Pharmacology Exam 3- Neurotransmission

Front 1

amino acid/primary amine NT synthesis location vs. peptide NT

Back 1

AA/primary amines synth'ed in the NERVE TERMINAL.

peptide nt is synthesized in the

Front 2

synth of NTs is regulated by ... (2)

Back 2

1) presence of precursor (choline, etc)
2) enzyme activity (e.g. tyrosine hydroxylase RLS)

Front 3

purpose of NT transport into vesicles (2)

Back 3

keeps NTs ready for release
protects from catabolism

Front 4

describe what happens to nerve terminal upon arrival of action potential (2)

Back 4

1) action potential opens voltage gated Ca++ channels
2) Ca++ influx causes docking of vesicles on membrane surface, fusion, and dumping of contents into synapse

Front 5

2 ways in which NT action is terminated

Back 5

1) reuptake into nerve terminal (repackaged or catabolized)
2) diffusion away from synapse and taken up by astrocytes

Front 6

definition of a neurotransmitter (5)

Back 6

1) synthesized in neuron
2) released upon arrival of action potential
3) in physiologically relevant amounts
4) and binds to specific receptor molecule
5) is then rapidly removed/deactivated

Front 7

criteria of NTs

Back 7

1) synthesis
2) storage
3) release by action potential (Ca++ influx)
4) presence in significant amounts
5) rapid termination by reuptake or enzyme degradation
6) can be miimic'ed by drugs
7) receptors on post synaptic neuron

Front 8

locations of dopaminergic neurons (4)

Back 8

1) substantia nigra projecting to striatum (caudate putamen)
2) ventral tegmentum area (VTA)-->cortex and limbic
3) VTA-->n. accumbens
4) hypothalamus-->pituitary

Front 9

DA cell bodies in substantia nigra-->caudate putamen: role

Back 9

posture/movement (parkinsons)

Front 10

DA cell bodies in VTA-->cortex and limbic system: role (2)

Back 10

1) target oriented behavior (goal oriented)
2) psychosis

Front 11

DA neurons in VTA-->n. accumbens (nuclei = group of specialized neurons): role

Back 11

addiction/reward behaviors

Front 12

HT-->pit DA neurons: role

Back 12

endocrine control

Front 13

cholinergic neuron locations (4) and their functions

Back 13

1) nucleus basalis-->cerebral cortex- learning and memory
2) diagonal band/medial septum-->hippocampus- learning/memory
3) pons-->thalamus, basal forebrain, reticular formation- sleep/arousal
4) striatum- motor control

Front 14

noradrenergic neuron locations (indicate which is the most) (2)

Back 14

1) locus coerulus*** --> cerebral cortex, thalamus, HT, spinal cord (projects everywhere)
2) midbrain-->limbic, cerebellum, spinal cord

Front 15

functions of noradrenergic neurons in the brain (4)

Back 15

1) integration of response to external sensory and motor stimuli (maintain homeostasis)
2) arousal/attention
3) learning/memory
4) mood/depression

Front 16

serotonergic neuron location (1) and their function (20

Back 16

1) raphe nuclei (this is a broad category of nuclei in the brainstem- they are divided into many clusters) medulla pons and midbrain- with diffuse projections into the CNS

function: sensory processing
homeostasis

Front 17

dysfunction of serotonergic neurons implicated in...(4)

Back 17

1) psychosis
2) depression
3) eating disorders
4) OCD

Front 18

associated pathways of histamine and 3 functions

Back 18

tuberomamillary

1) arousal
2) cerebral metabolism
3) neuroendocrine

Front 19

GABA location and 2 functions

Back 19

widespread
1) anxiolytic
2) anti convulsant

Front 20

glutamte location and 3 functions

Back 20

widespread
1) pro-convulsant
2) LTP
3) learning and memory

Front 21

DA neurons in VTA-->n. accumbens (nuclei = group of specialized neurons): role

Back 21

addiction/reward behaviors

Front 22

HT-->pit DA neurons: role

Back 22

endocrine control

Front 23

cholinergic neuron locations (4) and their functions

Back 23

1) nucleus basalis-->cerebral cortex- learning and memory
2) diagonal band/medial septum-->hippocampus- learning/memory
3) pons-->thalamus, basal forebrain, reticular formation- sleep/arousal
4) striatum- motor control

Front 24

noradrenergic neuron locations (indicate which is the most) (2)

Back 24

1) locus coerulus*** --> cerebral cortex, thalamus, HT, spinal cord (projects everywhere)
2) midbrain-->limbic, cerebellum, spinal cord

Front 25

functions of noradrenergic neurons in the brain (4)

Back 25

1) integration of response to external sensory and motor stimuli (maintain homeostasis)
2) arousal/attention
3) learning/memory
4) mood/depression

Front 26

serotonergic neuron location (1) and their function (20

Back 26

1) raphe nuclei (this is a broad category of nuclei in the brainstem- they are divided into many clusters) medulla pons and midbrain- with diffuse projections into the CNS

function: sensory processing
homeostasis

Front 27

dysfunction of serotonergic neurons implicated in...(4)

Back 27

1) psychosis
2) depression
3) eating disorders
4) OCD

Front 28

associated pathways of histamine and 3 functions

Back 28

tuberomamillary

1) arousal
2) cerebral metabolism
3) neuroendocrine

Front 29

GABA location and 2 functions

Back 29

widespread
1) anxiolytic
2) anti convulsant

Front 30

glutamte location and 3 functions

Back 30

widespread
1) pro-convulsant
2) LTP
3) learning and memory

Front 31

drugs can alter lvls of neurotransmitters how? (5)

Back 31

1) alter lvl of precursor
2) inhibit reuptake
3) inhibit vesicular repackaging
4) inhibit enzymes involved in synthesis
5) inhibit metabolic processing

Front 32

how do drugs alter release of neurotransmitter? (2)

Back 32

1) prevent action potential from entering neuron (sodium channel blocking)
2) prevent Ca++ influx into axon (calcium channel blockage)

Front 33

"recycle"- this term is associated with what step in neurotransmitter cycle?

Back 33

repackaging into vesicles

Front 34

how can drugs block action of neurotransmitter? (2)

Back 34

1) antagonist
2) inhibit subcellular effectors (like adenyl cyclase in transduction pathways)

Front 35

ligand gated ion channels vs. GPCRs in terms of speed of synaptic transmission

Back 35

ligand gated- very fast transmission
GPCR- may be involved in more prolonged synaptic events (10s of seconds to minutes)

Front 36

the action of a neurotransmitter is dictated by what?

Back 36

the subtype of receptor on the post synaptic neuron (i.e. TISSUE SPECIFIC)

Front 37

role/properties of voltage gated Na+ channels (3)

Back 37

1) nitiate action potentials
2) support rapid (due to being gated ion channels) propagation of impulses
3) some may be coupled to receptors

Front 38

location of voltage gated Ca++ and K+ channels (3)
what happens when the are activated (opened)?

Back 38

cell body
dendrites
initial segment
activation causes slower propagation of impulses

Front 39

chemically gated ion channels (ionotropic/ligand gated)- which receptors? (5)

Back 39

nicotinic ACh
5HT3
GABAa
glycine
NMDA

Front 40

ionotropic receptors are used for what type of transmission?

Back 40

fast synaptic transmission where opening of channel is brief

Front 41

chemically gated ion channels (metabotropic)- direct interaction of g-protein with Ca++ channels: types (4)
function

Back 41

1) D2 dopaminergic
2) GABAb
3) glutamate
4) alpha 2

decreases Ca++ channel function (pre-synaptic)

Front 42

chemically gated ion channels (metabotropic)- direct interaction of g-protein with K+ channels: types (4)
function

Back 42

M2
D2
GABAb
a2
(same ones as Ca++)

increases K+ conductance resulting in hyperpolarization (K+ efflux). mostly post synaptic.

Front 43

examples of indirect g protein interaction (metabotropic) with ion channels (4)
explain how signal is propagated

Back 43

all GABAb?
aminergic
peptidergic
glutamate

usually through secondary messengers like IP3, DAG, cAMP or Ca++

Front 44

nicotinic receptor- what type of receptor, what does it do

Back 44

ligand gated ion channel
excitatory-increases Na+ conductance (flow of sodium into the cell)

Front 45

muscarinic receptor-excitatory type (3)
what does it do

Back 45

GPCR
M1, 3, 5
decrease K+ conductance (decrease permeability to K+ so K+ stays inside cell, making it easier to depolarize?)

Front 46

muscarinic receptor- inhibitory type (2)
what does it do

Back 46

M2, M4
inhibitory- increase K+ conductance

Front 47

specificity of muscarinic drug action depends on...

Back 47

density of M receptor subtypes in brain regions

Front 48

dopamine receptors are what type?

Back 48

GPCR indirectly coupled to ion channel

Front 49

which 2 dopamine receptors activate adenyl cyclase?

Back 49

D1, D5-->increase in cAMP

Front 50

4 functions of D2 receptors (what do they do physiologically, what are the implicated in)

Back 50

implicated in schizophrenia and parkinson's

1) inhibits adenyl cyclase and decreases cAMP
2) suppresses PRE-synaptic Ca++ currents (no vesicle release)
3) activates POST-synaptic K+ currents (Hyperpolarize)
4) ergo pre/post synaptic inhibition

Front 51

D3,D4 receptors implicated in what disease? what type of receptor are they?

Back 51

indirectly activating ion channel GPCR that inhibits AC

implicated in schizophrenia

Front 52

serotonergic receptors- what kind are they? (2 subcategories)

Back 52

GPCR
ligand gated ion channel

Front 53

5HT1 receptors- describe the type and its type of action (inhibitory/excitatory, 2 effects it has on conductance)

Back 53

GPCR-->inhibits AC

inhibitory- decrease Ca++ conductance and increases K+ conductance

Front 54

5HT2, 5HT4 receptors- type, and actions on conductance (what pahtway) and whether it is inhibitory/excitatory

Back 54

GPCR
excitatory
PLC-->DAG/IP3-->decrease K+ conductance

Front 55

5HT3 receptor- type, actions on conductance, inhib/excite

Back 55

ligand gated ion channel
excitatory
increases Na+ conductance

Front 56

alpha 1 receptor- type, actions on conductance, inhib/excite

Back 56

GPCR
inhibitory
inhibits AC-->decrease cAMP
regulates K+/Ca++ channels (did not say how)

Front 57

alpha 2 receptor- type, actions on conductance, inhib/excite

Back 57

GPCR
inhibitory AND excitatory subtypes
activates PLC/PLA-->DAG/IP3 (excitatory)
inhibits by increasing K+ conductance and decreasing Ca++ conductance

Front 58

beta receptors- type, inhib/excite pathway

Back 58

excitatory GPCR
stimulates AC-->increase cAMP

Front 59

glutamate receptor type

Back 59

ionotropic receptor: ion channel

Front 60

AMPA/Kainate receptor- type of receptor, what does it do/what channels does it open

Back 60

glutamate ionotropic receptor
opens Na+, K+, Ca++ to mediate fast depolarization and normal synaptic transmission

Front 61

NMDA- type of receptor
what are its actions? (3)

Back 61

glutamate ionotropic receptor
1) mediates fast depolarization but is not activated until membrane depolarizes
2) this is because its function is to AMPLIFY glutamatergic signal
3) opens Ca++ channels and involved in LTP

Front 62

GABAa receptor- type, excite or inhib?

Back 62

ligand gated Cl- channel
inhibitory

Front 63

GABAb receptor- type, excite or inhib? what channels does it affect?

Back 63

GPCR
inhibits presynaptic Ca++ channel (inhibit vesicles) and increases post synaptic K+ channels conductance (Hyperpolarization)
inhibitory

Front 64

properties of peptide NTs (2) that make them different from normal NTs

Back 64

1) not synthed in nerve terminal (synthed in cell body)
2) not inactivated by reuptake- so longer lasting

Front 65

peptide NTs implicated in...(4)

Back 65

1) mood/depression (enkephalins- runner's high)
2) huntington's/alzheimers (substance P)
3) schizophrenia
4) eating disorders

Front 66

neurotrophic factors- what do they do?
produced by what? (3)

Back 66

EGF, nerve growth factor

promote neuronal repair and growth/plasticity

produced by neurons, glia or invading peripheral inflammatory/immune cells

Front 67

adaptive changes of neuronal receptors (4)

Back 67

1) receptors recycle (ligand binds, endocytosis of receptor into cell, then receptor goes back to membrane surface)
2) upregulate and downregulate depending on amount of stimulation (or lack thereof)
3) can change efficiency to which they bind to g proteins (maybe will go from binding 2 to 11 depending on need)
4) can change the type of g protein they couple to