Synapses 4

Question 1

neuromuscular junction

Answer 1

Synapse between neurons of the spinal cord + skeletal muscle
Brain & NS tell muscles when to contract

Question 2

An Action Potential in the motor axon ALWAYS causes an Action Potential on the muscle cell it innervates due to:

Answer 2

large size of synapse
large # of active zones on the presynaptic terminal
shallow folds on postsynaptic membrane, called motor end-plate creates large surface area with many receptors

Question 3

mechanisms of neurotransmitter release

Answer 3

Vesicles dumped by exocytosis - stimulated by influx of extracellular calcium, [Ca2+] through voltage-gated Ca++ channel
Vesicle membrane incorporated into presynaptic membrane
Neurotransmitter released
Vesicle re-formed by endocytosis

Question 4

types of neurotransmitters

Answer 4

amino acids, amines, peptides

Question 5

amino acids

Answer 5

Small organic molecules
e.g., Glutamate, Glycine, GABA
Released from synaptic vesicles (smaller)

Question 6

amines

Answer 6

Small organic molecules
e.g., Dopamine, Acetylcholine, Histamine
Released from synaptic vesicles (smaller)

Question 7

peptides

Answer 7

Short amino acid chains (i.e. proteins) stored in and released from secretory granules
e.g., Dynorphin, Enkephalins, endorphins
Released from secretory granules (larger)

Question 8

synthesizing amino acids and amines

Answer 8

Synthesizing enzymes are transported down to the axon terminal.
Once there, they synthesize the amine and amino acid NTs in the cytosol of the axon terminal.
Then special proteins called transporters that are embedded in the synaptic vesicle membrane are responsible for concentrating the NTs within the synaptic vesicles.

Question 9

synthesizing peptides

Answer 9

Synthesized in the rough ER, then sent to Golgi Body.
At Golgi body, protein is split into peptides which are concentrated in secretory granules, which then bud off from the Golgi body and move down the axon via anterograde transport to axon terminal.

Question 10

Mechanism for Amino Acids and Amines neurotransmitter release:

Answer 10

• Synaptic vesicles docked at active zone
• Action Potential reaches axon terminal causing voltage-gated calcium channels to open at the active zone; Ca2+ flows from outside cell to inside, down their concentration gradient
• Influx of Ca2+ stimulates exocytosis - vesicle membrane gets incorporated into presynaptic membrane and neurotransmitters released
• Vesicle is re-formed by endocytosis and refilled with neurotransmitters

Question 11

Mechanism for Peptides neurotransmitter release:

Answer 11

• Secretory granules not located at active sites and therefore not close to influx of Ca2+
  For exocytosis of granules to occur, requires series of high frequency of action potentials to elevate Ca2+ levels in the axon terminal to a high enough level to trigger release.

Question 12

Release of Peptides BLANK than release of amino acids and amines.

Answer 12

slower

Question 13

transmitter gated ion channels

Answer 13

neurotransmitter receptor on postsynaptic cell
Membrane-spanning proteins that change shape when NT attached
Directly allow ions through membrane
If Na+, will excite postsynaptic neuron; If K+ or Cl-, will inhibit

Question 14

Transmitter-gated ion channels (con’t)

Answer 14

If excitatory, depolarization causes excitatory postsynaptic potential (EPSP) → ACh, Glu
If inhibitory, hyperpolarization causes inhibitory postsynaptic potential (IPSP) → Gly, GABA

Question 15

g protein coupled receptors

Answer 15

Slower, longer-lasting actions

neurotransmitter receptor on postsynaptic cell

Question 16

g coupled protein receptors steps

Answer 16

a) NT molecule binds to receptor proteins on postsynaptic membrane
b) Receptors activate G-protein, which crawls along inside of membrane
c) G-protein activates “effector” protein, which might:
- Open a G-protein-gated ion channel OR
- Synthesize a second messenger to initiate other tasks within the cell

Question 17

excess neurotransmitter

Answer 17

If NTs not taken up, AP will continue out of control

If NTs left in neuromuscular junction, receptors desensitize (close), muscles fail

Question 18

how to prevent excess neurotransmitter

Answer 18

Some taken back into presynaptic terminal
Some diffuses away
Some taken in by glia (yay glia!)
Some broken down in cleft by enzymes

Question 19

autoreceptors

Answer 19

Neurotransmitter receptors in the Presynaptic neuron that respond to neurotransmitters released by the presynaptic terminal.
Typically G-protein-coupled receptor
Second messengers typically stop more neurotransmitter release or end the synthesis of neurotransmitters.
Way to regulate and prevent too much neurotransmitter released into the cleft.

Question 20

Processes for Neurotransmitter Removal:

Answer 20

Some sucked back into presynaptic terminal by transporter proteins in the presynaptic membrane (reuptake), then enzymatically destroyed or put back into vesicles.
Some diffuse away from synapse
Some taken in by glia by transporter proteins in their membranes and then broken down by enzymes.
Some broken down in cleft by enzymes
If neurotransmitters left in neuromuscular junction, receptors desensitize (channels close), muscles fail

Question 21

neuropharmacology

Answer 21

The study of the effects of drugs on nervous system tissue

Question 22

Receptor agonists:

Answer 22

Mimic actions of naturally occurring neurotransmitters

Question 23

Nicotine

Answer 23

binds to and activates (nicotinic) Ach receptors in skeletal muscle and in the CNS (addiction)
receptor agonist

Question 24

Receptor antagonists:

Answer 24

bind to the receptors and block normal action of the neurotransmitter (Inhibitors)

Question 25

Curare

Answer 25

blocks nicotinic ACh receptors causing weakness of muscles or asphyxiation due to paralysis of diaphragm (arrow poison used by South American indigenous people)

Question 26

Defective neurotransmission:

Answer 26

Root cause of neurological and psychiatric disorders

Question 27

Black Widow venom

Answer 27

Latrotoxin triggers ACh, norepinephrine, and GABA release until runs out; works by causing influx of Ca2+ which stimulates exocytosis – muscle cramping, rigidity, pain, stomach cramps, vomiting, sweating and fast pulse

Question 28

Taiwanese Cobra venom

Answer 28

Cobratoxin peptide binds to ACh receptors, blocking the signal to muscles, days to be remove - paralyzes diaphragm so can cause death, chest discomfort and difficulty breathing, fever, difficulty swallowing, weak limbs

Question 29

Botulinum

Answer 29

Clostridium botulinum bacterium that causes botulism (from poor canning)
Prevents docking of vesicles with ACh so blocks release of ACh into the synapse – respiratory muscle paralysis can cause death

Question 30

If transmitter gated ion channel allows Na+ to enter, then

Answer 30

Na+ flow into the postsynaptic neuron causing depolarization and a graded potential flows to the axon hillock which can help trigger an action potential.

Question 31

If transmitter gated ion channel allows Cl- to enter, then

Answer 31

Cl- flows into the postsynaptic neuron causing hyperpolarization, decreasing the chance the cell will fire an action potential. (hyperpolarization can occur from K+ flowing out of cell.)

Question 32

na+

Answer 32

depolarize the postsynaptic membrane causing it to reach threshold
Excitatory Post-Synaptic Potential (EPSP)

Question 33

cl-

Answer 33

hyperpolarize the postsynaptic membrane

Inhibitory Post-Synaptic Potential (IPSP)

Question 34

If excitatory, depolarization causes

If inhibitory, hyperpolarization causes

Answer 34

excitatory postsynaptic potential (EPSP) → ACh, Glu

inhibitory postsynaptic potential (IPSP) → Gly, GABA

Question 35

Neural Integration

Answer 35

– combining the signals coming from the synapses to get a net change in membrane potential at the Axon Hillock.
after synaptic transmission