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Pharmacology Test #6 > Neuropharmacology Intro > Flashcards

Neuropharmacology Intro Flashcards

1
Q

Cholinergic transmission is important for

A

cognitive function, sensitization to incoming stimuli, movement control

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2
Q

Describe the difference between nACh receptors and mACh receptors.

A

nAch receptors are ligand gated cation channels whereas mACh receptors are GPCRs

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3
Q

Where are cholinergic neurons?

A

concentrated in the basal forebrain and pons, but numerous cholinergic interneurons are found int he cortex and basal ganglia

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4
Q

Dopamine transmission is important for

A

natural rewards and motor function

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5
Q

Problems in dopamine transmission is implicated in diseases or disorders such as

A

schizophrenia, parkinsons disease, addiction, depression and ADHD

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6
Q

Two varieties of GPCR dopamine receptors

A

D1-type (D1 and D5) and D2-type (including D2, D3, and D4)

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7
Q

Where are dopamine neurons?

A

situated in the midbrain, either the ventral tegmental area or the substantia nigra pars compacta

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8
Q

Norepinephrine activates

A

adrenergic receptors (GPCRs), ainly alph1 and/or alpha2 in the CNS

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9
Q

NE is involved in

A

memory, pain transmission, and salience

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10
Q

NE transmission is altered in

A

depression and addiction

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11
Q

NE neurons are located in

A

the pons, specifically the locus coeruleus

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12
Q

Serotonin activates

A

either 5-HT3 ligand gated cation channels, or GPCR-type 5-HT receptors

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13
Q

Serotonin is important in

A

reward, learning, and mood/affect, and is thought to play a major role in depression and possibly schizophrenia

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14
Q

Where are serotonin neurons located?

A

in the midbrain/pons, specificially inthe raphe

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15
Q

GABA is produced from

A

glutamate

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16
Q

Major inhibitory neurotransmitter in the CNS

A

GABA

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17
Q

GABA activates

A

GABAA type ligand gated Cl- channels, and GABAB and GABAC receptors which are GPCRs

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18
Q

Where is GABA produced?

A

produced throughout the brain by numerous cell types, and is altered in many disorders, including epilepsy, muscle spasticity, and addictions such as alcoholism

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19
Q

Main excitatory neurotransmitter in the brain

20
Q

What does glutamate bind to?

A

Ion channels (AMPA, NMDA) and GPCRs (mGluRs)

21
Q

Glutamate may be a useful pharmacologic target in which diseases?

A

epilepsy and schizophrenia

22
Q

Two categories of ligand-gated

A

ion channels and G protein coupled receptors

23
Q

HCN channels are

A

cyclic nucleotide-gated channels

24
Q

Ligand that modifies HCN channels

A

cAMP or cGMP

25
Describes what happens when a GIRK channel is activated
activating a GPCR coupled to a GIRK channel results in enhanced outward K+ currents, which serve to hyperpolarize the membrane potential and keep the cell "clamped" near the equilibrium potential for K+, which is around -90mV
26
Where are NT transporters usually located?
usually located presynaptically where they remove NT molecules from the synaptic cleft and return them back inside the presynaptic terminal
27
Which ion do most neurotransmitter transporters use?
most are Na+ symporters, making them electrogenic
28
How is electrical activity altered by drugs
by directly affecting the function of ion channels, or indirectly by changing the overall number or function of important targets in the CNS
29
Where do drugs act?
NT synthesis, NT storage, NT reuptake, autoreceptors, presynaptic receptors, postsynaptic receptors
30
What will decreasing the action of NT transporters do?
will decrease re-uptake, and therefore prolong the action of drugs released into the synaptic cleft
31
Difference between blocking a presynaptic autoreceptor versus a postsynaptic receptor.
Blocking an inhibitory autoreceptor on the presynaptic side will increase activity of the synapse whereas blocking a receptor on the postsynaptic side can decrease the output of a synapse
32
BBB formed by
tight junctions between endothelial cells, which contributions from astrocytes as well
33
BBB typically restricts
microscopic objects (bacteria, viruses) and hydrophilic molecules, but allows small hydrophobic molecules (hormones, gases) and glucose
34
Two ways drug affinity for receptors is measured
saturation assays and competition assays
35
Describe saturation assays
directly measures drug affinity for receptor, but require the test drug to be radiolabeled, therefore a large amount of prior knowledge about the drug and its candidate receptor must be in hand
36
What is Kd?
the concentration of the radioligand where 50% of receptors are bound
37
What is Bmax?
the total number of receptors in a preparation
38
Describe competition assays
they're done with a known, labeled drug and unlabeled test drugs which are used to compete off the labeled drug. Provides an indirect assessment of affinity of the drug for the receptor because it is measuring how well it can displace the labeled drug
39
What is the Ki?
the concentration of drug where 50% of the radioligand is displaced
40
Functional Assays
Biochemical: enzyme function Second messenger response assay Transporter function assay: uptake and/or efflux assay Patch clamp electrophysiology (ion channel function)
41
Describe patch clamp electrophysiology
involves placing a glass pipette onto the surface of the cell expressing the channel of interest, followed by forming a high-resistance seal between the glass and the cell membrane
42
Where do full agonists bind?
binds at the orthosteric binding site where the natural ligand binds, and activates the receptor as well as the natural ligand
43
Where do partial agonists bind?
binds the receptor and activates it, but can never achieve full activation of the receptor population like a full agonist can - also has antagonist activity
44
Where do antagonists bind?
bind at the orthosteric binding site, do not have any ability to actiate the receptr on its own, but will prevent the ability of the natural ligand or an agonist to activate the receptor?
45
What does an inverse agonist do?
reduces the activity of a receptor to levels BELOW what they would be if no ligand is present at all

Pharmacology Test #6 (12 decks)

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