Synaptic Transmission And Neurotransmitters

Question 1

Electrical synapses

1. Conductance is thru __ junctions
2. Uni or bidirectional?
3. Is there a synaptic delay?

Answer 1

1. Gap
2. Bi
3. No

Question 2

Chemical synapse:

1. Transduce __ impulses into __ signals
2. Neurotransmitters are __ and __ by neurons
3. Neurotransmitter release by presynaptic terminal is dependent on __. why?

Answer 2

1. Electrical into chemical
2. Synthesized and stored
3. Ca; needed for depolarization

Question 3

What needs to happen to open the voltage gated Ca channels?

Answer 3

AP needs to reach terminal

Question 4

1. Ionotropic and metabotropic are types of __synaptic receptors
2. Ionotropic vs metabotropic?

Answer 4

1. Post

2. Ion= opens an ion channel; metabo=G coupled receptor

Question 5

How are neurotransmitters removed from the synaptic cleft? (4)

Answer 5

Terminal reuptake, glial reuptake, diffuse away or enzymatically transformed to inactive substances

Question 6

Ionotropic post synaptic receptors:

1. __ gated ion channels
2. Open rapidly or slowly?
3. Stay open for long or short?
4. Name an excitatory NT
5. Name 2 inhibitory

Answer 6

1. Ligand
2. Rapidly
3. Short
4. Glutamate
5. GABA and glycine

Question 7

Metabotropic:

1. Slow or fast, why?
2. Stay open for longer or shorter

Answer 7

1. Slow - G protein coupled receptors show a delayed opening

2. Stay open longer

Question 8

1. Difference between EPSP and IPSP

2. Both are caused by opening of what kind of channels?

Answer 8

1. EPSP induces depolarization of postsynaptic membrane; IPSP induces hyperpolarization
2. Ligand gated

Question 9

1. Dominant NTs in CNS
2. PNS?
3. 2 common other ones

Answer 9

1. GABA and glutamate
2. ACh and norepinephrine
3. Serotonin and dopamine

Question 10

1. EPSP receptor activation opens what kind of channels?
2. How does this lead to depolarization
3. IPSP receptor activation opens what kind of channels?
4. How does this lead to hyperpolarization

Answer 10

1. Nonselective cation channels (Na, K, Ca)
2. Cation influx
3. Cl or K channels
4. Move according to gradients - Cl will enter neuron to increase negative charge; K leaves the cell so the membrane moves closer to Keq potential

Question 11

Hyperpolarization leads to __ membrane excitability

Answer 11

Decreased (IPSP)

Question 12

1. Temporal summation
2. Spatial summation
3. Both result in?
4. Would spatial summation be increased if the axons being stimulated were close or far from each other
5. Why are these summations important

Answer 12

1. Stimulating the same axon again and again
2. Stimulating 2 different axons at the same time
3. Greater depolarization
4. Closer = increased
5. With enough input, they can initiate an AP

Question 13

1. Can EPSPs and IPSPs cancel each other out?

2. Give an example using patellar reflex

Answer 13

1. Yes
2. Stimulating stretch receptor of extensor muscle generates an AP that produces a small EPSP in motor neuron of extensor muscle and IPSP in flexor

Question 14

5 ways that drugs can affect presynaptic strength?

Answer 14

1. Can increase/decrease the degradation of NT in terminal
2. Can increase/decrease NT release
3. Can block NT release
4. Inhibit NT synthesis
5. Reduce NT reuptake/degradation

Question 15

1. From previous slide, what does Botox do?

2. What do SSRI and AChE inhibitors do?

Answer 15

1. Block NT

2. Reduce NT reuptake or degradation

Question 16

1. How do agonist drugs affect postsynaptic?
2. Antagonist?
3. Other effect drugs can have on postsynaptic?

Answer 16

1. Evoke same response as NT
2. Block response to NT
3. Can alter channel function

Question 17

From last slide, which do Benzos do?

Answer 17

Alter the channel function

Question 18

Name what category the following NTs are in:

1. ACh
2. Glutamate, GABA, and histamine
3. Dopamine, epinephrine and NE
4. Serotonin

Answer 18

1. Cholinergics
2. Amino acid NTs
3. Catecholamines
4. Indolamines

Question 19

1. Glutamate subsection (another AA)
2. GABA subsection and its location
3. Location of histamine neurons and function
4. Location of catecholamines and indolamines neurons

Answer 19

1. Aspartate
2. Glycine; spinal cord
3. Hypothalamus; involved in wakefulness
4. Brainstem neurons

Question 20

Glutamate:

1. Originates from?
2. Uses what 2 receptors for fast excitation
3. Glutamate __ is implicated in some neurodegenerative disorders
4. When get it be neurotoxic?
5. Target of some general __

Answer 20

1. Either alpha ketoglutarate or astrocyte-derived glutamine
2. AMPA and NMDA receptors
3. Excitotoxicity
4. Excess release or poor synaptic clearance
5. Anesthetics

Question 21

Glutamate:

1. Ionotropic post synaptic receptors are excitatory or inhibitory?
2. Metabotropic

Answer 21

1. Excitatory

2. Could be either

Question 22

Glutamate: NMDA receptor

1. How does this receptor amplify depolarization
2. Why can overactivation of this receptor be neurotoxic?
3. What inhibits receptor opening?
4. 2 drugs that are NMDA antagonists
5. This receptor is key for
6. What normally blocks Ca inside the channel?

Answer 22

1. It has a role as a Ca channel
2. Too much intracellular Ca
3. Zinc
4. PCP and Ketamine
5. Synaptic plasticity
6. Mg

Question 23

Glutamate AMPA receptors:

1. What does receptor trafficking do and what is it critical for
2. What promotes insertion of more AMPA receptors
3. What effect do inhibitory NTs have on these receptors?

Answer 23

1. Regulates neuronal excitability and synaptic plasticity; learning and memory
2. Ca influx
3. Can remove them

Question 24

GABA:

1. 4 main locations
2. Involved in what brain functions
3. Main function of glycine
4. How is synaptic cleft cleared of GABA

Answer 24

1. Brain, interneurons, projection neurons, and spinal cord
2. Sensation, memory, mood, etc.
3. Mediates fast inhibitory transmission in the brainstem and spinal cord
4. Transporters on presynaptic neuron and astrocytes

Question 25

1. GABAa receptor is what type 2. What does it do to the cell and why 3. GABAb receptor is what type 4. Difference between GABAb pre and post synaptic receptors

Answer 25

1. Ionotropic 2. Hyperpolarizes because of Cl- influx 3. Metabotropic 4. Pre are inhibitory; post are usually inhibitory but could be excitatory

Question 26

1. GABA deficiencies lead to neuronal __ | 2. GABA dysfunction could be a key factor in etiology of

Answer 26

1. Excitability | 2. Seizures

Question 27

1. Excitotoxicity of glutamate can result in 2. Decreased cholinergic input to cerebral cortex can result in 3. Decreased dopamine can lead to 4. Dopamine circuits in striatum and frontal lobe reinforce effects of 5. Central NE and serotonin systems are involved in

Answer 27

1. Cell death in acute chronic neurologic diseases 2. Memory loss and confusion 3. Parkinsons 4. Addictive drugs 5. Anxiety and depression

Question 28

Neuropeptides: where are they found and function 1. Substance P 2. Orexin (hypocretin) 3. Name the 3 endogenous opiates

Answer 28

1. Pain related; in spinal cord and peripheral nerves 2. Regulates hunger and sleep; hypothalamus 3. Enkephalins, dynorphins, and beta endorphins

Question 29

What are retrograde messengers Give 3 examples

Answer 29

Released from post synaptic neuron to regulate NT release from pre synaptic neurons (typically suppression) NO, CO and endocannabinoids