Synaptic Transmission

Front 1

What is the readily releasable pool?

Back 1

1. Vesicles full or proteins docked at the vesicle docking site

Front 2

What channels does an AP activate in order to release NTs into the cleft?

Back 2

1. CaV2

Front 3

What toxins degrade vesicle docking proteins in the membrane?

Back 3

1. Botulinum toxin

2. Tetanus toxin

Front 4

What is the focus of botulinum toxin action?

Back 4

1. NM junction

2. Destroys docking proteins

3. Blocks release of Ach

Front 5

How is botulinum toxin taken up into the presynaptic terminal?

Back 5

1. Endocytosis

2. Proteases target docking proteins

Front 6

What is the location and action of acetylcholinesterase in the NM junction?

Back 6

1. Lies in basolateral membrane between pre- and postsynaptic surfaces

2. Breaks down Ach

Front 7

What is the relative speed of AchE?

Back 7

1. VERY fast

Front 8

Why doesn't AchE break down all Ach in the NMJ?

Back 8

1. First wave of Ach is "suicide wave"

2. Subsequent waves overwhelm available AchE

Front 9

What is the transporter molecule for glutamate in the CNS?

Back 9

1. EAAT---pre- and postsynaptic and glial cells (surround the synapse)

Front 10

What is the MC pathway for glutamate?

Back 10

1. Presynaptic knob--> glial cell---

2. Glutamate processed to glutamine by glial cell

3. Glutamine passes to post-synaptic terminal

4. Glutamine converted to glutamate, ready to be used

Front 11

How is NE taken up out of the cleft?

Back 11

1. Specific NE transporter

Front 12

What drugs block NE reuptake?

Back 12

1. NE reuptake inhibitors (more later)

2. Antidepressants

3. Also available for serotonin/NE and solely serotonin

Front 13

What effect can SSRIs that inhibit NE have on pain?

Back 13

1. Provide analgesic effects

2. Useful for tx of chronic pain

Front 14

What are the subunits of a GPCR?

Back 14

1. a

2. B

3. y

Front 15

What is the role of the By complex in GPCRs?

Back 15

1. Activate downstream effector proteins

2. SLOW

Front 16

What is the GIRK channel?

Back 16

1. Inward-directing K channel

2. Increased K activity=inhibition

3. Located in post-synaptic terminal

Front 17

What activates the GIRK channel?

Back 17

1. By subunit---

2. Original stimulus CAN BE opioids--- suppression of pain

Front 18

What targets u-opioid receptor?

Back 18

1. Opiate drugs--- morphine, oxycodone, etc.

Front 19

What is the relationship between GIRK channels and Ca channels?

Back 19

1. Inhibition of Ca channels leads to inhibition of AP---- blockage of pain impulse

Front 20

What is the relationship between GIRK channels and u-opioid channels?

Back 20

1. Positive-- no inhibition

Front 21

What is the role picrotoxin?

Back 21

1. Blocks GABA A channels--- leads to epileptic behavior

Front 22

What is the black box warning for botox?

Back 22

1. Local injections can spread throughout the body and can produce generalized muscle weakness, diplopia, ptosis, dysarthria, urinary incontinence, and breathing difficulties

Front 23

What is the postsynaptic density?

Back 23

1. Area with high density of NT receptors on postsynaptic bouton.

Front 24

What structures are used by neurons to receive input from other neurons?

Back 24

1. Soma

2. Dendrite

Front 25

What is the nature of the interaction between CaV2 channels and proteins holding the synaptic vesicles?

Back 25

1. Physical interaction--- docking proteins bind Ca that enters through CaV2

Front 26

How are most NTs removed from the cleft?

Back 26

1. Transport proteins

Front 27

What is the target of TCAs and SNRIs?

Back 27

1. Transport proteins for NTs

Front 28

What do TCAs block?

Back 28

1. Reuptake of serotonin

Front 29

Where are most inhibitory synapses located?

Back 29

1. Soma