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MBOD Week 6 > Drugs at the Synapse > Flashcards

Drugs at the Synapse Flashcards

1
Q

What are the divisions of the PNS?

A

the autonomic (ANS) and somatic nervous systems

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2
Q

What is the role of the ANS in the body?

A

It is concerned primarily with visceral functions such as cardiac output, blood flow distribution, and digestion, which are necessary for life

It is largely independent (autonomous) in that its activities are not under direct conscious control

NOTE: There is growing evidence that it also has immune function (through the vagus nerve) and can influence cancer progression

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3
Q

What is the role of the somatic nervous system in the body?

A

largely responsible for consciously controlled functions such as movement, respiration, and posture.

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4
Q

Does the nervous system operate through electrical or chemical synapses?

A

Chemical.

Chemical transmission takes place through the release of small amounts of transmitter substances from the nerve terminals into the synaptic cleft and subsequent fusion with a postsynaptic membrane

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5
Q

What are the major divisions of the ANS?

A

sympathetic (aka thoracolumbar) and the parasympathetic (aka craniosacral)

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6
Q

The sympathetic preganglionic fibers leave the CNS through the which spinal nerves?

A

thoracic and lumbar spinal nerves.

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7
Q

The parasympathetic preganglionic fibers leave the CNS through which nerves?

A

the cranial nerves (especially 3, 7, 9, and 10) and the third and fourth sacral spinal nerve roots.

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8
Q

What are the types of preganglionic fibers of the sympathetic nervous system and where do they terminate?

A

1) paravertebral chains that lie on either side of the spinal column. (shorter fibers)
2) prevertebral ganglia, which lie in front of the vertebrae, usually on the ventral surface of the aorta (longer fibers)

From the ganglia, postganglionic sympathetic fibers run to the tissues innervated

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9
Q

The majority of parasympathetic preganglionic fibers terminate on ganglion cells distributed diffusely or in networks in the walls of the innervated organs. Which ones terminate in parasympathetic ganglia located outside the organs innervated?

A

the ciliary, pterygopalatine, submandibular, otic, and several pelvic ganglia

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10
Q

What is the enteric nervous system (ENS)?

A

a large and highly organized collection of neurons located in the walls of the gastrointestinal (GI) system. It is sometimes considered a third division of the ANS and is involved in both motor and secretory activities of the gut.

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11
Q

What are the two plexuses that make up the ENS?

A

myenteric plexus (the plexus of Auerbach) and the submucous plexus (the plexus of Meissner).

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12
Q

Does the ENS receive ganglionic fibers from both the sympathetic and parasympathetic systems?

A

Yes. The neural networks of the ENS receive preganglionic fibers from the parasympathetic system and postganglionic sympathetic axons

They also receive sensory input from within the wall of the gut.

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13
Q

Do the ganglionic fibers from the parasympathetic and sympathetic systems that enter the ENS provide an excitatory, inhibitory, or modulatory role?

A

A modulatory role, as indicated by the observation that deprivation of input from both ANS divisions does not abolish GI activity

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14
Q

What is the role of the ENS?

A

Fibers from the neuronal cell bodies in the myenteric and submucous plexuses travel forward, backward, and in a circular direction to the smooth muscle of the gut to control motility (especially of the colon) and to secretory cells in the mucosa to sense and influence their actions

The ENS also provides the necessary synchronization of impulses that, for example, ensures forward, not backward, propulsion of gut contents and relaxation of sphincters when the gut wall contracts.

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15
Q

How does the ENS work in a semiautonomous manner?

A

it utilizes input from the motor outflow of the ANS for modulation of GI activity and sends sensory information back to the CNS

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16
Q

Are they effects of neurotransmitter release at an ANS synapse more localized or more spread than neuromuscular synapses? Are they quicker or closer?

Why?

A

More spread out and slower

Junctions between autonomic neuron terminals and effector cells (smooth muscle, cardiac muscle, glands) differ from classic synapses in that transmitter is often released from a chain of varicosities in the postganglionic nerve fiber in the region of the smooth muscle cells rather than from boutons (as in neuromuscular synapses and most neuron-neuron synapses), and autonomic junctional clefts are wider than somatic synaptic clefts.

Effects are thus slower in onset and discharge of a single motor fiber often activates or inhibits many effector cells.

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17
Q

Peripheral ANS fibers that release acetylcholine as a neurotransmitter are called?

A

cholinergic.

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18
Q

Which ganglionic fibers in the PNS are cholinergic in nature?

A

All preganglionic efferent autonomic fibers, the somatic (nonautonomic) motor fibers to skeletal muscle, most parasympathetic postganglionic, and a few sympathetic postganglionic fibers

Thus, almost all efferent fibers leaving the CNS are cholinergic

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19
Q

Most postganglionic sympathetic fibers release which neurotransmitter?

A

norepinephrine (except sweat glands- acetylcholine)

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20
Q

Fibers which release norepinephrine as a neurotransmitter are called?

A

noradrenergic

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21
Q

What neurotransmitters do adrenal medullary cell secrete?

A

norepinephrine and epinephrine

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22
Q

What are the five key features of neurotransmitter function that provide potential targets for pharmacologic therapy?

A

synthesis, storage, release, termination of action of the transmitter, and receptor effects

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23
Q

What are VAMPs?

A

vesicle-associated membrane proteins (VAMPs), which serve to align vesicles with release sites on the inner neuronal cell membrane and participate in triggering the release of transmitter

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24
Q

What are SNAPs?

A

synaptosomal nerve-associated proteins (SNAPs). These are involved with fusion of VAMPs on the inner membrane of the presynaptic nerve membrane to aid in release of the transmitter

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25
Q

VAMPs and SNAPs are aka?

A

fusion proteins

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26
Q

Acetylcholine is synthesized from choline and acetyl CoA through the actions of which enzyme? Where in the neuron?

A

choline acetyltransferase (ChAT); cytoplasm

Acetyl-CoA is synthesized in mitochondria, which are present in large numbers in the nerve ending

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27
Q

T or F. Choline is synthesized in the cytoplasm of the neuron?

A

F. It is synthesized in the extracellular matrix

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28
Q

How is choline imported into the cytoplasm of the neuron at the pre-synaptic neuron terminal?

A

by a sodium-dependent membrane choline transporter (CHT)

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29
Q

What do the group of drugs called hemicholiniums do?

A

they block choline transporter (CHT)

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30
Q

Once acetylcholine is synthesized in the cytoplasm of the neuron, where is it transported to and what is it transported by?

A

Transported from the cytoplasm into the vesicles by a vesicle-associated transporter (VAT) that is driven by proton efflux

NOTE: Most of the vesicular acetylcholine is bound to negatively charged vesicular proteoglycan (VPG).

31
Q

What does the drug vesamicol do?

A

blocks vesicle-associated transporters (VAT) involved with transporting acetlcholine from the cytoplasm to vesicles

32
Q

Specifically, what are the names of the VAMPs and SNAREs involved in binding of transmitter in vesicles to the inner membrane of the pre-synaptic neuron

A

VAMP- v-SNAREs, especially synaptobrevin

SNARE- t-SNAREs, especially syntaxin and SNAP-25

33
Q

What stimulates the fusion of v-SNAREs on the vesicle and t-SNAREs on the membrane of the pre-synaptic neuron? How does this work?

A

Influx of Calcium interacts with the VAMP synaptotagmin on the vesicle membrane and triggers fusion of the vesicle membrane with the t-SNAREs on the terminal membrane, resulting in the opening of a pore into the synapse.

The opening of the pore and inrush of cations results in release of the acetylcholine from the proteoglycan and exocytotic expulsion into the synaptic cleft.

NOTE: One depolarization of a somatic motor nerve may release several hundred quanta into the synaptic cleft. One depolarization of an autonomic postganglionic nerve varicosity or terminal probably releases less and releases it over a larger area. In addition to acetylcholine, several cotransmitters are released at the same time

34
Q

What does botulinum toxin do?

A

Blocks the acetylcholine vesicle release process through the enzymatic removal of two amino acids from one or more of the fusion proteins

35
Q

After release from the presynaptic terminal, acetylcholine molecules may bind to and activate what?

A

an acetylcholine receptor (cholinoceptor)

36
Q

What causes the breakdown of acetylcholine in the synaptic cleft?

A

acetylcholinesterase (AChE): splits it into choline and acetate which don’t have a transmitter effect and are recycled

37
Q

What does metyrosine do?

A

It is a tyrosine analog that inhibits norepinephrine (catecholamine) synthesis from tyrosine in adrenergic neurons via prevents synthesis of a pre-cursor, dopa

38
Q

What does reserpine do?

A

Inhibits a high-affinity antiporter for catecholamines located in the wall of the storage vesicle (vesicular monoamine transporter, VMAT)

39
Q

What does NET do?

A

carries norepinephrine and similar molecules back into the cell cytoplasm from the synaptic cleft.

NET is also commonly called uptake 1 or reuptake 1 and is partially responsible for the termination of synaptic activity

40
Q

What drug can inhibit NET?

A

cocaine

41
Q

T or F. Release of the vesicular transmitter store from noradrenergic nerve endings is similar to the calcium-dependent process previously described for cholinergic terminals

A

True

42
Q

What effect do amphetamines, ephedrine, and tyramines have on noradenergic processes?

A

capable of releasing stored transmitter from noradrenergic nerve endings by a calcium-independent process.

These drugs are poor agonists (some are inactive) at adrenoceptors, but they are excellent substrates for monoamine transporters. As a result, they are avidly taken up into noradrenergic nerve endings by NET. In the nerve ending, they are then transported by VMAT into the vesicles, displacing norepinephrine, which is subsequently expelled into the synaptic space by reverse transport via NET. Results in increased sympathetic system output.

Amphetamines also inhibit monoamine oxidase and have other effects that result in increased norepinephrine activity in the synapse.

43
Q

Why can an estimate of catecholamine turnover can be obtained from measurement of total metabolites in a 24-hour urine sample?

A

Because the metabolic products are excreted in the urine

NOTE: due to the high activity of monoamine oxidase in the mitochondria of the nerve terminal, there is significant turnover of norepinephrine even in the resting terminal. Lower values of total metabolites would indicate a potential issue

44
Q

What are the primary mechanisms for termination of noradrenergic transmission?

A

simple diffusion away from the receptor site (with eventual metabolism in the plasma or liver), and

reuptake into the nerve terminal by NET or into perisynaptic glia or other cells.

45
Q

T or F. the vesicles of both cholinergic and adrenergic nerves contain other substances in addition to the primary transmitter (aka cotransmitters), sometimes in the same vesicles and sometimes in a separate vesicle population

A

T. Although the cotransmitters for each process may be different

46
Q

What are the main functions of cotransmitters?

A

In some cases, they provide a faster or slower action to supplement or modulate the effects of the primary transmitter. They also participate in feedback inhibition of the same and nearby nerve terminals.

In the case of acetylcholine, which when released can impact both the parasympathetic and sympathetic systems, they can aid in micromanagement of the sympathetic system response. (local control over global sympathetic response)

47
Q

What are the main autonomic nervous system receptors?

A

muscarinic and nicotinic cholinoceptors, and

a, β , and dopamine adrenoceptors

48
Q

How are the sub-types of autonomic nervous system receptors classified?

A

on the basis of both agonist and antagonist selectivity and on genomic grounds.

49
Q

What are the main transmitters of noncholinergic neurons found in the enteric system (NANC neurons)?

A

peptides, nitric oxide synthase, and purines

NOTE: Capsaicin, a neurotoxin derived from chili peppers, can cause the release of transmitter from enteric neurons

50
Q

Autonomic and receptor cell function is regulated by what MAIN process?

A

Negative feedback (there are others, but this is the main)

51
Q

How do α2 receptors regulate pre-synaptic terminals during norepinephrine release?

A

Ex. of negative feedback. This receptor is activated by norepinephrine and similar molecules; activation diminishes further release of norepinephrine from these nerve endings by distributing the calcium current

52
Q

How do beta receptors regulate pre-synaptic terminals during norepinephrine release?

A

Ex. of positive feedback at the pre-synaptic terminal. It is synthesized by norepinephrine and facilitates the release of more norepinephrine from some adrenergic neurons.

53
Q

What are autoreceptors?

A

Presynaptic receptors that respond to the primary transmitter substance released by the nerve ending are called autoreceptors.

Autoreceptors are usually inhibitory, but in addition to the excitatory β receptors on noradrenergic fibers, many cholinergic fibers, especially somatic motor fibers, have excitatory nicotinic autoreceptors.

54
Q

What are heteroreceptors?

A

Receptors on the pre-synaptic terminal that may be activated/deactivated by substances released from other nerve terminals that synapse with the nerve ending (aka not the primary transmitter as in autoreceptors)

55
Q

Post-synaptic regulation arises from what two main processes?

A

modulation by previous activity at the primary receptor (which may up- or down-regulate receptor number or desensitize receptors), and

modulation of the primary transmitter-receptor event by events evoked by the same or other transmitters acting on different postsynaptic receptors

56
Q

What is denervation supersensitivity?

A

An extreme form of up-regulation of post-synaptic receptor affinity occurring after denervation of some tissues. Receptors can be found in places outside the post-synaptic terminal in this case.

57
Q

How can pharmacological drugs cause denervation supersensitivity?

A

occurs in autonomic effector tissues after administration of drugs that deplete transmitter stores and prevent activation of the postsynaptic receptors for a sufficient period of time.

For example, prolonged administration of large doses of reserpine, a norepinephrine depleter, can cause increased sensitivity of the smooth muscle and cardiac muscle effector cells served by the depleted sympathetic fibers.

58
Q

How do EPSPs and IPSPs regulate post-synaptic terminals?

A

binding of an appropriate ligand to post-synaptic receptor results in fast excitatory postsynaptic potentials (EPSP) (evokes a propagated action potential if threshold is reached). This event is often followed by a small and slowly developing but longer-lasting hyperpolarizing afterpotential—a slow inhibitory postsynaptic potential (IPSP).

The combination of these two events regulate initiation of an AP at the post-synaptic neuron

59
Q

T or F. Drugs that block action potential propagation (local anesthetics and some natural toxins) are very nonselective in their action, since they act on a process that is common to all neurons

A

T. All neurons have APs

60
Q

How does lidocaine work?

A

Prevents AP propagation by blocking Na+ influx channels. It is a local anesthetic that prevents pain reception from reaching the brain

61
Q

How does Phentolamine work?

A

It is a reversible nonselective alpha-adrenergic antagonist that causes vasodilation (in response to hypertension) due to α1 blockade.

62
Q

What is isoproterenol?

A

a medication used for the treatment of bradycardia (slow heart rate), heart block, and rarely for asthma. In humans, it is a non-selective beta-adrenergic agonist

Basically, it makes the heart starts pumping harder

63
Q

What is propranolol?

A

beta- blocker (aka beta antagonist)

When they are blocked by propranolol the heart is made to beat more slowly and with less force. This reduces the pressure at which the blood is pumped out of the heart and around the body. This in turn reduces blood pressure, which means that propranolol can be used to treat high blood pressure

64
Q

What does nicotine do?

A

It is very similarly shaped to acetylcholine, so it can function as a ‘mimic’. It can also stimulate dopamine release

65
Q

How does atropine work?

A

Works as a nonselective muscarinic acetylcholinergic antagonist, increasing firing of the sinoatrial node (SA) and conduction through the atrioventricular node (AV) of the heart, opposes the actions of the vagus nerve, blocks acetylcholine receptor sites, and decreases bronchial secretions. Administered in response to brachycardia and heart block

66
Q

How does neostigmine work?

A

Use for treating myasthenia gravis.

Neostigmine is a cholinesterase inhibitor. It works by improving the transmission of nerve impulses in muscles so that the muscles are better able to work.

67
Q

How doe tranylcypromine work?

A

Tranylcypromine is a monoamine oxidase inhibitor (MAOI)

Tranylcypromine is used to treat major depressive episode in adults.

These are typically not prescribed anymore because monoamine oxidases are not effective against tyramine

68
Q

What are the main affects of stimulation of a1 adrenergic receptors?

A

Smooth muscle contraction, mydriasis, vasoconstriction in the skin, mucosa and abdominal viscera & sphincter contraction of the GI tract and urinary bladder

These bind norepinephrine most commonly

69
Q

What are the main affects of stimulation of a2 adrenergic receptors?

A

norepinephrine (noradrenaline) inhibition at presynaptic terminal platelet activation

These bind epinephrine most commonly

70
Q

What are the main affects of stimulation of b1 adrenergic receptors?

A

Positive Chronotropic, Dromotropic and inotropic effects, increased amylase secretion (aka makes the heart pump harder)

These bind isoprenaline most commonly

71
Q

What are the main affects of stimulation of b2 adrenergic receptors?

A

Smooth muscle relaxation

These bind isoprenaline most commonly

72
Q

What are the main metabolizers of norepinephrine?

A

monomamine oxidase and catechol-O-methyltransferase (COMT)

73
Q

What is the fundamental difference between the methods of inactivation of acetylcholine vs. that of norepinephrine?

A

Ach is broken down by AchE enzyme but NE is taken up (90%) into the pre-synaptic terminal and also diffuses away from cleft or is absorbed post-synaptically

74
Q

What does bethanechol do?

A

Muscarinic receptor agonist

MBOD Week 6 (7 decks)

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