NP Midterm 2 Flashcards

1
Q

Gap junctions between cells is found in what type of synapses?

A

Electrical

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2
Q

Where in the body are electrical synapses found?

A

Cardiac Muscle
Visceral Smooth Muscle
A few CNS synapses

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3
Q

What type of synapse occurs across a space filled with interstitial fluid?

A

Chemical

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4
Q

T or F

Chemical synapses are very fast and can travel in both directions through gap junctions?

A

False!

Electrical synapses are fast and use gap junctions

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5
Q

What is a synaptic knob?

A

An axon ending having a presynaptic terminal

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6
Q

How are synapses named?

A

First for the structure of the presynaptic neuron that contacts the post synaptic cell and secondly for the structure of the post synaptic cell that receives input.

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7
Q

What are the most typical chemical synapse?

A

Axo-dendritic

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8
Q

The most powerful excitatory chemical synapse is? Why is it the most powerful?

A

Axo-somatic
Local current flow experiences little resistance due to the large surface are of the cell body -> non decremental conduction.

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9
Q

When is an axo-axonic synapse inhibitory?

A

When the synapse is on the axon hillock

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10
Q

How can an axo-axonic veto excitatory effects of the axo-dendritic, and ado-somatic synapses?

A

By blocking or decreasing the frequency of action potentials generated by an EPSP on the soma

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11
Q

When will an axo-axonic synapse exert presynaptic facilitation or inhibition?

A

When the synapse is onto the synaptic ending of the post synaptic cell.

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12
Q

What type of synapse can only be electrical due to gap junctions?

A

Dendo-dendritic

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13
Q

Name the variations in the Presynaptic Events of Synaptic Transmission.

A
  • Regulation of Ca++ entry and the # of vesicles releasing NT
  • # of Vesicles and NT available for release.
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14
Q

What are the different mechanisms for changing the # of vesicles and NT available to be released?

A

Synthesis of NT
Inhibition of Synthesis of NT
Re-Uptake of NT
Inhibition of re-uptake
Destruction of NT by cytoplasmic enzymes
Depletion of vesicles = synaptic fatigue
Blockage of a NT release due to destruction of cytoskeleton

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15
Q

Give an example of the inhibition of re-uptake of NT?

A

Mode of action of drugs like Prosac

Serotonin re-uptake inhibitor increases the effectiveness of the release of Serotonin

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16
Q

Give an example of Destruction of NT by cytoplasmic enzymes:

A

Mono amino oxidases (MAO) enzymes oxidize the mono amines: Serotonin, Dopamine, and Norepi

17
Q

What do MAO inhibitors actually do?

A

They block the destruction of the monoamine NT’s inside the presynaptic cell and increase the availability of monoamines to be released.

18
Q

What enzyme will destroy Norepinephrine and Dopamine?

A

Catecholamine-O-methyl transferase COMT

19
Q

What enzyme converts Acetyl Choline to Acetate and Choline?

A

Acetyl Cholinesterase

20
Q

T or F

Drugs that inhibit COMT can decrease the effectiveness of the synapse

A

False

The drug will increase the effectiveness of the synapse because more will be available since it is not being destroyed.

21
Q

What are the variations in events in the synaptic cleft that will effect a synapse?

A
  1. Enzymatic Destruction of Neurotransmitters by enzymes in the Synaptic Cleft
  2. Presence of Antibodies against NT receptors
22
Q

When are Anti-acetyl Cholinesterase drugs used?

A

To increase the number of Ach molecules that reach the post synaptic cell membrane to compete with the Antibodies in the synaptic cleft.

23
Q

What are the ways in which Ca++ entry is regulated?

A

Frequency of AP
Presynaptic Inhibition
Presynaptic Facilitation
Increased Calcium in the presynaptic cell due to the release of Nitric Oxide by the post synaptic cell

24
Q

Describe the properties of receptors that are ion channels:

A
Open rapidly
Short Acting
Stay open for a brief time
Generally excitatory Na+ or Ca++ channels
Few sits for regulation of activity
25
Q

Give an example of when the Blockage of NT actions by molecules that bind to NT’s receptors discussed in class.

A

Curare the plant product binds to Nicotinic Acetyl Choline receptors on skeletal muscles -> paralysis

26
Q

Alpha and Beta Adrenergic blockers block the action of what monoamine?

A

Norepi

27
Q

Give an example of a receptor that is also an ion channel?

A

Nicotinic Acetyl Choline Receptor

28
Q

T or F

Nicotine binds to Ach receptors, closes the ion channel and remains bound also activating the Ach receptor

A

False

Nicotine binds to Ach receptors OPENS the ion channel and remains bound also INACTIVATING the Ach receptor.

29
Q

What remains open longer? G protein related channels or receptor ion channels?

A

G protein remain open or closed for longer periods of time - up to a number of seconds.

30
Q

Some neurotransmitters block the actions of other neurotransmitters how?

A

By working through receptors that cause the activation or inhibition of enzymes that block the mechanism of action of the other neurotransmitters.

31
Q

What do Phosphodiesterases do?

A
  • They destroy second messenger molecules whose structure contains two phosphoesters.
  • These enzymes are specific for either cyclic AMP or cyclic GMP.
32
Q

A NT that increases cyclic AMP - phosphodiesterase activity can diminish what mechanism?

A

The effectiveness of Norepi when it binds to Beta receptors and stimulates the production of cyclic AMP

33
Q

Give examples of phosphodiesterase inhibitors

A

Caffeine and Theophylline