Copyright ©Mark Nelson, 2002. All rights reserved.
Chapter 6: Synaptic Transmission
What you need to know

(exam questions will be a drawn from this subset of material)

What's the difference between electrical and chemical synaptic transmission?  (p. 133-139, Table 6-1)
    electrical: fast, reliable, no chemical intermediary, uses gap junctions, no postsynaptic receptors, consistent response
    chemical: slight delay; neurotransmitter intermediary; postsynaptic response depends on receptor properties,  modifiable

What's the difference between excitatory and inhibitory synaptic transmission?  (p. 133-139, Table 6-1)
    excitatory: moves Vm closer to spike threshold (generally depolarizing); increases likelihood of AP generation in postsynaptic neuron
    inhibitory: moves Vm away from spike threshold (generally hyperpolarizing ), decreases likelihood of AP in postsynaptic neuron

What's the difference between classical and neuromodulatory chemical transmission?  (p. 133-139, Table 6-1; p 149, Table 6-2)
    classical: mediated by ionotropic receptors; direct, rapid, short-lasting effects on ion channels in the postsynaptic membrane
    neuromodulatory: mediated by metabotropic receptors; indirect, slow, long-lasting postsynaptic effects

What are the five main steps in chemical synaptic transmission?  (p. 139-141; Figure 6-3)
    1) synthesis, 2) storage, 3) release, 4) postsynaptic effects, 5) inactivation

What is a ligand-gated channel?  (p. 140)
    a channel that changes its conductance state by binding a specific chemical substance (neurotransmitter)
    (in contrast with voltage-gated channels, where the conductance state depends on Vm)

What is nAChR?  (p. 140-141)
    nAChR is an abbreviation for the nicotinic acetylcholine receptor; it is a ligand-gated channel; it is an ionotropic receptor

What molecule(s) normally activate nAChR?  (p. 140)
   acetylcholine (ACh); a neurotransmitter found at vertebrate neuromuscular junctions as well as other places in the CNS

What molecule(s) normally pass through the pore of the nAChR?  (p. 140)
    primarily Na+ ions and K+ ions, as well as some Ca++ ions

How many subunits does the nAChR contain?  (p. 140)

About how large is a single nAChR?  (p. 140, Fig. 6-4)
    roughly 10 nm (about 8 nm in diameter and 14 nm in length)

Why is the nAChR called "nicotinic"?  [not in text]
    the chemical nicotine selectively activates this type of ACh receptor.
    nicotine is not a is a plant alkaloid that happens to stimulate certain types of ACh receptors
    potent nervous system effects of nicotine are evidenced by the widespread use of tobacco products

What's the difference between an EPSP and an EPP?  (p. 141-142, Figure 6-5)
    an excitatory postsynaptic potential (EPSP) is a transient depolarization caused by ionic flow through an activated ligand-gated channel
    an end plate potential (EPP) is functionally the same as an EPSP, but the term EPP is used for muscle cells and EPSP for neurons

What is the reversal potential(p.142-143, Figure 6-6)
    the reversal potential is a term that can apply to a single ligand-gated channel or to an entire synapse (multiple channels)
    it is the membrane potential at which no net ionic current flows through the synapse/channel
    if the membrane potential of a neuron is below the reversal potential, activation of the synapse/channel will cause depolarization
    if the membrane potential is above the reversal potential, activation will cause hyperpolarization
    if the membrane potential is at the reversal potential, activation will cause no change in membrane potential
    hence the reversal potential is the voltage at which the postsynaptic effect reverses sign

Where are action potentials initiated?  (p. 144-145, Fig. 6-7)
    axon potentials are generated in special regions of the neuron termed spike initiation zones
    in vertebrate neurons, this region is often at the location where the axon meets the soma, the so-called axon hillock

What is an IPSP?  (p. 145)
    an inhibitory postsynaptic potential (IPSP) is a transient hyperpolariztion caused by ionic flow through an activated ligand-gated channel

What's the difference between presynaptic and postsynaptic inhibition?  (p. 145-147; Fig. 6-10)
    presynaptic inhibition acts on the presynaptic axon terminal of an excitatory synapse onto a target neuron,
    postsynaptic inhibition acts directly on the soma or dendrites of the target neuron

What is GABA?  (p. 148)
    GABA stands for gamma-aminobutyric acid; it is a common neurotransmitter at inhibitory synapses in the vertebrate CNS.
    You'll often here it referred to as an "inhibitory neurotransmitter"
    Strictly speaking GABA itself is not inhibitory,  rather the postsynaptic receptors that it activates are usually inhibitory.

What is a second messenger?  (p. 148)
    a chemical intermediary released inside a cell that triggers a biochemical cascade which in turn cause changes in neural responses
    second messengers are often involved in neuromodulatory transmission

What type of receptor is the muscarinic AChR?  (p. 149)
    it is a ligand-gated receptor that binds ACh; unlike the nAChR it does not contain a central pore; it is a metabotropic receptor
    it acts indirectly on a particular class of K channels (M-type) through a second messenger

What is a G protein?  (p. 149-151)
    G proteins are intracellualr membrane proteins that, when activated by a ligand-gated receptor,
a biochemical cascade which in turn cause changes in neural response properties

What is a protein kinase?  (p. 152)
    an enzyme that promotes binding of a phophate to a protein;
    phosphorylation of channel proteins is often the last step in a second messenger cascade

What are the three main mechanisms of neurotransmitter inactivation?  (p. 154-155, Fig. 6-13)
    1) diffusion, 2) enzymatic degredation, 3) reuptake

What enzyme breaks down the ACh?  where is it found in the CNS? (p. 154-155)
    acetylcholinesterase (AChE);  it is found  in both pre- and post-synaptic membranes near CNS synapes