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 release.

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)
    synaptic transmission 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 presynaptic terminal
How do Ca++ ions enter the presynaptic terminal?  (p. 160)
    through voltage-gated Ca++ channels in the presynaptic membrane
What happens when Ca++ enters the presynaptic terminal?  (p. 160)
    presynaptic calcium triggers the fusion of synaptic vessicles with the cell membrane, causing neurotransmitter release
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 release of
        transmitter from one or two presynaptic vesicles
What happens when external  Mg++ is applied to a synapse?  (p. 161)
    external Mg++ 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 200
About how many neurotrasmitter molecules are in a single vesicle?  (p. 161)
    about 10,000
What are the two main pools of synaptic vesicles in the presynaptic terminal.?  (p. 163-164)
    the storage pool and the release pool
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?  (p. 164)
    synapsin-I
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?  (p. 172-173)
   1) synthesized in presynaptic neuron; 2) stored in presynaptic neuron; 3) released from presynaptic neuron, and
   4) have a postsynaptic effect that mimic the natural response
What are the three main groups of neurotransmitter molecules?  (p. 173-175, Table 7-2)
    amino acids,  amines,  and peptides
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 7-3)
    1) epinephrine (adrenaline); 2) norepinepherine (noradrenaline); 3) Ach; 4) serotonin (5-HT)
What is a catecholamine?  (p. 174-175; Table 7-2)
    amines neurotransmitters that contain a catechol group (6-carbon ring with two OH units): dopamine, epinepherine; norepinepherine
What is the synthesis pathway for __________?  (p. 176-178)
    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?  (p. 180)
    dopamine
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?  (p. 180)
   L-dopa
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