Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NESC 2570 > Croll > Flashcards

Croll Flashcards

1
Q

neurons communicate with one another by…..

A

releasing chemical messengers called neurotransmitters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

main excitatory neurotransmitter

A

glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

main inhibitory neurotransmitter

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how to evoke synaptic response

A

binding to and activating neurotransmitter receptors, yielding any possible modes of synaptic signalling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

after activating neurotransmitter receptors, neurotransmitter are removed from synaptic cleft by…

A

neurotransmitter transporters or degradative enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 different classes of neurotransmitters

A

1) classical (small molecule transmitters
- ACh, amino acids, biogenic amines derived from amino acids, purines

2) peptides
- endorphins etc.

3) non-classical, small molecule
- NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

neuropeptides

  • examples
A
  • relatively large transmitter molecules (3-36 amino acids)

- endophrins, enkephalins, neuropeptide Y, vasoactive intestinal peptide, substance P, FMRDamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

small molecule transmitter

A
  • individual amino acids (ex: glutamate, GABA)
    and transmitters (ACh, serotonin, histamine)
  • smaller than neuropeptides
  • divided into: acetycholine, amino acids, purines, biogenic amines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are biogenic amines

  • examples
  • subgroup
A
  • small molecule transmitter (subgroup)
  • similar chemical properties and postsynaptic actions
  • examples: dopamine, norepinephrine, epinephrine, serotonin, histamine
  • catcholamines (subgroup)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are catcholamines?

A
  • biogenic amine subgroup

- hydroxylated benzene ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acetylcholine
- basic processes to all chemical synapses (4)

  • where is it made?
A
  • synthesis
  • package and release
  • reception
  • removal (simple slow diffusion)
  • made in cytoplasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

synthesis of ACh

  • precursors (2)
  • enzyme
  • transporter
A
  • synthesized in nerve terminals, from precursors acetyl coenzyme A (kreb cycle) and choline
  • enzyme: reaction catalyzed by choline acetyl transferase (ChAT or CAT)
  • transporter: after synthesis in cytoplasm, vesicular ACh transporter loads ~10 000 molecules of ACh into cholinergic vesicle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how to determine the evolution of ACh?

how do we know which tranmitter is used by which neuron for which function?

A
  • raise antibodies against ChAT (enzyme)
  • knockout genes (synthesis of ChAT)
  • any mutation of the enzyme is quickly lethal mutation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

locations of ACh in vertebrate nervous system

A
  • all motor neurons= spinal cord and brainstem
  • autonomic nervous system (sympathetic and parasympathetic divisions)- fight or flight
  • modulatory neurons in brainstem and basal forebrain- often involved with levels of activation (sleep/wake)- susceptible to Alzheimer’s (boost ACh to relieve some symptoms)
  • intrinsic neurons= basal ganglia, tectum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

reception of ACh- 2 major types of receptors

A

1) nicotinic receptors

2) muscarinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

nicotinic receptors

  • example found..?
  • iono/metabo
  • conduct?
  • made up of.. ?
A
  • important for reception of ACh
  • ex: found neuromuscular junction
  • ionotropic
  • conduct both Na and K (depolarizing- net flow of Na override outflow of K)
  • composed of 5 subunits with 3-4 transmembrane domains which form a channel with central membrane-spanning pore
  • ligand-gated channel - binding ACh, causes conformational change, rearranges receptor domains, opening gate, permittion ions to diffuse through pore
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

where does ACh bind on nicotinic ACh receptors?

A

on the alpha-subunit

usually has 2 alpha subunits at neuromuscular junction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

muscarinic receptors

  • example, found where?
  • iono/metabo
  • when do you want to use these?
  • structure
A
  • ex: targets of parasympathetic postganglionic neurones
  • found on receptors of parasympathetic nervous system, heart muscles
  • metabotropic receptor
  • use ACh to speed up/slow down processes (ex: beating of heart)

structure:
- 7 transmembrane domains
- extracellular site to bind neurotransmitter
- intracellular site to bind G-protein
- activate inward rectifier K channels or Ca-activated-K channels, exerting inhibitory influence on dopamine-mediated motor effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

subtypes of muscarinic receptors

how does ACh bind?

A

M1, M2, M3, M4, M5

  • different binding characteristics
  • different reactions to drugs
  • no subunits, each protein forms a complete receptor with its transmembrane domains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

G-protein receptors

  • iono/metabo
  • how does it work
  • 2 examples
A
  • metabotopic receptor
  • work indirectly to regulate activity in numerous other proteins including channels
  • receptor lies within membrane, can mind to transmitter, has intercellular domain that can react to G-protein
  • heterotrimeric or monomeric
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

2 differences between ionotropic and metabotropic receptors

A

1) speed (fast vs long lasting effects)
- fast= ionotropic
- slow= metabotropic

2) multiple actions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

how any subtypes of muscrinic receptors are there?

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

removal of ACh

A
  • post synaptic actions of ACh at many cholinergic synapses, is terminated by hydrolytic enzyme= acetylcholinesterase
  • enzyme is concentrated in synaptic cleft, ensuring rapid decrease in ACh concentration after its release from presynaptic terminal
  • choline produced by ACh hydrolysis, is RECYCLED by being transported back into nerve terminals, where it is used to re-synthesize ACh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Why is the process of chemical synapses of ACh important?

A
  • differential effects of toxins and drugs– pharmacology
  • Agonists (drug mimics specific transmitter)
  • antagonists (blocks transmitter)
  • disease affecting cholinergic transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is agonist and antagonist

A
  • agonist= mimic endogenous ligand

antagonist= block endogenous ligand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

example of nicotinic agonist

A

cholinergic substance

nicotine
- nicotine binds to nicotinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

nicotinic antagonist

A
  • a-bungarotoxin from krait (used by snake, paralyze prey), prevents ACh from opening postsynaptic ion channels
  • A-neurotoxin from cobra (blocks nicotinic receptor)
  • curare (used as poison on darts to kill animals, blocks nicotinic receptors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

3 examples of muscarinic agonist and antagonist

A
  • muscarine from the Amarita mushroom
  • Summer flower
  • Atropine from deadly nightshade (autumn berry)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

effects of myasthenia gravis on neurotransmission and basis of treatment

A
  • myasthenia gravis= disease that interferes with transmission between motor neurons and skeletal muscle fibers
  • effects: autoimmune destruction of nicotinic receptors
  • immunse responses reduced number of functional receptors at neuromuscular junction, eventualyl destroys them, diminishing efficiency of synaptic transmission
  • muscle weakness occurs b/c motor neurons are less capable of exciting the postsynaptic muscle cells
  • inhibitors increase concentration of ACh at synaptic cleft, allowing more effective activation of postsynaptic receptors not yet destroyed by immune system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

each transmitter must always have mechanism for (4)

A
  • synthesis
  • package and release
  • reception
  • removal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Glutamatergic synapse

  • synthesis
  • packaging
A

glutamate= non essential amino acid, does not cross blood-brain barrier, therefore must be synthesized in neurons from local precursors
- every cell in body has glutamate

Synthesis
- glutamate can be synthesized from glutamine

packaging
- into synaptic vesicles by variety of vesicular glutamate transporters (VGLUT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

locations of glutamate in vertebrate nervous system

A
  • most common fast transporter in the brain
  • many primary sensory cells (ex: photoreceptors, olfactory receptors)
  • many higher order/relay sensory cells (ex: retinal ganglion cells)
  • many cells in cortex, and sub-cortical nuclei (ex: basal ganglia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

2 classes of glutamate receptors

A

1) ionotropic

2) metabotropic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

structure of metabotropic glutamate (mGlu) receptors

A
  • similar to muscarinic receptors
  • 7 transmembrane domains
  • extracellular site to bind neurotransmitter
  • intracellular site to bind G-protein
  • metabotropic= slow
  • many classes
  • glutamate can mediate excitatory vs inhibitory actions into postsynaptic cells depending upon receptor type
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

structure of ionotropic glutamate receptors

A
  • similar to nicotinic receptor
  • 3-4 common transmembrane domains
  • with only 4 sub-units per channel
36
Q

3 subgroups of ionotropic glutamate receptors

A

1) AMPA
2) Kainate
3) NMDA (aka non-NMDA)

these receptors are

  • glutamate- gated cation channels that allow passage of Na and K (similar to nicotinic)
  • always produce excitatory post synaptic responses
37
Q

Non-NMDA receptors

A

(ionotropic glutamate receptors)

  • generally non-selective for monovalent cations (both Na and K)
  • excitatory
  • generally fast opening and closing
38
Q

gating NMDA receptor

A
  • Ca in addition to K and Na
  • glycine has to be binding to NMDA receptor
  • Mg tends to block so nothing can cross (at hyperpolarized membrane potentials), inside the pore, have to depolarize the postsynaptic membrane to push Mg out
  • NMDA receptors pass cations only when postsynaptic membrane potential is depolarized (during activating of strong excitatory inputs or during AP firing in postsyanptic cell)
39
Q

if want Ca into cell that responds to glutamate, what should you do?

A
  • have NMDA receptor present in cell (b/c permeable to K, Na and Ca)
40
Q

NMDA receptor could act as “coincidence detector” how??

A
  • parallel with classical conditioning
  • – need 2 stimuli, release glutamate and other pathway allowing depolarization
  • implications for understanding how we learn
    (block NMDA receptor, often block learning)
41
Q

glutamatergic synapse

- removal

A
  • reuptake using excitatory amino acids transports (EATTs)
  • uptake by glial cell
  • – conversion to glutamine (via enzyme glutamine synthetase)
  • – uptake by presynaptic terminal
  • – reconversion to glutamate
42
Q

insufficient removal of glutamate in extracellular space causes…

(what happens during ischemia (stroke))

A
  • excess depolarization
  • leads to more glutamate release
  • leads to more depolarization
  • leads to more glutamate release
    (vicious circle of EXCITOTOXICITY)
  • runaway depolarization
  • massive Ca influx
  • mechanisms unclear but may involve activation of caspases leading to cell death
43
Q

GABAergic synapse

  • synthesis and packaging
  • removal
A

synthesis

  • from glutamate
  • glutamic acid decarboxylase (glutamate with 1 carboxyl group chopped off)

packaging
- get into vesicles by vesicular inhibitory amino acid transporter (VIATT)

removal
- GABA transporter (GAT)

44
Q

where are GABAergic synapses?

A
  • GABA= most abundant inhibitory transmitter (fast)
  • found throughout the brain
  • mostly local circuit neurons but also projection neurons (Purkinje cells of cerebellum)
45
Q

GABA receptors (3)

A

GABAb= metabotropic

  • generally increase K currents
  • tend to hyperpolarize cells
  • inhibitory

GABAa and GABAc= ionotropic

  • composed of multiple subunits
  • Cl is main permeanant ion
  • activation of the receptors cause influx of negatively charged Cl that inhibits the postsynaptic cells
46
Q

ionotropic GABA receptors

A
  • mediate inhibition through increase Cl permeability (hyperpolarize cell)
  • multiple binding sites for GABA and variety of antagonists and modulators
    (benzodiazepine, barbituates, steroids, picrotoxin)
47
Q

4 types of agonist/antagonist ionotropic GABA receptor

A

1) Benzodiazepine
- agonist
- increase inhibition, decrease activity in brain

2) barbituates
- agonist
- binding sites are located within pore of domain

3) steroids
- interact with some extracellular receptors
- binding sites are located within pore of domain

4) Picrotoxin
- antagonist
- binding sites are located within pore of domain

48
Q

glycine is ____ transmitter found in the ___ ___

A

inhibitory transmitter

in the spinal cord

49
Q

Glycinergic synapse

  • synthesis
  • packaging
  • reception
A
  • synthesized from serine
  • uses VIATT (vesicular inhibitory amino acid transporter) to package into vesicles (loads GABA into vesicles)
  • used glycine transporter for uptake to terminals and glia
  • receptors are ligand-gated Cl channels
    (inhibition, hyperpolarizing)
  • structure mirrors GABAa receptors
50
Q

styrchnine

A
  • glycine antagonist
  • blocks inhibitory synapses in spinal cord
  • over excitation of most muscles (including breathing)
  • comes from tree in eastern asia
  • rat poison
51
Q

biogenic amines

small molecule transmitters

A
  • all are simple modifications from common amino acids
  • catecholamines derive from tyrosine
  • indolamines derive from tryptophan
  • imidazolamines drive from histadine
52
Q

5 biogenic amine neurotransmitters

A

3 are catacholamines- derived from tyrosine

1) dopamine
2) norepinephrine
3) epinephrine

4) histamine
5) serotonin

53
Q

synthesis of catacholamines (5)

A

1) tyrosine
- tyrosine hydroxylase (add hydroxyl group)

2) L-DOPA
- DOPA decarboxylase

3) Dopamine
- Dopamine Beta Hydroxylase
- reward pathway

4) norepinephrine
- PRMT

5) epinephrin

54
Q

what is Parkinsons disease caused from

- how to treat

A
  • Parkinson’s disease= death of dopamine containing cells

- treat by adding L-DOPA, will provide enough dopamine cells to run system

55
Q

where does dopamine originate from?

- where is it found

A

originated in substantia nigra and VTA

  • found in projections throughout brain
56
Q

dopaminergic synapse

  • synthesis
  • packaging
  • removal
  • metabotropic receptors
A
  • synthesized by tyrosine
  • packaging using vesicular monoamine transporter (VMAT)

removal

  • reuptake: high affinity, Na-dependent dopamine transporter (DAT
  • catabolism of dopemine enzymes: monoamine oxidase (MAO) and catechol O-methyltransferase (COMT)
  • once release, dopamine acts exculsively by activating G-protein coupled receptors

Metabotropic receptors

  • D1-4, which work primarily through inhibitory and excitatory actions on adenylyl cyclase, thus regulating cAMP levels
  • activating/inhibiting adenyly cyclase
57
Q

importance of dopamine (4)

A

1) Parkinson’s disease
- death of many monoaminergic (dopaminergic, adrenergic, serotonergic) cells, particularly cells of substantic nigra which project to striatum
- motor deficits
- treatment with L-DOPA

2) schizophrenia
- treatment with D2/D4 antagonists
- drugs working as antipsychotics

3) reward and addiction
- ex; self-stimulation pathwyas

4) drugs
- amphetamines facilitate the release and block re-uptake of dopamine (and other catacholamines)
- cocaine: block re-uptake mechanism

58
Q

cocaine

A
  • blocks dopamine re-uptake
  • prolongs its action at synapse
  • too much dopamien, have symptoms of cocaine
  • cocaine reduce psychotropic effects by inhibiting DAT, increasing dopamine concentrations in synaptic cleft
59
Q

where is norepinephrine originated?
- where is it found?

  • influences?
A
  • originated in locus coeruleus
  • found in projections throughout brain and spinal cord
  • also the transmitter used by the sympathetic ganglion cells to control peripheral targets
  • influences sleep and wakefulness, attentiona and feeding behaviour
60
Q

where does epinephrine originate?

- where is it found?

A
  • originates in medullary neurones

- found in projections to brainstem (hypothalamus) and spinal cord

61
Q

adrenergic/noradrenergic synapse

- what does it do?

A
  • epinephrine and norepinephrine, importnat in autonomic nervous system and hormonal system
  • mediate responses to dangerous/stressful stimuli and account for increase heart rates, dilated airways, shunting of bloodflow from digestive system and into muscles (etc)
  • also involved in other visceral functions like bladder control and sexual arousal
62
Q

adrenergic/noradrenergic synapse

  • synthesis
  • packaging
  • removal
  • metabotropic receptors
A
  • synthesis: from tyrosine to L-DOPA to dopamine
  • packaging using same VMAT (vesicular monoamine transporter)

removal

  • re-uptake: high affinity norepinephrine transporter (NET)
  • monoamine oxidase (MAO)
  • catechol O-methyltransferase (COMT)

metabotropic receptors

  • a1, a2 (alpha)
  • b1, b2, b3 (beta)
63
Q

serotonergic synapse

  • synthesis
  • packaging
  • removal
  • multiple receptors
A

synthesis: from typtophan
packaging: with VMAT (vesicular monoamine transporter)

removal

  • re-uptake: serotonin selective transporter (SERT)
  • MAO (monoamine oxidase) - break down

multiple receptors

  • ionotroic: 5-HT 3
  • metabotropic: 5-HT 1,2,4,5,6,7
64
Q

where is serotonin originated

-where is it found

A

originates in raphe nuclei

  • found in projections throughout brain and spinal cord
65
Q

LSD

A
  • serotonin agonist

- overstimulation of serotonergic pathways

66
Q

histaminergic synapse

  • synthesis
  • packaging
  • removal
  • metabotropic receptors
A

synthesis: from histadine
packaged: VMAT (vesicular monoamine transporters)

removal/degradation: by MAO and histamine methyltransferase

metabotropic receptors
- H1, H2, H3

67
Q

where is histamine found

role

A
  • neurons in hypothalamus
  • projections throughout nervous system
  • plentiful in mast cells involved with inflammatory processes throughout the body

role

  • projections mediate arousal and attention
  • allergic reactions or tissue damage cause release of histamine from mast cells in bloodstream
68
Q

roles of monoamines in affective disorders

A
  • monoamine oxidase inhibitors (MAO-I) are effective anti-depressants
  • tricyclic anti-depressants inhibit re-uptake transporters for all monoamines
  • serotonin selective re-uptake inhibitors (SSRIs) are among most precribed medications
69
Q

purines as transmitters

- 2 examples

A
  • ATP
  • Adenosine
  • often packaged together with other more conventional transmitters
70
Q

2 types of purine receptors

A

metabotropic and ionotropic receptors
- broad classes of both

metabotropic= A and P2Y receptors
ionotropic= P2X receptors
71
Q

effects of caffeine

A
  • purine antagonist

- disrupt the adenosine pathways in brain

72
Q

5 broad classes of neuropeptides in vertebrates

A

1) brain-gut peptides
2) opioid peptides
3) pituitary peptides
4) hypothalamic-releasing peptides
5) miscellaneous peptides

73
Q

opioids tend to be ___

  • come from
  • example of drug that binds
A
  • tend to antidepressants
  • come from the poppy
  • heroin has specific receptors in cells bind to opium (?)
74
Q

3 endogenous substances that bind to the same proteins as opium derivatives

A

1) endorphins
- mimic actions of morphine

2) enkephalins
3) dynorphines

75
Q

synthesis of peptides from larger precursor protein

A
  • often multiple copies of small peptides on precursor

- need large amounts because they are secreted

76
Q

where are peptides synthesized and packaged?

  • are they able to be recycled?
A
  • ER and Golgi located in the soma

- metabolically expensive, cannot recycle

77
Q

peptidergic transmission depends directly upon..

A

axonal transport to supply transmitter to synapse

78
Q

peptidergic synapse

  • synthesis
  • packaging
  • removal
  • receptors
A

synthesis: from amino acids
packaging: in Golgi apparatus, plus axonal transport
removal: by diffusion, relatively no selective extracellular peptidases (no recycling)

receptors

  • metabotropic and often varied for each peptide
  • µ, (delta), K receptors for opiates
  • often release with other transmitters
79
Q

non-covential transmitters

  • involved with..
  • release
A
  • involved with intercellular signalling
  • release regulated by Ca
  • non-vesicular release (not stores in SV)
  • not confined by cellular membrnaes
  • often associated with retrograde signalling (post–> presynaptic cells)
80
Q

endocannabinoids

  • derived from
  • action
  • depolarization effects
A
  • derived form fatty acids
  • endogenous signals that interact with cannabinoid receptors
  • anandamide
  • 2-AG

action: inhibition of communication between postsynaptic cells and their presynaptic input

depolarization of postsynaptic neuron causes transient reduction in inhibitory postsynaptic transmission

  • depolarization reduces synaptic transmission by elevating [Ca] within postsynaptic neuron
  • rise in Ca triggers synthsis and release of endocannabinoids from post synaptic cell
81
Q

nitric oxide (NO)

  • synthesis
  • specializations at synapses (transmission)
  • direction of pathways
A
  • endogenous structure
  • gaseous neurotransmitter
  • synthesis in presynaptic cell, release regulated by Ca
  • no normal membrane specializations at synapses, the presynaptic cell could be a postsynaptic cell (retrograde transmission)
  • pathway is not always in one direction
82
Q

other possible non-covential transmitters (2)

A

CO and H2S

- also some other gaseous neurotransmitters

83
Q

are transmitters same across animal kingdom?

A
  • some animals use them differently

ex: insects, visual system uses histamine (as opposed to glutamate in vertebrates)

84
Q

diversity of transmitters in invertebrates

A
  • many molluscs have only 10s of thousands of neurones (as opposed to 10s of billions of neurones in our brains)
  • molluscs contain many neurotransmitters as vertebrates
85
Q

molluscan neurotransmitters (8)

A

1) serotonin
2) histamine
3) catecholamines (dopamine, norepinephrine)
4) Acetylcholine
5) glutamate
6) GABA
7) Nitric oxide
8) numerous peptides (some same as vertebrates, some different - FMRFamide)

NESC 2570 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions