Functional Properties Of Neurons Iii

Front 1

2 main groups of chemical transmitters

Back 1

small molecule transmitters (classical) & peptide transmitters

Front 2

4 examples of small molecule transmitters

Back 2

1. Ach
2. amino acids
3. monoamines
4. purines

Front 3

which small molecule NT is not removed by transporters ?

Back 3

Ach

Front 4

where are small molecule neurotransmitters made?

Back 4

nerve terminal

Front 5

where are the enzymes that help make small molecule NTs synthesized?

Back 5

RER (of cell body)

Front 6

where are the peptide NTs made?

Back 6

RER (of cell body)

Front 7

where are peptide NTs packaged into vesicles?

Back 7

in the golgi of the cell body

Front 8

where are small NTs packaged into vesicles?

Back 8

at the nerve terminal by vesicular transport proteins

Front 9

T/F many small molecule NTs are made in a pre-pro form

Back 9

F. Peptide NTs are the ones that are made in a pre-pro form, and must be cleaved by processing enzymes.

Front 10

which NTs, peptide or small molecule NTs, produce slow effects?

Back 10

peptide NTs (and small molecule NTs can do both fast and slow)

Front 11

what's packaged inside large dense core vesicles?

Back 11

neuropeptide transmitters (vs. small clear core vesicles)

Front 12

where do you find large dense core vesicles?

Back 12

farther away from the plasma membrane of the nerve terminal, unlike the small clear core vesicles that stay docked close to the plasma membrane surface

Front 13

prolonged high frequency stimulation would most likely induce stimulation of what type of NT? (small NTs or peptide)

Back 13

peptide

Front 14

how many types of receptors can a given neuron have? (1, 2, 3 or more?)

Back 14

multiple.

Front 15

what is one possible function of autoreceptors on nerve terminals?

Back 15

enable feedback inhibition of the transmitter release and synthesis

Front 16

what types of receptors respond to opiod peptides and substance P?

Back 16

GPCR (these are both peptide NTs that modulate SLOW effects through GPCRs)

Front 17

what type of NT is substance P?

Back 17

peptide NT

Front 18

peptide NTs that depress synaptic transmission

Back 18

opiod peptides

Front 19

3 classes that opiod peptides can fit into

Back 19

endorphins, enkephalins, and dynorphins

Front 20

representative of the peptide family called tachykinins

Back 20

substance P

Front 21

peptide NT found in sensory neurons in DRG

Back 21

substance P

Front 22

substance P responds to what type of stimuli when found in sensory neurons?

Back 22

noxious stimuli (mechanical, chemical, thermal)

Front 23

this peptide NT responds to capsaicin

Back 23

substance P

Front 24

role of substance P in the PNS

Back 24

respond to noxious stimuli (found in sensory neurons of DRG)

Front 25

role of substance P in the CNS

Back 25

motor function as acts as co-transmitter w/ GABA

Front 26

what is the function of substance P?

Back 26

depends on what brain region you're in. In PNS, it plays a sensory role, while in CNS, it plays a motor role.

Front 27

precursor for glutamate

Back 27

glutamine

Front 28

most prevalent excitatory NT in the CNS

Back 28

glutamate

Front 29

what role does aspartate play in the CNS?

Back 29

fast excitatory action just like glutamate, however, unknown/controversial whether or not asparate functions in the brain

Front 30

transporters for glutamate are found where? (3 places)

Back 30

1. presynaptic
2. postsynaptic
3. glial cells

Front 31

AMDA receptors respond to what NT?

Back 31

glutamate

Front 32

3 ionotropic glutamate receptors

Back 32

AMPA, NMDA, kainate

Front 33

3 major roles of glutamate receptors

Back 33

1. excitatory
2. neuronal plasticity
3. cell death

Front 34

3 modulatory sites on the NMDA receptors

Back 34

1. glycine site (necessary co-agonist)
2. PCP binding site (responsible for psychotomimetic effects of PCP and other drugs)
3. Mg2+ site (responsible for Mg2+ block)

Front 35

which glutamate receptor is responsible for fast and normal transmission?

Back 35

AMPA receptor

Front 36

which glutamate receptor is responsible for the slower excitation that produces a late phase of the EPSP?

Back 36

NMDA receptor

Front 37

NMDA receptors are permeable to

Back 37

Na+ and Ca2+

Front 38

functions of NMDA receptors

Back 38

excitotoxity and plasticity

Front 39

what is the effect of Mg2+ bound to NMDA receptor?

Back 39

Mg2+ blocks the cell at normal resting potential so that it is normally closed. Only when the cell membrane becomes depolarized by AMPA receptor, then these receptor channels will open.

Front 40

doubly gated glutatmate receptors

Back 40

NMDA receptors (cell must be depolarized and NT must be bound)

Front 41

ability of synapses to change their strength

Back 41

plasticity

Front 42

when NMDA receptors are activated a little bit they lead to what?

Back 42

plasticity

Front 43

when NMDA receptors are activated a whole lot they lead to what?

Back 43

excitotoxicity

Front 44

what glutatmate receptor is responsible for excitoxocity and plasticity?

Back 44

NMDA receptors (special ability to pass Ca2+ which triggers these 2 phenomena)

Front 45

long term potentiation first characterized in what part of the brain?

Back 45

hippocampus so thought LTP associated with memory formation but know involved in many different pathways

Front 46

schaffer collateral synapses are the best studied form of _______

Back 46

LTP

Front 47

T/F LTP only occurs at synapses that receive strong activation

Back 47

T.

Front 48

what protein is activated as a result of flow of Ca2+ through NMDA receptors?

Back 48

CaMKII

Front 49

what role does CaMKII play in plasticity?

Back 49

it is activated by Ca2+ entry through the NMDA receptor, and in turn adds more AMPA receptors into the postsynaptic membrane

Front 50

what effects does phosphorylating the AMPA receptors have?

Back 50

increases their conductance, which plays a role in long term potentiation

Front 51

early phase of long term potentiation involves

Back 51

insertion of more AMPA receptors

Front 52

late phase of long term potentiation involves

Back 52

synthesis of new proteins involved in new synaptic contacts through PKA mediated activation of CREB (a transcriptional activator protein which goes on to activate synaptic growth and remodeling)

Front 53

brief high frequency stimulation leads to LTP while low frequency stimulation for longer periods leads to ________

Back 53

LTD (long term depression)

Front 54

activates protein phosphatases and removes AMPA receptors via clathrin dependent endocytosis

Back 54

LTD (long term depression)

Front 55

opposes LTP to prevent it from reach a "ceiling" level of maximum efficacy

Back 55

LTD

Front 56

structural change of dendrites associated w/ LTP

Back 56

increases # of dendritic spines

Front 57

LTD is activated by

Back 57

a smaller more prolonged rise in Ca2+

Front 58

excitotoxicity is seen when there are sustained and diffuse increases in what NT?

Back 58

glutamate

Front 59

important cause of cell death associated with ischemia

Back 59

excitotoxicity mediated through rising levels of glutamate

Front 60

once glutatamate levels rise, how does it kill neurons?

Back 60

Ca2+ activates biochemical cascades (proteases and endonucleases that destroy DNA, activates enzymes that produce free radicals) & leads to production of free radicals which are toxic