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Physiology > Lecture 3-Synaptic Transmission > Flashcards

Lecture 3-Synaptic Transmission Flashcards

1
Q

What is the AP (Action Potential) and how is it generated?

A

The AP is a rapidly propagating electrical wave. During the AP, the membrane potential changes due to the flow of Na+ (in to the neuron) and K+ (out of the neuron) ions through voltage-gated channels in the cell membrane.

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2
Q

Define Depolarization

A

Becomes less negative.

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3
Q

Define Hyperpolarization

A

Becomes more negative

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4
Q

Define Inward Current

A

Net + charge moves into the cell. Ex: The Na+ current is inward and depolarized the cell.

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5
Q

Define Outward Current

A

Flow of + charge out of a cell. Ex: Outward K+ current hyperpolarizes the cell.

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6
Q

Define AP Threshold

A

The point to which the membrane must be depolarized to in order to generate an AP. Generally 15-30 mV less negative than the resting potential.

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7
Q

Define Overshoot

A

The positive part of the AP above 0mV

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8
Q

Define Refractory Period (RP)

A

Another AP cannot be elicited. During the Absolute RP. During the Relative RP a larger than normal stimulus may cause another AP.

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9
Q

Define All or None

A

The AP either happens or it does not.

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10
Q

Define Repolarization

A

Na+ channels inactivate and close, whilst K+ channels open and K+ leaves the cell. (Cell becomes more negative)

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11
Q

Define Afterhyperpolarizing Potential (AHP)

A

For a brief period, K+ conductance is higher than normal and the membrane potential swings towards Ek. K+ conductance then returns to normal levels and the membrane is back at rest.

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12
Q

What makes up a gap junction in an electrical synapse?

A

Hemichannels or connexons

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13
Q

What is a connexon made up of?

A

6 connexin subunits, each about 7.5 nm long with 4 membrane spanning regions.

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14
Q

What are the advantages of electrical synapses?

A
  1. Speed
  2. Coordinating activity in large groups of cells
  3. Allow transfer of metabolites between cells (cAMP and small peptides.
  4. Gap Junctions can close in response to unfavorable conditions.
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15
Q

What is Charcot-Marie-Tooth disease?

A

A disease in which Connexin32 is defective. Demylenating.

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16
Q

Where is Connexin 26 found and what can mutations lead to?

A

Epithelial cells of the inner ear, deafness.

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17
Q

What is Oculodentodigital Dysplasia?

A

A disease in which Connexin 43 is defective. Symptoms include enamel hypoplasia, craniofacial anomalies and cardiac dysfunction.

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18
Q

What does the arrival of an AP at a presynaptic terminal lead to? (1st step in synaptic transmission)

A

The depolarization and opening of the voltage-gated Ca2+ channels.

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19
Q

When the Ca2+ enters the presynaptic terminal, where does Ca2+ concentration increase? (2nd step in synaptic transmission)

A

When the Ca2+ enters the presynaptic terminal, the concentration near the Active Zone.

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20
Q

What does the Ca2+ causes vesicles to fuse with and what is released? (3rd step in synaptic transmission)

A

Ca2+ causes vesicles to fuse with the presynaptic membrane. Neurotransmitter (NT) is released into the synaptic cleft via exocytosis.

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21
Q

What do the NT molecules bind to? (4th step in synaptic transmission)

A

NT molecules diffuse across the synaptic cleft and bind to postsynaptic receptors.

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22
Q

What does the NT receptor binding lead to? (5th step in synaptic transmission)

A

An opening of ion channels and a change in current flow through the postsynaptic cell and the generation of the postsynaptic potential.

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23
Q

What are the Receptors?

A

Proteins that span the membrane with an extracellular site that recognizes and binds NT. They have an effector function that can excite or inhibit a cell. It typically they gate the opening or closing of ion channels.

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24
Q

What are Ionotropic receptors?

A

Receptors that have direct effects on ion channels. Relatively FAST. (Nicotinic ACh receptor)

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25
Q

What are Metabotropic receptors?

A

Receptors that have an indirect, and SLOWER actions through second messenger systems. (Think G-proteins) (Muscarinic ACh receptor)

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26
Q

Where is ACh released in the Neuromuscular Junction (NMJ)

A

ACh is released from small vesicles in the boutons into the junctional folds of the underlying postsynaptic muscle fiber.

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27
Q

Where are Nicotinic ACh receptors concentrated at the NMJ?

A

At the top of the junctional folds at a density of about 10K recepters per micrometer2

28
Q

Where are Na+ Channels found in the NMJ?

A

At the base of the junctional folds.

29
Q

What is Acetylcholinesterase?

A

An enzyme that causes the hydrolysis of ACh. It is present in the synaptic cleft.

30
Q

What happens following an ACh release in the NMJ?

A

ACh diffuses and binds to the postsynaptic nicotinic receptors. The opening of the channels allows for Na+ and K+ to flow across the postsynaptic membrane and generates the end plate potential. If the depolarization is large enough, it will open Na+ channels and trigger an AP in the muscle.

31
Q

What does Curare do?

A

It is a drug that blocks the binding of ACh to receptors. Used to study the End Plate Potential.

32
Q

What does the Patch Clamp Technique study?

A

The opening and closing of a single ACh gated channel in muscle cells.

33
Q

What is alpha Bungarotoxin?

A

Toxin from snake venom. Binds irreversibly to alpha subunit of nicotinic receptor and blocks it. Can be used to measure density of ACh receptors at the end plate.

34
Q

What is the Botulinum Toxin?

A

A neurotoxin produced by Clostridium botulinum bacteria. Results in muscle paralysis by blocking release of ACh at the NMJ by clipping SNARE proteins. Botox.

35
Q

What is Myasthenia gravis?

A

Autoimmune disease in which antibodies are made to the neuromuscular ACh receptor. Fewer functional receptors result in muscle weakness.

36
Q

What do Cholinesterase inhibitors do?

A

Enhance transmission in Myasthenia Gravis patients by extending the life of ACh in synaptic cleft by inactivating the acetylcholinesterase.

37
Q

Compare Electrical vs. Chemical Transmission

A

Electrical is MUCH faster.

Synapse structure is different. Electrical synapses have continuous cytoplasm of cells and the distance between pre/post is 3 nm. In chemical synapses there is no cytoplasmic continuity and cleft is 20-40 nm wide.

Transmission is usually bi-directional at electrical and unidirectional at chemical.

Amplification is possible at chemical synapses.

38
Q

What are the two broad classes of Neurotransmitters?

A 
Small molecule (Rapidly acting: ACh, glutamate and nitric oxide)
Neuroactive peptides (Slowly acting: gastrin, angiotensin II and bradykinin)
39
Q

What is Co-release of NT?

A

Where two kinds of NT can be released from the same vesicle. EX: Small molecule transmitter and neuropeptide could both be released from a large, dense-core vesicle.

40
Q

Where is epinephrine released?

A

Directly into the bloodstream.

41
Q

What is Synaptic Integration?

A

A central neuron receives thousands of synaptic inputs from other neurons. Some can be excitatory or inhibitory. Lot’s of different NTs and receptors are involved. Synaptic integration is the term used to describe how neurons ‘add up’ these inputs before the generation of a nerve impulse, or action potential.

42
Q

Where are excitatory synapses often found? What about inhibitory?

A

Excitatory: Dendrites
Inhibitory: Soma

43
Q

Where are AP’s generated?

A

The Axon Hillock, or the initial segment of the axon. Na+ channels are concentrated here.

44
Q

What does it mean when you say, Chemical synapsis are plastic?

A

Effectiveness of chemical synapses can be altered in the short term or longterm via changes within the neuron or extrinsic factors such as input from other cells.

45
Q

What is the most common excitatory transmitter in the CNS?

A

L-glutamate

46
Q

What are the 3 types of ionotropic glutamate receptors that mediate excitatory responses? What are they blocked by?

A

AMPA, Kainate, and NMDA.

AMPA and Kainate are blocked by CNQX and NMDA is blocked by APV

47
Q

What are Metabotropic Glutamate Receptors do? What does the binding of glutamate lead to?

A

Mediate excitatory or inhibitory responses. They are activated by ACPD. The binding of glutamate stimulates phospholipase C (PLC) which leads to the second messengers of DAG and IP3.

48
Q

What receptors are involved in the EARLY part of the Excitatory Post-Synaptic Potential (EPSP)?

A

AMPA and Kainate. They conduct Na+ and K+.

49
Q

What receptors are involved in the LATE part of EPSP?

A

NMDA receptors.

50
Q

What are 3 unusual featers of the NMDA receptor?

A
  1. The high conductance channel opened by NMDA is PERMEABLE BY Ca+ as well as Na+ and K+
  2. GLYCINE is required as a co-factor for channel opening.
  3. At hyperpolarized potentials, Mg2+ BLOCKS THE CHANNEL.
51
Q

Explain the mechanism of how Mg2+ blocks NMDA’s channel?

A

At the cell’s resting potential Mg2+ enters the receptor-channel and binds tightly. Following depolarization, Mg2+ is ejected from the channel allowing Na+ and Ca2+ to enter the cell.

52
Q

What is Activity-Dependent Synaptic Modification?

A

If a presynaptic neuron fires repeatedly, EPSP’s will summate, resulting in a larger depolarization. More Ca2+ will enter the cell and will trigger Ca2+ dependent processes, such as enzyme activity.

Thought to be involved in learning and memory.

53
Q

What is Spacial Summation?

A

When two or more presynaptic inputs arrive at the same time at the postsynaptic cell and act at different sites.

54
Q

What is Temporal Summation?

A

When tow or more consecutive presynaptic inputs at the same site are added together in the postsynaptic cell.

55
Q

What is Glutamate Excitotoxicity?

A

Too much glutamate can be toxic, causing excess Ca2+ to enter through the NMDA receptor. Can lead to stroke, seizures, neurodegeneration and cell death.

56
Q

What two things mediate inhibitory synaptic transmission?

A

GABA and Glycine

57
Q

What type of receptor is the GABAa receptor? What is it’s equilibrium potential?

A

Ionotropic receptor that gates a chloride channel. Equilibrium potential is about -90mV.

58
Q

What does activation of the GABAa receptor lead to?

A

Net influx of Cl-, or an outward current. Hyperpolarization or inhibition.

59
Q

What type of receptor is GABAb?

A

A metabotropic receptor which activates K+ channels.

60
Q

What are the effects of an activated GABAb receptor?

A

Outward K+ current, resulting in hyperpolarization. Ca2+ channels may also be inhibited via a second messenger pathway.

61
Q

Where is glycine present and what does it activate?

A

Spinal cord and activates ionotropic receptors that open Cl- channels.

62
Q

What two things block glycine receptors? What happens when glycine is blocked?

A

Strychnine and tetanus. Muscle spasms, eventually resulting in opisthotonos. (Think of the picture)

63
Q

What is the structure of GABA receptors?

A

Similar to ACh. 5 subunits. 2 alpha, 2 beta and 1 gama. All subunits are similar and GABA can bind to anyone.

64
Q

What is the structure of the glycine receptor?

A

Similar to ACh. 3 alpha and 2 beta subunits. Glycine binds to alpha subunits.

65
Q

What does benzodiazepines (such as diazepam) do when bound to the gamma subunit of the GABAa channel?

A

Increase Cl- conductance through the channel, enhancing the inhibitory affect of GABA.

Alcohol and barbiturates also enhance the effect of GABA.

Physiology (2 decks)

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