Synaptic transmission

Question 1

What modulates the gap junction channel?

Answer 1

1. Intracellular pH2. Calcium3. Neurotransmitters and second messenger

Question 2

What makes up a gap junction?

Answer 2

Two connexons, each made up of six connexin proteins

Question 3

What are the properties of electrical synapses?

Answer 3

1. Most are bidirectional 2. Rapid transmission, little or no delay allows synchronous activity 3. Low selectivity

Question 4

What is the significance of electrical synapses and/or gap junctions?

Answer 4

1. Found in most types of tissue (nervous, myocardial, intestinal smooth muscle, cochlea)2. Mediate chemical coupling in a network3. Synchronize electrical activity among populations of neurons

Question 5

What are the ways in which a chemical synapse can transmit a signal?

Answer 5

1. Endocrine - via vascular system2. Paracrine - local chemical mediators3. Synaptic - NT binds to target cell receptor4. Autocrine - receptors on presynaptic cell for NT it releases

Question 6

What is the definition of a hormone?

Answer 6

Released into blood stream by a neuron

Question 7

What is the definition of a neurotransmitter?

Answer 7

1. Distributed locally by diffusion2. Released at a synapse by a neuron3. Synaptic mechanism when postsynaptic cell is very close4. Paracrine mechanism when several nearby cells

Question 8

What are the properties of the CNS synapse?

Answer 8

1. Pre and postsynaptic membranes held close together by extracellular matrix and transmembrane proteins such as neurexins2. Presynaptic density - docking complex3. Postsynaptic density - receptors, binding proteins4. Active zone - part of presynaptic membrane that is specialized for the vesicular release of NTs

Question 9

What are the general features of a chemical synapse?

Answer 9

1. Unidirectional transmission 2. Impact can be excitatory or inhibitory

Question 10

What are the presynaptic events of NT release?

Answer 10

1. NT packed into vesicles, vesicle docking2. Membrane depolarization by AP3. Activation of Ca channels (influx) 4. Elevation of intracellular Ca5. Vesicle fusion and NT release (exocytosis)6. Membrane repolarization 7. Vesicle recycling

Question 11

What is the SNARE complex?

Answer 11

1. Several specific transmembrane proteins located at vesicles and presynaptic plasma membrane form a helix complex for vesicle docking and fusion 2. Calcium binding proteins serve as sensors of calcium levels

Question 12

What are the properties of the recovery phase?

Answer 12

1. Presynaptic terminal repolarizes as K leaves through voltage gated K channels2. Voltage gated Ca channels close3. Ca stops flowing into the synaptic terminal4. Free ionized Ca in the terminal is removed from cytoplasm5. Vesicle recycling

Question 13

What are the fates of calcium during the recovery phase?

Answer 13

1. Can diffuse away from docking complex2. Can be sequestered by cytoplasmic Ca binding proteins3. Can be pumped into SER cisterns4. Can be pumped out of the cell into the extracellular fluid by secondary active transport Na/Ca exchange transporters

Question 14

What are the postsynaptic events of NT release?

Answer 14

1. Binding of transmitters to postsynaptic receptors2. Activation of receptors 3. Elicit postsynaptic responses4. Induce action potentials5. Activate postsynaptic signaling cascades

Question 15

What are the two classes of postsynaptic receptors?

Answer 15

1. Ionotropic2. Metabotropic

Question 16

What are the properties of ionotropic receptors?

Answer 16

1. Ligand gated ion channel receptors2. One macromolecule may both bind transmitters and form channel3. Binding of NT directly changes channel’s permeability to ions4. Responsible for fast chemical synaptic transmission5. Rapid changes in membrane potential

Question 17

What are the properties of metabotropic receptors?

Answer 17

1. G protein coupled receptors2. Slower acting on membrane potential than ionotropic 3. Elicit different physiologic effects

Question 18

Is the EPSP mediated by ionotropic receptors or metabotropic?

Answer 18

Ionotropic

Question 19

What is the major excitatory NT in the brain and spinal cord?

Answer 19

Glutamate

Question 20

What is the effect of glutamate on ionotropic glutamate receptors?

Answer 20

1. Binding opens Na/K channel 2. Net influx of Na3. Depolarization

Question 21

What are the properties of the EPSP at glutamatergic synapses?

Answer 21

1. EPSP brings Vm closer to firing threshold, thus increasing likelihood of AP generation2. EPSP is a local potential so there is decremental spread (momentary disturbance of polarization of membrane potential, effect of synapse depends on location of synapse)

Question 22

What is the major inhibitory NT in the brain and spinal cord?

Answer 22

GABA

Question 23

What is the effect of GABA on ionotropic GABA receptors?

Answer 23

1. Chemical force on Cl is stronger than electrical 2. Influx of chloride ions will hyperpolarize membrane - inhibition 3. Local potential with decremental spread

Question 24

What is synaptic delay?

Answer 24

Time interval between when AP invades the presynaptic terminal and when a membrane potential change begins in the postsynaptic cell

Question 25

How do metabotropic receptors cause excitatory effects?

Answer 25

1. Decreasing conduction through chloride or potassium channels2. Relatively slow change in Vm

Question 26

How do metabotropic receptors cause inhibitory effects?

Answer 26

1. Increasing conduction through chloride or potassium channels2. Relatively slow change in Vm

Question 27

How are NTs removed from the synaptic cleft?

Answer 27

1. Diffusion2. Enzymatic degradation3. Transmitter reuptake either into presynaptic terminal or into adjacent astroglia

Question 28

Where does cocaine bind?

Answer 28

1. DA/NE/5-HT transporters at presynaptic terminals 2. Results in increase in synaptic DA levels

Question 29

What are the properties of spatial summation?

Answer 29

1. Occurs when two or more separate postsynaptic potentials reach the initial segment simultaneously2. Initial segment is usually the most electrically excitable part of neuron

Question 30

What are the properties of temporal summation?

Answer 30

1. Occurs when a single presynaptic terminal has two or more APs in rapid succession2. First postsynaptic potential has not died away when next occurs3. Temporal overlap enables potentials to sum

Question 31

What are the properties of the NMJ structure?

Answer 31

1. Presynaptic - as motoneuron axon approaches termination it loses myelin sheath and divides into many terminal boutons2. Postsynaptic membrane - junctional folds, motor end plate3. Active zone - part of the presynaptic membrane that is specialized for the vesicular release of NT

Question 32

What are the unique features of the NMJ?

Answer 32

1. Skeletal muscle cell innervated by one motor neuron2. One large motor end plate per extrafusal muscle fiber3. Excitatory - no inhibitory synapses (inhibition means inhibition of the alpha motor neuron)4. Only Ach is released5. Only nicotinic Ach receptor

Question 33

How many active zones are there at a CNS synapse?

Answer 33

One

Question 34

What makes a NMJ different from a CNS synapse?

Answer 34

1. Multiple active zones2. High level of mitochondria in both terminals3. Junctional folds

Question 35

What characterizes the NMJ synaptic transmission?

Answer 35

1. Depolarization opens voltage gated channels - influx of calcium 2. Ach is released 3. Ionotropic Ach receptor activated and Na flows in causing end plate depolarization (EPP - local) 4. Depolarization spreads to skeletal muscle membrane containing Na channels5. EPP terminated by hydrolysis of Ach 6. Reuptake of choline into motor neuron

Question 36

What is the effect of anticholinesterases?

Answer 36

Inhibit acetylcholinesterase - prolongs EPP and makes it longer

Question 37

What are the effects of botulinum toxin?

Answer 37

1. Cleave proteins on either synaptic vesicle or presynaptic plasma membrane (motor neuron) 2. Interferes with release of NT at NMJ 3. Effects include focal dystonia, strabismus, facial wrinkles

Question 38

What is Eaton-Lambert syndrome?

Answer 38

1. Caused by autoimmune attack on voltage gated calcium channels in terminals of somatic motor nerves2. Less calcium enter presynaptic terminals so less Ach is released - muscle weakness3. Frequently seen in patients with small cell carcinoma of the lung

Question 39

What is myasthenia gravis?

Answer 39

1. Autoimmune disease tha treduces the number of Ach receptors at postsynaptic NMJ 2. EPP is smaller than normal 3. If EPP is too small skeletal muscle cell will not generate an AP, causing weakness and possibly paralysis

Question 40

What are the effects of tetanus toxin?

Answer 40

1. Cleaves SNARE protein in an interneuron2. Disinhibition leads to hyperexcitability and tetanic contraction

Question 41

What does neostigmine do in myasthania gravis?

Answer 41

1. Reversible AchE inhibitor2. Indirectly enhances function of existing AchR by increasing extracellular Ach levels 3. Slows enzymatic breakdown of Ach and lets released transmitter interact longer with remaining AchR

Question 42

What is tubocurarine?

Answer 42

1. AchR blocker2. Causes paralysis

Question 43

What is bungarotoxin?

Answer 43

Irreversibly blocks nAchR

Question 44

What is the effect of nicotine on nAchR?

Answer 44

Agonist