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
response
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)
five
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 neurotransmitter...it 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,
trigger 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