
while chemical is slower but more controlled amd selective (larger in abundance) and has asynchromous firing, up to 0.5 sec delay
Electrical synapses transmit information
quickly
via changes in electrical potential
through relatively large pores (connexons)
across very narrow synapses (< 4nm)
where/when do electrical synapse occur? there are 5 places…
the retina
hormone secreting neurons in the hypothalamus
neuromuscular junctions involved in rapid escape response
cardiac rhythems
fight/flight
connexon
also known as a connexin hemichannel, is an assembly of six proteins called connexins that form the pore for a gap junction between the cytoplasm of two adjacent cells.
innexin
gap junction proteins expressed in invertebrates,
hemichannels
–The connexon of the presynaptic neuron fits directly onto the connexon of the post-synaptic neuron, forming two
This allows comingling of cytoplasm, and fast transmission.
may be formed by connexons of similar or different molecular composition.
connexin vs connexon
connexin is singular
connexon is plural
When a signal reaches an axon terminal, changes in
membrane potential
postsynaptic conductance
postsynaptic conductance
determine the probability that an AP
will be propagated in the postsynaptic cell.
Ability of synaptic input to trigger neuronal output depends on
- magnitude and timing of incoming potentials
- postsynaptic neuron morphology
- postsynaptic neuron synapse location
- voltage-gated channels’ locations and densities
postsynaptic potential (PSP)
membrane potential change caused by neurotransmitter binding to a postsynaptic membrane channel.
excitatory
releases excitatory neurotransmitter (e.g., glutamate)
this triggers opening of Na+ ion channels
Na+ current changes membrane potential
inhibitory
releases inhibitory neurotransmitter(s) (e.g., GABA, serotonin)
this triggers opening of K+ ion channels
K+ leaks out, Cl- leaks in
cytosol becomes relatively more negative
Excitatory PostSynaptic Potential (EPSP)
depolarizes the membrane
increases likelihood of PSP propagation.
Inhibitory PostSynaptic Potential (IPSP)
hyperpolarizes the membrane
decreases likelihood of PSP propagation
summation
A neuron has many synapses, and can receive PSPs from one or more of them that is needed to reach depolarization threshold
net eff: excitatory - inhibitory will most likely cancel out but u can usually have both for a threshold to be met
the synapses will lose amplitude over time as they travel
Probability of triggering an postsynaptic action potential depends on
the number of incoming signals
whether an incoming signal is an EPSP or an IPSP
the location of the synapse, relative to the hillock like axosomatic or axodendritic
axosomatic synapse
connect to the soma
(relatively close to the hillock) so it has greater effect with impulse
axodendritic synapse
connect to a dendrite
(relatively far from the hillock)
lose the most amplititude b/c its more far away
axonomic synapse
are passed from axon to axon
spatial summation
recipient neuron sums PSPs from multiple neurons connected to it at different locations
arrive at the same time
most likrly to depolarized when summed
temporal summation
recipient neuron sums PSPs from the same neuron over time
potetntials arrive at a short time after each other
define neurotransmitters
chemical messengers. They send information between neurons by crossing a synapse.
synthesized in presynaptic terminal cytoplasm
stored in presynaptic terminal vesicles
As membrane depolarization increases, what happens to the vesicles?
more and more of them will release neurotransmitters
quantum (pl. = quanta)
The contents of one vesicle (usually several thousand molecules like neurotransmitters)
what does the vesicle SNARE interaction mean?
(Soluble N-Ethylmaleimide-sensitive factor) Attachment REceptor
synapsin
it attaches the vesicle to the actin fillaments
when phosphorylated, it releases the vesicle
step 1 of SNARE is Tethering but what occurs
- Vesicle is attached to actin filaments by synapsin.
- Phosphorylation of synapsin causes it to release the vesicle.
- Vesicle migrates to a terminal membrane active zone.
- The vesicle is reversibly tethered to the active zone.
(syntaxin is held in an inactive configuration by Munc18)
Step Two: Docking
occurs when synaptobrevin binds to syntaxin and SNAP-25.
This step is irreversible.
step three: stabilization
Complexin protein stabilizes the vesicle at the active zone.
step 4: vesicle priming
- Ca+2 ions enter the cell via voltage-gated channels
xxxin response to an action potential. - The ions bind to synaptotagmin.
step 5: vesicle fusion
- The synaptagmin-Ca+2 complex binds to the SNARE proteins.
- This displaces complexin and triggers formation of a fusion pore.
- Neurotransmitter passes through the pore and into the synapse.
when the snare complex diassembles what happens?
the vesicles are released from the terminal membrane
name 2 types of vesicle recycling
classical and kiss/run
classical recycling
Clathrin proteins interact to form a lattice
around the membrane to be removed.
They facilitate the “pinching off” of the vesicle from the membrane.
spiky appearance and gets recycled as well
kiss/run
opens just enough (think of not tongue kissing but just a little open ) then pinches off and recycles
diff btwn snare and recycling vesicles
snare is exocytosis
3 types of neurotransmitter removals
diffusion
enzymatic degradation
neurotransmitter reuptake
diff for neurotransmitters
Neurotransmitter molecules simply diffuse away from the synaptic cleft
enzymatic degradation
Specialized enzymes may be employed to break down specific neurotransmitters that are in synaptic cleft
For example, acetyocholinesterase breaks down acetylcholine at neuromuscular junctions.
Breakdown products can be recycled into the presynaptic neuron
to be used as raw materials to build new neurotransmittters.
neurotransmitter reuptake
mainly reabsorbs the neurotransmitters back into the presynaptic
allows recycling of neurotransmitters
allows regulation of neurotransmitter concentration in the synapse
this can determine how long the signal lasts
ionotropic receptor
ligand-gated ion channels
opened by neurotransmitter binding
allows ions into postsynaptic neuron
produce a rapid, transient effect
metabotropic receptor
G-protein coupled receptors
triggered by neurotransmitter binding
initiates a signalling cascade in the postsynaptic cell
produce a slow, longer-lasting effect
effect can be more widespread throughout the cell than ionotropic effect
agonist
substance that binds to receptors
and mimics the effects of a neurotransmitter.
antagonist
substance that blocks the receptor,
preventing the effects of a neurotransmitter.
inverse agonist
binds to receptors and elicits an effect opposite that of the appropriate neurotransmitter.
neuromodulator
substance that can act locally or at a distance,
increasing or decreasing the effect of neurotransmitters.
The neuromodulator itself does not initiate depolarization.
Slow (metabotropic) synaptic transmissions
operate by opening G-protein coupled (metabotropic) channels
may be either excitatory or inhibitory
are mediated by biogenic amine and peptide neurotransmitters and involve
second messengers
cleaving of proteins
cleavage of high-energy phosphate bonds
usually take many biochemical steps to complete.
take hundreds of milliseconds to affect target cells
Fast (ionotropic) synaptic transmissions
operate by opening ligand-gated (ionotropic) ion channels may be either excitatory or inhibitory
are mediated by specific neurotransmitters, for example:
glutamate (excitatory)
GABA (inhibitory)
affect their target cells in less than a millisecond
Most fast EPSPs are triggered by
glutamate
Most fast IPSPs are triggered by
GABA and glycine
