Ch. 3: Synapses & Synaptic Transmission Flashcards
Amount of NT release is proportional to:
number of action potentials arriving at presynaptic terminal
2 postsynaptic potentials
- EPSP
- IPSP
Clearing Synapse
- Enzymes
- Reuptake Transporter
3 types of synapses
- Axodendritic
- Axosomatic
- Axoaxonic
EPSP
- Excitatory postsynaptic potential
- Excitatory=depol
- Na+ or Ca++ into cell
IPSP
- Inhibitory postsynaptic potential
- Inhibit=hyperpolarizes
- Cl- in or K+ out
Presynaptic Facilitation
- Always axoaxonic
- “interneuron” stimulates presynaptic neuron to release more NT (by causing more Ca++ to enter)
- Makes intended signal stronger
Direct Activation of Ion channels
- Fast-Acting
- Direct binding to ion channel
- Quick open & short lived response
2 presynaptic potentials
- Presynaptic Inhibition
- Presynaptic facilitation
A ligand can be a NT or neuromodulator based on:
- where it is released
- Nuromodulator: not in synapse; released in extracellular fluid
NT
- ligand released into synapse & binds to ligand-gated membrane receptor
- Fast or slow based on what it binds to
Presynaptic Inhibition
- Axoaxonic
- “interneuron” inhibits more Ca++ influx so intended signal is weaker (because less NT released)
2nd Messenger
- cAMP
- Used in indirect stiulation (g-protein)
1st Messenger
NT
Exogenous Ligands
- NT produced outside the body
- Ex. Drugs/Meds
Endogenous Ligands
- NT produced in the body
- Ex. Glutamate
Up Regulation
- Put more receptors on post-synaptic membrane or turn on receptors on post-synaptic membrane
- in response to decreased levels of NT, so there is increased binding
Down Regulation
- Removal of post-synaptic receptors or turning off receptors
- in response to high signal levels to decrease binding
Antagonist
- Substance that blocks NT action
- (blocks release of NT or binds to receptor so NT can’t bind)
- Ex. botox antagonist to Ach by blocking Ca++ channels–>NT not relseased
Agonist
- Substance that acts like a NT & causes the same effect
- Ex. Nicotine is an Ach agonist
7 events at synapse
- action potential arrive at presynaptic terminal
- depol opens Ca++ channels
- Ca++ move vessicles to end of neuron
- Vessicles bind with membrane and release NT
- NT diffuse through synapse and bind to receptors
- Binding initiates change
- Clearing of synapse (enzymes/reuptake transporter)
Neuromodulator
- Released outside synapse (extracellular fluid)
- bind to channels that slowly leak–partially depol cell so it facilitates the depol from the NT
- Modulates many neurons
Indirect activation of ion channels
- Slow acting
- indirect binding to gated ion channel via receptor on g-protein
- channels open slower and have a longer response
- indirect activation of intracellular enzymes
GABA
Location: CNS (fast or slow acting)
Action: INHIBITORY at ligand gated channels
*Most prevalent fast acting inhibitory NT of CNS
Ach
Location: PNS (at NMJ), ANS/CNS (fast)
Action: bind to ligand gated channel, EXCITATORY
Glutamate
Location: CNS (Fast/slow)
Action: bind to ligand gated channel–EXCITATORY
*Most prevalent excitatory NT in CNS
G-Protein receptor activation cause:
-Slow and prolonged opening and closing of ion channels using a second messenger
G protein-mediated Receptors (with 2nd messenger)
- NT bind to g protein receptor
- GDP–>GTP
- GTP complex binds to g-protein
- increase production of ATP
- ATP converted to cAMP
- cAMP activates channels
- complex inactivates and returns to start
Ligand-Gated Ion channels
- Direct activation
- NT binds to receptor on channel
- Gate open and closes quickly
2nd messenger system causes
- Slow and prolonged change in cell function
- membrane channels to open for long time
- change Ca++ metabolism
G-protein mediated receptors (indirect)
- NT binds to g-protein complec
- GDP–>GTP
- Complex to channel & binds to open channel (ions enter)
- Complex inactivated and returns to receptor
Myasthenia Gravis
- Autoimmune blockade or destruction of nicotinic Ach receptor on post-synaptic membrane–>
- Decreased Ach binding (not enough receptors to bind Ach and recycle Ach to keep contraction going)
- Treatment: Anti-cholinesterase to keep Ach in synapse longer
