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Year 1 Physiology > Synaptic transmission > Flashcards

Synaptic transmission Flashcards

1
Q

What modulates the gap junction channel?

A
  1. Intracellular pH2. Calcium3. Neurotransmitters and second messenger
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2
Q

What makes up a gap junction?

A

Two connexons, each made up of six connexin proteins

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3
Q

What are the properties of electrical synapses?

A
  1. Most are bidirectional 2. Rapid transmission, little or no delay allows synchronous activity 3. Low selectivity
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4
Q

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

A
  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
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5
Q

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

A
  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
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6
Q

What is the definition of a hormone?

A

Released into blood stream by a neuron

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7
Q

What is the definition of a neurotransmitter?

A
  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
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8
Q

What are the properties of the CNS synapse?

A
  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
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9
Q

What are the general features of a chemical synapse?

A
  1. Unidirectional transmission 2. Impact can be excitatory or inhibitory
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10
Q

What are the presynaptic events of NT release?

A
  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
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11
Q

What is the SNARE complex?

A
  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
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12
Q

What are the properties of the recovery phase?

A
  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
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13
Q

What are the fates of calcium during the recovery phase?

A
  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
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14
Q

What are the postsynaptic events of NT release?

A
  1. Binding of transmitters to postsynaptic receptors2. Activation of receptors 3. Elicit postsynaptic responses4. Induce action potentials5. Activate postsynaptic signaling cascades
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15
Q

What are the two classes of postsynaptic receptors?

A
  1. Ionotropic2. Metabotropic
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16
Q

What are the properties of ionotropic receptors?

A
  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
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17
Q

What are the properties of metabotropic receptors?

A
  1. G protein coupled receptors2. Slower acting on membrane potential than ionotropic 3. Elicit different physiologic effects
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18
Q

Is the EPSP mediated by ionotropic receptors or metabotropic?

A

Ionotropic

19
Q

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

A

Glutamate

20
Q

What is the effect of glutamate on ionotropic glutamate receptors?

A
  1. Binding opens Na/K channel 2. Net influx of Na3. Depolarization
21
Q

What are the properties of the EPSP at glutamatergic synapses?

A
  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)
22
Q

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

A

GABA

23
Q

What is the effect of GABA on ionotropic GABA receptors?

A
  1. Chemical force on Cl is stronger than electrical 2. Influx of chloride ions will hyperpolarize membrane - inhibition 3. Local potential with decremental spread
24
Q

What is synaptic delay?

A

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

25
Q

How do metabotropic receptors cause excitatory effects?

A
  1. Decreasing conduction through chloride or potassium channels2. Relatively slow change in Vm
26
Q

How do metabotropic receptors cause inhibitory effects?

A
  1. Increasing conduction through chloride or potassium channels2. Relatively slow change in Vm
27
Q

How are NTs removed from the synaptic cleft?

A
  1. Diffusion2. Enzymatic degradation3. Transmitter reuptake either into presynaptic terminal or into adjacent astroglia
28
Q

Where does cocaine bind?

A
  1. DA/NE/5-HT transporters at presynaptic terminals 2. Results in increase in synaptic DA levels
29
Q

What are the properties of spatial summation?

A
  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
30
Q

What are the properties of temporal summation?

A
  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
31
Q

What are the properties of the NMJ structure?

A
  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
32
Q

What are the unique features of the NMJ?

A
  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
33
Q

How many active zones are there at a CNS synapse?

A

One

34
Q

What makes a NMJ different from a CNS synapse?

A
  1. Multiple active zones2. High level of mitochondria in both terminals3. Junctional folds
35
Q

What characterizes the NMJ synaptic transmission?

A
  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
36
Q

What is the effect of anticholinesterases?

A

Inhibit acetylcholinesterase - prolongs EPP and makes it longer

37
Q

What are the effects of botulinum toxin?

A
  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
38
Q

What is Eaton-Lambert syndrome?

A
  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
39
Q

What is myasthenia gravis?

A
  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
40
Q

What are the effects of tetanus toxin?

A
  1. Cleaves SNARE protein in an interneuron2. Disinhibition leads to hyperexcitability and tetanic contraction
41
Q

What does neostigmine do in myasthania gravis?

A
  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
42
Q

What is tubocurarine?

A
  1. AchR blocker2. Causes paralysis
43
Q

What is bungarotoxin?

A

Irreversibly blocks nAchR

44
Q

What is the effect of nicotine on nAchR?

A

Agonist

Year 1 Physiology (66 decks)

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