LG 1.10 Synaptic Transmission

Question 1

What must the membrane potential rise to to cause another action potential?

Answer 1

-50 mVs

Question 2

What is EPSP?

Answer 2

Change in membrane potential towards an action potential (-50 mV) [Na+ moving in or K+ moving out]

Question 3

What is IPSP?

Answer 3

change in membrane potential away from an action potential. Usually this is from Cl- moving in the cell.

Question 4

What is summation?

Answer 4

Multiple EPSPs combine to raise the membrane potential to threshold (-50mV)

Question 5

What are the two types of summation?

Answer 5

Temporal and spatial

Question 6

What is a temporal summation?

Answer 6

One neuron causing multiple EPSPs within a short time frame.

Question 7

What is a spatial summation?

Answer 7

At least two neurons causing an EPSP around the same time

Question 8

What is Lambert Eaton Syndrome?

Answer 8

Autoantibodies to the voltage gated Ca+2 channels on the presynaptic terminal

Question 9

What is the effect of Botulism Toxin?

Answer 9

Destroys SnRPs, which prevents synaptic vesicle from releasing neurotransmitters

Question 10

What is the effects of Myasthenia Gravis?

Answer 10

Autoantibodies to the postsynaptic acetylcholine receptors.

Question 11

Define a non-gated ion channel

Answer 11

• “Open” all the time
• Also known as leak channels
• Used to help control the resting membrane potential.
• Think of the potassium leak channels with regular action potentials.

Question 12

Define Voltage Gated channels

Answer 12

1) Respond to changes in membrane potential.
2) Found on
a) Axons of nerve cells (Na+ gated)
b) Presynaptic nerve endings (VG-Ca+2 channels releases NTs)

Question 13

What is a mechanically gated channel?

Answer 13

• These channels respond to environmental stimuli
• Ex: Pressure receptors found in the skin such as pacinian corpuscles, merkel discs, meissner’s corpuscles, and ruff ini endings. Hair cell transductive mechanochannels responding to sound.

Question 14

What are Ligand channels?

Answer 14

• Ion or molecule that forms a complex
• Neurotransmitters or ligands.
• Divided into metabotropic and ionotropic

Question 15

What are the general characteristics of Metabotropic?

Answer 15

• G-protein coupled
• Made up of seven transmembrane proteins
• Wide array of effects [illustrated on the next slide]
• Activates secondary (G-proteins) proteins that will open an ion channel, enhance transcription, or cause the release of other enzymes.
• Slower response
• One unit as a seven transmembrane (requires only one gene)

Question 16

What are the general characteristics of ionotropic receptors

Answer 16

• Fast Excitatory or Inhibitory
• Local effects (once the ligand binds the channel opens)
• Fast response
• Multiple protein subunits (influenced by multiple genes)

Question 17

What are the general characteristics of Nicotinic Acetylcholine Receptors?

Answer 17

• Ionotropic
• Peripherally on postganglionic neurons
• Located on skeletal muscle end plates
• Adrenal Gland

Question 18

What are the general characteristics of muscarinic acetylcholine receptors?

Answer 18

• Metabotropic

- Located on target organs for postsynaptic neurons of parasympathetic nervous system and sweat glands

Question 19

Which receptor do most anti-cholinergic drugs target?

Answer 19

Most anti-cholinergic drugs used are muscarinic and not nicotinic

Question 20

Which receptor do most anesthetic drugs target?

Answer 20

Nicotinic

Question 21

What is the only type of postsynaptic receptors found at the ganglionic synaptic clefts?

Answer 21

Nicotinic

Question 22

What would happen if you game a anti-nicotinic drug?

Answer 22

Both the sympathetic and parasympathetic nervous systems would be depressed.

Question 23

What happens if you destroy or inhibit acetylcholinesterase or something that acts as a nicotinic agonist?

Answer 23

• Prevents the muscles from relaxing (unregulated high Ach levels)
• Ex: Organophosphates (insecticides – think of farmers), Nerve gas, nicotine

Question 24

What are examples of anti-cholinergic drugs?

Answer 24

• Low potency typical antipsychotics
• Atypical antipsychotics
• Tricyclic antidepressants (TCA’s)
• Anti-histamines 1st generation
• Anti-muscarinic drugs for asthma
• Scopolamine – used for motion sickness

Question 25

What do triptans work against?

Answer 25

Are 5-HT1B & D agonists

Question 26

What do Ondansetron (anti-emetics) do?

Answer 26

5-HT3 blockers

Question 27

What body activities is serotonin involved with?

Answer 27

-Emesis, GI motility, Anxiety, GI smooth muscle contraction, sleep, feeding, thermoregulation, hallucinations

Question 28

What are the types of Serotonin receptors?

Answer 28

• 7 families of receptors (numbered 1 – 7)

* All are G protein receptors (metabotropic) except 5-HT3, which is ionotropic

Question 29

What is Tyrosine Kinases?

Answer 29

Tyrosine kinases becomes activated when a growth factor, cytokine, or insulin binds to the receptors. Growth in general is a multicellular activity that needs to be coordinate so it makes sense that growth factors activates a pathway with a lot of components. Insulin also uses RTK and if your body has decreased amounts or becomes desensitized to insulin as with diabetes you will have a decrease in signaling from receptor tyrosine kinase. If you decreased signaling from receptor tyrosine kinase it will affect a lot of different pathways, which helps to explain why complications from diabetes are with multiple organs.

Question 30

What are the main factors of Receptor Tyrosine Kinase?

Answer 30

• Ligands associated with RTKs include: growth factors, cytokines, and pancreatic beta cells for insulin.
• There can be up to 10 different responses after these ligands bind to RTKs. This indicates that there are multiple ways to regulate growth.
• RTK mutations are associated with cancers if a mutation causes the RTK to become constantly activated.

Question 31

What is the end activity of activation of Receptor tyrosine kinase?

Answer 31

Will lead to the activation of a protein that binds to a promoter region of DNA to upregulate transcription.