Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/98

Click to flip

98 Cards in this Set

  • Front
  • Back
what are the two types of synapses and how do they differ?
electrical synapse allows direct, passive electrical current to pass through gap junction from one neuron to another

chemical synapse releases neurotransmitter from one neuron across synaptic cleft to another neuron, where binding to receptors causes opening or closing of ion channels and subsequently an electrical signal that acts on post-synaptic neuron and is either inhibitory or excitatory
how does calcium enter the pre-synaptic neuron and what does it do?
action potential depolarizes the cell, allowing voltage-gated calcium channels to open

calcium enters through open channels and stimulates fusion of synaptic vesicles with the pre-synaptic plasma membrane for neurotransmitter release
describe the transmission that occurs between electrical synapses
transmission of large molecules by direct passive electrical current through gap juction that links two neurons

paired channels form a pore

ATP, 2nd messengers

transmission is bidirectional and very fast
describe the cycle of transmission between electrical synapses
action potential generates electrical current, which flows directly from one neuron to another through pore in that comprises gap junction

transmission is bidirectional and very fast
what is the function of electrical synapses? give examples
synchronize electrical activity among populations of neurons

brainstem neurons - breathing
hormone-secreting neurons: all cells fire action potential at the same time to release a burst of hormone into the circulation - mammary glands
coordinated intercellular signaling and metabolism (glial cells form large interconnected networks)
describe the cycle that occurs at chemical synapses (10 steps)
1. neurotransmitter synthesized and stored in synaptic vesicles at nerve terminal
2. action potential invades nerve terminal, depolarizing pre-synaptic neuron
3. depolarization opens voltage-gated calcium channels, allowing calcium influx into cell
4. increased calcium concentration stimulates fusion of synaptic vesicles with plasma membrane of pre-synaptic neuron
5. neurotransmitter released into synaptic cleft via exocytosis
6. neurotransmitter binds to receptors on post-synaptic neuron membrane
7. post-synaptic ion channels open or close
8. ions flow into or out of open/closed ion channels, creating an electrical current through the post-synaptic cell
9. this current causes a change in post-synaptic potential, which changes the excitability of the post-synaptic cell
10. vesicle membrane is retrieved from plasma membrane of pre-synaptic cell. it is recycled to make a new synaptic vesicle
name 3 places where acetylcholine acts
released by vagus nerve to regulate heartbeat

neuromuscular junctions of striated muscles

visceral motor system
what are the 2 types of neurotransmitters and how do they differ?

distinguish between how they are released and what type of synaptic actions they mediate
small molecule neurotransmitters (subset of this group is the biogenic amines) and peptide neurotransmitters

small molecule transmitters are released by low frequency activity and mediate rapid synaptic actions

peptide transmitters are releasted by high frequency activity and mediate slower, ongoing synaptic actions
what is a co-transmitter and what is its significance?
neurons often store and release 2 or more neurotransmitters (co-transmitters)

a neuron can be excited by 1 type of neurotransmitter and inhibited by another type
name the 3 criteria that define a neurotransmitter
1. substance must be present within pre-synaptic neuron

2. substance must be released in response to depolarization of the pre-synaptic cell membrane and release must be Ca-dependent

3. specific receptors for the substance must be present on the post-synaptic cell membrane
describe the differences in synthesis, storage, and transport between small molecule neurotransmitters and peptide neurotransmitters

location of synthesis
transport
vesicles
enzymes needed to synthesize small molecule neurotransmitters are produced in the neuronal cell body and transported to the nerve terminal by slow axonal transport

precursor molecules are taken into the cell by transporter proteins

small molecule neuropeptides are synthesized at the nerve terminal and stored in small clear-core synaptic vesicles

neuropeptides are synthesized in the cell body of the neuron and transported to the nerve terminal by fast axonal transport

neuropeptides are transported and stored in large dense-core vesicles
name 4 components of neurotransmitter removal from synaptic cleft
1. diffusion away from post-synaptic receptors

2. re-uptake into pre-synaptic nerve terminal by transporter proteins

3. uptake into nearby glial cells

4. degradation by specific enzymes
what are the two types of neurotransmitter receptors and how do they differ?

distinguish between both speed and duration of post-synaptic response
ionotropic receptor = ligand-gated ion channel = molecule that is both receptor and ion channel allows fast post-synaptic response that lasts only a short time

metabotropic receptor = molecule that is a receptor only, not an ion channel allows slower post-synaptic response that persists for a longer time
give 4 examples of small molecule neurotransmitters
Ach

GABA

glycine

glutamate
name the 5 biogenic amines
the catecholamines: dopamine; epi; norepi

serotonin

histamine
name the 2 precursors and the enzyme used to synthesize Ach
Acetyl CoA (from glucose metabolism) and choline

enzyme is CAT = choline acetyltransferase
where does the choline for Ach synthesis come from?
choline is present in the plasma at high concentrations

it is taken up into the pre-synaptic neuron by a Na-dependent choline transporter
what are the breakdown produces of Ach and what enzyme produces them?

what happens to the breakdown products?
acetylcholinesterase breaks Ach down into acetate + choline

choline is transported back into the nerve terminal
what happens if acetylcholinesterase is inhibited?
Ach accumulates at the synapse, depolarizing the post-synaptic neuron

the post-synaptic neuron is thus refractory to subsequent Ach release: can't open ion channels in the cell

result is neuromuscular paralysis
what are the inhibitors of acetylcholinesterase?
organophosphates, e.g. Sarin
describe the structure and function of a nicotinic Ach receptor
activated by both nicotine and Ach

same molecule is both receptor and cation channel (ionotropic receptor / ligand-gated ion channel)

large protein complex with 5 subunits around a central membrane-spanning pore

each subunit has 4 transmembrane domains that comprise the ion channel pore and a long extracellular region where the Ach binds

intimate association of Ach with channel pore allows rapid (ionic) response to Ach

results in excitatory post-synaptic responses
alpha-bungarotoxin
binds to nicotinic Ach receptors at neuromuscular junctions but not at neuronal junctions
describe the function of a muscarinic Ach receptor
activated by both muscarine and Ach

just a receptor, not an ion channel (metabotropic)

mediates most of the effects of Ach in the brain
name 3 places where muscarinic Ach receptors are important
1. forebrain

2. ganglia of PNS

3. autonomic effector organs: heart; smooth muscle; exocrine glands
give 3 examples of blockers of muscarinic Ach receptors that have therapeutic value
1. atropine - pupil dilation

2. scopolamine - prevent motion sickness

3. ipratropium - treats asthma
atropine
pupil dilation

blocker of muscarinic Ach receptor
scopolamine
prevents motion sickness

blocker of muscarinic Ach receptor
ipratropium
asthma treatment

blocker of muscarinic Ach receptor
how does cocaine work?
it binds to DAT (dopamine transporter that transports dopamine out of synaptic cleft), increasing the dopamine concentration so dopamine is more available to receptors
conotoxin peptides
toxins that block nicotinic Ach receptors
what is the function and significance of biogenic amines?
regulate many brain functions

defects lead to psych disorders

psych drugs and drugs of abuse act on pathways, synthesis, receptor binding, and catabolism of biogenic amines
tyrosine hydroxylase
converts tyrosine to DOPA in first and rate-limiting step of catecholamine synthesis

requires oxygen and tetrahydrobiopterin as co-factors
DOPA decarboxylase
coverts DOPA to dopamine
dopamine-beta-hydroxylase
converts dopamine to norepi
phenylethanol-amine-N-methyl transferase
converts norepi to epi
pathway of catecholamine synthesis
tyrosine to DOPA to dopamine to norepi to epi

tyrosine hydroxylase catalyzes rate-limiting step
dopamine
motivation, reward, reinforcement - dopamine transporter blocked by cocaine so more dopamine available to receptors

present in coprus striatum, which coordinates body movements

in Parkinson's disease, substantia nigrans degenerates so no more input to corpus striatum so motor dysfunction
VMAT
vesicular monoamine transporter

loads dopamine into synaptic vesicles at the nerve terminal
DAT
Na-dependent dopamine transporter

transports dopamine from the synaptic cleft into nerve terminals and glial cells

inhibited by cocaine
MAO
dopamine catabolism enzyme contained in both neurons and glia

monoamine oxidase

inhibited by antidepressants
COMT
dopamine catabolism enzyme contained in both neurons and glia

catechol-O-methyl transferase

inhibited by antidepressants
how does dopamine work?
it activates G-protein-coupled receptors
Ach post-synaptic effect
excitatory
Ach precursors
acetyl CoA + choline
Ach synthesis rate-limiting step
CAT (choline acetyl transferase)
Ach removal
degraded by acetylcholinesterase
Ach storage vesicle
small clear-core vesicle
glutamate post-synaptic effect
excitatory
glutamate precursors
glutamine
glutamate synthesis rate-limiting step
glutaminase
Ach properties
excitatory post-synaptic effect

rate-limiting step is CAT (choline acetyl transferase)

precursors are choline + acetyl CoA

removal is by acetylcholinesterase

storage vesicles are small clear-core vesicles
glutamate properties
excitatory post-synaptic effect

glutamine is precursor

rate-limiting step in synthesis is glutaminase

removal is by transporters

storage vesicles are small clear-core vesicles
glutamate removal
transporters
glutamate storage vesicles
small clear-core vesicles
GABA post-synaptic effect
inhibitory
GABA precurors
glutamine
GABA synthesis rate-limiting step
GAD
GABA removal
transporters
GABA storage vesicles
small clear-core vesicles
GABA properties
inhibitory post-synaptic effect

precursor is glutamine

rate-limiting step in synthesis is GAD

removal is by transporters

vesicles are small clear-core vesicles
glycine post-synaptic effect
inhibitory
glycine precurors
serine
glycine synthesis rate-limiting step
phosphoserine
glycine removal
transporters
glycine vesicles
small clear-core vesicles
glycine properties
inhibitory post-synaptic effect

precursor is serine

rate-limiting step in synthesis is phosphoserine

removal is by transporters

vesicle is small clear-core vesicle
catecholamine post-synaptic effect
excitatory
catecholamine precursor
tyrosine
catecholamine synthesis rate-limiting step
tyrosine hydroxylase
catecholamine removal
transporters; MAO; COMT
catecholamine vesicles
small dense-core vesicles

large irregular dense-core vesicles
catecholamine properties
excitatory post-synaptic effect

precursor is tyrosine

rate-limiting step in synthesis is tyrosine hydroxylase

removal is by transporters, MAO, and COMT

vesicles are small clear-core vesicles and large irregular dense-core vesicles
serotonin post-synaptic effect
excitatory
serotonin precursor
tryptophan
serotonin synthesis rate-limiting step
tryptophan hydroxylase
serotonin removal
transporters, MAO
serotonin vesicles
large dense-core vesicles
serotonin properties
post-synaptic effect is excitatory

precursor is trp and rate-limiting step in synthesis is trp hydroxylase

removal is by transporters and MAO

vesicles are large dense-core vesicles
histamine post-synaptic effect
excitatory
histamine precursor
histidine
histamine synthesis rate-limiting step
histidine decarboxylase
histamine removal
transporters
histamine vesicles
large dense-core vesicles
histamine properties
excitatory post-synaptic effect

precuror is histidine and rate-limiting step is histidine decarboxylase

removal is by transporters

vesices are large dense-core vesicles
ATP post-synaptic effect
excitatory
ATP precursor
ADP
ATP synthesis rate-limiting step
mitochondrial ox-phos and glycolysis
ATP removal
hydrolysis to AMP and adenosine
ATP vesicles
small clear-core vesicles
ATP properties
excitatory post-synaptic effect

precursor is ADP

rate-limiting steps are glycolysis and mitochondrial ox-phos

removal is by hydrolysis to adenosine and AMP

vesicles are small clear-core vesicles
neuropeptides post-synaptic effect
excitatory and inhibitory
neuropeptides precursors
amino acids
neuropeptides synthesis rate-limiting step
synthesis in neuronal cell body and fast axonal transport (ATP-dependent) in large dense-core vesicles to nerve terminal
neuropeptides removal
proteases
neuropeptides vesicles
large dense-core vesicles
neuropeptides properties
post-synaptic effects are excitatory and inhibitory

precursors are amino acids

rate-limiting steps are synthesis in neuronal cell body and ATP-dependent fast axonal transport to nerve terminal

removal is by proteases

vesicles are large dense-core vesicles
which neurotransmitters have inhibitory post-synaptic effects?
GABA and glycine

sometimes neuropeptides

all others have excitatory post-synaptic effects
Parkinson's disease
dopaminergic neurons of substantia nigra degenerate

substantia nigra input to corpus striatum is compromised, resulting in motor dysfunction