Copyright ©Mark Nelson, 2002. All rights reserved.
Chapter 7: Neurotransmitters and Their Release
What you need to know
(exam questions will be a drawn from this subset of material)
Who were Katz and Miledi? (p. 157-158)
Katz and Miledi
made pioneering discoveries in the 1960s on the mechanisms of neurotransmitter
How is the amplitude of the presynaptic potential
related to the amplitude of the postsynaptic response? (p. 158, Fig. 7-1)
Small amounts of presynaptic
depolarization (less than about 45 mV) fail to elicit a postsynaptic response.
Above this threshold, the amplitude of the postsynaptic
response is strongly dependent on the presynaptic amplitude (Fig. 7-1)
How did Katz and Miledi manipulate the voltage amplitude in the presynaptic
terminal? (p. 158)
They applied varying amounts
of TTX to the synapse...TTX blocks voltage-dependent Na+ channels.
By controlling the amount of TTX applied, they could
vary the amplitude of the presynaptic depolarization.
Does TTX have a direct effect on the ligand-gated channels on the postsynaptic
side of the synapse? (p. 158)
No, TTX does not have
a direct effect on the postsynaptic ligand-gated channels...it acts on
the presynaptic voltage-gated channels
What is iontophoresis? (p. 158-159)
a method for controlling
the release of charged ions from a microelectrode by passing electrical current
through the electrode
What happens to synaptic transmission if external [Ca++] is
reduced to zero? (p. 158)
will be abolished
When does external [Ca++] need to be available in order for
synaptic transmission to be successful? (p. 158)
external calcium needs
to be made available just before the arrival of the action potential in the
How do Ca++ ions enter the presynaptic terminal? (p. 160)
Ca++ channels in the presynaptic membrane
What happens when Ca++ enters the presynaptic terminal?
presynaptic calcium triggers
the fusion of synaptic vessicles with the cell membrane, causing neurotransmitter
What normally keeps the internal Ca++ levels low in the presynaptic
terminal? (p. 160)
active removal of Ca++
from the cell and sequestration in the endoplasmic reticulum and mitochondria
What is quantal release? (p. 160-161)
the idea that neurotransmitter
is released in discrete packets (quanta), each representing the contents
of a single vesicle
What is a miniature end plate potential (mepp)? (p. 161)
the small postsynaptic
response recorded at a neuromuscular junction arising from spontaneous
transmitter from one or two presynaptic
What happens when external Mg++ is applied to a synapse?
can block Ca++ channels. By controlling external Mg++ levels,
one can control
how much Ca++ enters
the presynaptic terminal, and thus how much transmitter is released
At the neuromuscular junction, about how many vesicles are released during
a full-sized EPP? (p. 161)
About how many neurotrasmitter molecules are in a single vesicle?
What are the two main pools of synaptic vesicles in the presynaptic terminal.?
the storage pool and the
What happens to vesicles in these two pools when Ca++ enters
the presynaptic terminal? (p. 164)
1) release of transmitter
from vesicles in the release pool
2) mobilization of vesicles from the storage pool to
the release pool
What molecule keeps vesicles in the storage pool locked in place?
What are NSF, SNAP, v-SNARE, t-SNARE, VAMP, SNAP-25? (p. 165-167)
these are all molecules
involved in the docking and release of vesicles
(AND THAT'S ALL YOU'RE EXPECTED TO REMEMBER)
Where do new vesicles come from? (p. 169-170)
they are recycled; when
vesicles release neurotransmitter, their membrane fuses with the cell membrane
the membrane gets pushed up along the synapse to an
area where new vesicles are "pinched off"
the recycling process only takes a minute or two
How do non-spiking neurons communicate? (p. 170-171)
they release transmitter
in a graded fashion (graded transmission);
in graded transmission, the amount of transmitter release
is roughly proportional to the level of presynaptic depolarization
How does neurotransmitter get into the vesicles? (p. 171-172)
transporter proteins embedded
in the vesicle membrane shuttle neurotransmitter molecules into the vesicle
the transport process is driven by a proton
gradient that is initially established by ATP-dependent proton transport
in some cases, vesicles are filled in the cell body
and transported to the release site by axonal transport
What four criteria are used to establish a chemical as a neurotransmitter?
1) synthesized in presynaptic
neuron; 2) stored in presynaptic neuron; 3) released from presynaptic neuron,
4) have a postsynaptic effect that mimic the natural
What are the three main groups of neurotransmitter molecules? (p. 173-175, Table 7-2)
amino acids, amines,
What are some examples of neurotransmitters that don't fit into these categories?
(p. 175, Table 7-2)
ACh, ATP, NO, CO
Name three amino acid neurotransmitters; three amines, and three peptide
neurotransmitters. (p. 175, Table 7-2)
choose your favorites
from Table 7-2
Identify the transmitter released by: 1) adrenergic, 2) noradrenergic, 3)
cholinergic, and 4)serotonergic neurons (p. 176. Tab;e
1) epinephrine (adrenaline);
2) norepinepherine (noradrenaline); 3) Ach; 4) serotonin (5-HT)
What is a catecholamine? (p. 174-175; Table 7-2)
that contain a catechol group (6-carbon ring with two OH units): dopamine,
What is the synthesis pathway for __________? (p.
Don't worry about it...you
can always look it up in your textbook if you need it.
Which neurotransmitter system is disrupted in patients with Parkinson's disease?
What are some of the symptoms of Parkinson's disease? (p. 180)
problems with motor
control; rigidity, tremor, slow or delayed movements, poor balance
What dopamine precursor is sometimes used to treat Parkinson's disease?
Name some famous people that have Parkinson's disease? (not in text; not on exam)
Muhammad Ali, Johnny Cash, Michael J. Fox, Katharine
Hepburn, Janet Reno, Pope John Paul II