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OPT 535 > Synapses and Synaptic Transmission > Flashcards

Synapses and Synaptic Transmission Flashcards

1
Q

What does an action potential trigger, as it reaches the presynaptic terminal?

A

Voltage-gated calcium channels open, allowing influx of this ion. This triggers release of neurotransmitter into the synaptic cleft.

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2
Q

What sort of action at the postsynaptic terminal might produce an EPSP?

A

Influx of sodium or calcium.

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3
Q

What sort of action at the postsynaptic terminal might produce an IPSP?

A

Influx of chlorine or efflux of potassium.

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4
Q

What is the difference between a neurotransmitter and a neuromodulator?

A

A neurotransmitter acts directly on the postsynaptic membrane; a neuromodulator is released into the extracellular fluid and can adjust the activity of many neurons.

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5
Q

True or false: A substance can be either a neurotransmitter or a neuromodulator, but it cannot be both.

A

False. A substance may act as a neurotransmitter in one location and as a neuromodulator in another. (Substance P is one example.)

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6
Q

What does ACh have to do with myasthenia gravis?

A

Myasthenia gravis is an autoimmune disease that destroys ACh receptors on skeletal muscle.

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7
Q

Which amino acid neurotransmitters are excitatory?

A

Glutamate and aspartate.

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8
Q

Which amino acid neurotransmitters are inhibitory?

A

GABA and glycine.

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9
Q

True or false: Amino acid neurotransmitters are typically fast-acting.

A

True.

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10
Q

How might low levels of GABA and/or glycine affect a person?

A

This can cause neural overactivity, which can lead to seizures, muscle spasms, and anxiety.

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11
Q

Name a few of the common amine neurotransmitters.

A

Dopamine, norepinephrine, serotonin, histamine.

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12
Q

True or false: Amine neurotransmitters are typically fast-acting.

A

False. Amine neurotransmitters are typically slow-acting.

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13
Q

Dopamine affects ____________.

A

motor activity, cognition, and behavior.

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14
Q

Where is dopamine produced?

A

In the substantia nigra and in the ventral tegmental area.

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15
Q

What role does NE play?

A

It helps maintain active surveillance by increasing attention to sensory information. (be aware of any (NE) one.)

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16
Q

In the CNS, where is NE produced?

A

Brainstem nuclei, hypothalamus, and thalamus. (Almost any (NE) thalamus.)

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17
Q

What can overactive NE systems do?

A

They produce fear and panic, even in response to things that are normal.

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18
Q

What role does serotonin play?

A

It affects mood and perception of pain, adjusts general arousal level, and can suppress sensory information.

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19
Q

What is the role of histamine, and where is it concentrated?

A

It increases arousal and is concentrated in the hypothalamus.

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20
Q

Name a few peptide neurotransmitters.

A

Substance P, calcitonin gene-related peptide, galanin, and opioid peptides.

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21
Q

What is the role of substance P?

A

It is thought to be involved in the pathology of pain syndromes where innocuous stimuli are perceived as painful. (substance P = Pathology of Pain, stimuli Perceived as Painful)

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22
Q

What is the role of calcitonin gene-related peptide?

A

It phosphorylates the ACh receptor, decreasing the likelihood that ACh will activate said receptor. (the Peptide Phosphorylates the receptor.)

23
Q

What is the role of galanin?

A

It helps regulate food intake, cognition and moods, alertness, seizures, and pain perception. It also helps inhibit insulin release. (food=Glut, coGnition, ALertness, seizures, and pAiN perceptIoN.)

24
Q

What is the role of opioid peptides?

A

They help decrease the perception of pain.

25
Q

What important functions does NO have?

A

It is involved in LTP and excitotoxicity.

26
Q

True or false: All of the amines and substance P bind to and activate G-protein receptors.

A

True.

27
Q

What are receptor tyrosine kinase most commonly involved in?

A

Cell growth, cellular movement, and cell death.

28
Q

What type of receptor do peptides and hormones typically activate?

A

Receptor tyrosine kinase.

29
Q

Loss of nicotinic receptor-expressing neurons in the brain have been associated with what disease?

A

Alzheimer’s disease.

30
Q

What type of receptors are nicotinic receptors?

A

They are ligand-gated ion channels, for sodium and calcium.

31
Q

What type of receptors are muscarinic receptors?

A

G protein receptors.

32
Q

True or false: All glutamate receptors are ionotropic.

A

False. Glutamate receptors may be ionotropic or metabotropic.

33
Q

What are some ionotropic receptors that bind glutamate?

A

AMPA, kainate, NMDA.

34
Q

What are the two types of receptors for GABA?

A

GABA-A, which is an ionotropic chlorine channel, and GABA-B, which is a metabotropic receptor.

35
Q

True or false: Dopamine receptors all use second messenger systems.

A

True. They are used to suppress the activity of calcium channels.

36
Q

What are the two types of NE receptors?

A

Alpha and Beta. Beta receptors in the heart increase the force and rate of heart contraction. Activation of Alpha receptors in the gut relaxes intestinal smooth muscle.

37
Q

After ACh is degraded by AChE, what happens to the resulting molecules?

A

Choline is reuptaken through active transport, acetic acid diffuses.

38
Q

Where are neuromodulators released?

A

At axoaxonic synapses in order to either facilitate or inhibit the release of neurotransmitter.

39
Q

True or false: Nicotonic receptors are always excitatory.

A

True.

40
Q

True or false: Muscarinic receptors are always excitatory.

A

False. They can be excitatory or inhibitory.

41
Q

How does botulinum toxin exert its effect?

A

It blocks release of ACh into the synaptic cleft.

42
Q

What types of receptors does NE activate?

A

Alpha1, alpha2, beta1, and beta2.

43
Q

How do MAO inhibitors help treat depression?

A

They stop the reuptake of NE by MAO, allowing NE to remain in the synapse longer, exerting its effect. (Cocaine also blocks NE reuptake.)

44
Q

True or false: Amphetamines block NE reuptake.

A

False, they stimulate additional NE release.

45
Q

Which neurotransmitters do optometrists have to deal with most?

A

ACh, NE, glutamate, aspartate, glycine, GABA, serotonin, and dopamine.

46
Q

Why is myasthenia gravis an important disease for optometrists to be familiar with?

A

Ptosis is the presenting symptom in many patients.

47
Q

What is the difference between symptoms and signs?

A

Symptoms are what the patient tells us; signs are what we see.

48
Q

True or false: In MG, manual elevation of one eyelid causes increased contralateral ptosis.

A

True.

49
Q

What is Cogan’s sign?

A

Occuring in MG, it is when, after looking in downgaze, a patient is instructed to look foward. The eyelid will elevate and then drop slightly.

50
Q

How would saccades be affected in MG?

A

They would slow with fatigue.

51
Q

How would the orbicularis be affected in MG?

A

Orbicularis be weakened. Have patient try to keep their eyes shut, then try to manually open their eyelids. They will open relatively easily.

52
Q

How can you test in-office for MG?

A

Two-minute upgaze test.
Ice test: 2 minutes improves ptosis, EOMs approve after 5 minutes.
Rest test: Ptosis improves after 20 minutes with eyes closed.

53
Q

How can you treat MG?

A

Anticholinesterase medications, removal of thymus gland, plasmapheresis.

OPT 535 (8 decks)

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