1Two types of synapse?
and
Two types of synapse?
Electrical and chemical
2Gap junctions often found where? Bidirectional or unidirectional?
a.Found in +
b.
Gap junctions often found where? Bidirectional or unidirectional?
a.Found in cardiac + smooth muscle
b.Bidirectional
3What are gap junctions made up of?
a. pores = connexons
What are gap junctions made up of?
a. Hexametric pores = connexons
4What are the three chemical synapses? Bidirectional or unidirectional?
a. , , and membrane
b.
What are the three chemical synapses? Bidirectional or unidirectional?
a. Presynaptic, Synaptic, and Postsynaptic membrane
b. Monodirectional
5How are neurotransmitters released?
dependent at the membrane on
How are neurotransmitters released?
Ca2+ dependent exocytosis at the pre-synaptic membrane on DEPOLARIZATION
6** What determines the concentration of neurotransmitter released?
a. Extracellular
** What determines the concentration of neurotransmitter released?
a. Extracellular Ca2+ concentration
7What does the presence of Ca2+ do?
Causes with the . Neurotransmitters than bind to proteins on .
What does the presence of Ca2+ do?
Causes fusion with the presynaptic membrane. Neurotransmitters than bind to proteins on postsynaptic membrane.
8***What are the 3 criteria for neurotransmitter?
1. Must be present in
2. Must be released by
3. receptors must be present
***What are the 3 criteria for neurotransmitter?
1. Must be present in PRESYNAPTIC
2. Must be released by DEPOLARIZATION
3. Specific receptors must be present
9How are small neurotransmitters sent? Large?
Small are packages into small vesicles
Peptides are synthesized in and , dense core vesicles
How are small neurotransmitters sent? Large?
Small are packages into small clear-core vesicles
Peptides are synthesized in ER and packaged into large, dense core vesicles
10What are Ionotropic receptors?
= change in =
What are Ionotropic receptors?
= change in ion conductance = FAST
11What are Metabotropic?
= change in ion conductance using =
What are Metabotropic?
= change in ion conductance using secondary messenger = SLOW
12Types of Ionotropic receptors: Cation channels produce? Anion channels produce?
channels produce fast . produce fast
Types of Ionotropic receptors: Cation channels produce? Anion channels produce?
Cation (+) channels produce fast EPSP. Anion channels (-) produce fast IPSP.
13What is EPSP summation?
a.Neurons add to produce using and summation
What is EPSP summation?
a.Neurons add EPSP to produce depolarization using spatial and temporal summation
14What is a local potential?
a. Result from neurotransmitters binding to receptors that cause a change of charge across
What is a local potential?
a. Result from neurotransmitters binding to receptors that cause a change of charge across post-synaptic membrane
15What are the two outcomes of local potentials? How are the summed?
a. = postsynaptic potential ( )
b. = postsynaptic potential ( )
c. Summed BOTH and
What are the two outcomes of local potentials? How are the summed?
a. Excitatory = postsynaptic potential (EPSP)
b. Inhibitory= postsynaptic potential (IPSP)
c. Summed BOTH spatially and temporally
16EPSP and IPSP are associated with what (depolarization or hyperpolarization)?
a.EPSP = , IPSP =
EPSP and IPSP are associated with what (depolarization or hyperpolarization)?
a.EPSP = depolarization, IPSP = hyperpolzarization
17What do excitatory neurotransmitters do? What do inhibitory neurotransmitters do?
Excitatory = creates , stimulate
Inhibitory = creates , probability that neuron shows
What do excitatory neurotransmitters do? What do inhibitory neurotransmitters do?
Excitatory = creates EPSP, stimulate actional potential
Inhibitory = creates IPSP, reduce probability that neuron shows action potential
18What do glutamate and glycine do?
They stimulate , producing
What do glutamate and glycine do?
They stimulate NMDA, producing EPSP
19What are examples of inhibitory neurotrasmitters?
What are examples of inhibitory neurotrasmitters?
Glycine
20Difference between behavioral vs. neural effects?
Something can inhibit part of the but cause in person’s behavior
Difference between behavioral vs. neural effects?
Something can inhibit part of the brain but cause excitation in person’s behavior
21Where is acetylcholine found? What are the types of receptors? What is it needed for Too much or too little?
a.Found in organs of
b. (excitatory), (excitatory and inhibitory)
c.Excitation or inhibition of , movement of ,
d.Too much =
e.Too little =
Where is acetylcholine found? What are the types of receptors? What is it needed for Too much or too little?
a.Found in organs of autonomic NS
b.Nicotinic (excitatory), Muscarinic (excitatory and inhibitory)
c.Excitation or inhibition of target organs, movement of muscle, learning
d.Too much = muscle contractions
e.Too little = paralysis
22Where is norepinephrine found? What are the two types? What is the effect of too much or too little?
a. Found in , ,
b. and
c. Too much =
d. Too little = u
Where is norepinephrine found? What are the two types? What is the effect of too much or too little?
a. Found in brain, spinal cords, target tissues
b. NE alpha and NE beta
c. Too much = overarousal, mania, cardiac issues
d. Too little = under arousal, depression, cardiac issues
23Where is dopamine found? How many types? Overall effect? Too much? Too little?
a.Found in
b. subtypes
c. EFFECT
d.Too little = disease (give )
Where is dopamine found? How many types? Overall effect? Too much? Too little?
a.Found in brain (substania nigra)
b.5 subtypes
c.Inhibitory EFFECT
d.Too little = Parkinson’s disease (give L-DOPA)
24Where is serotonin (5HT) found? What are the subtypes? Overall effects? Too little? Too much?
a.Found in and
b. AND
c.Too little = and
d.Too much = – which causes , , ,
Where is serotonin (5HT) found? What are the subtypes? Overall effects? Too little? Too much?
a.Found in brain and spinal cord
b.Inhibition AND excitation
c.Too little = depression and sleep disorders
d.Too much = serotonin syndrome – which causes confusion, twitching, trembling, dilated pupils
25What is GABA? What do GABA receptors respond to? What do benzodiazepines mimic? Too much causes? Too little causes?
a. Main neurotransmitters
b. Respond to
c. mimic or act like GABA
d. Too much =
e. Too little =
What is GABA? What do GABA receptors respond to? What do benzodiazepines mimic? Too much causes? Too little causes?
a. Main inhibitory neurotransmitters
b. Respond to alcohol
c. Benzodiazepines mimic or act like GABA
d. Too much = oversedation
e. Too little = anxiety
26What is glutamate? What condition is it significant for? What is its main role in the condition it causes?
a. neurotransmitter
b. Significant role in
c. Disrupts
What is glutamate? What condition is it significant for? What is its main role in the condition it causes?
a. Excitatory neurotransmitter
b. Significant role in schizophrenia
c. Disrupts DA, NE, Ach, 5HT
27What is glycine? How does it function? What prevents its function?
a. neurotransmitter
b. Regulates
c. poisoning
What is glycine? How does it function? What prevents its function?
a. Inhibitory neurotransmitter
b. Regulates motor activity
c. Strychinine poisoning
28What is a neuromodulator? How do they work?
a. Does not directly excite or inhibit neuron
b. They alter response of
What is a neuromodulator? How do they work?
a. Does not directly excite or inhibit postsynaptic neuron
b. They alter response of postsynaptic cells
29What do endorphins do?
Regulate and feeling of
What do endorphins do?
Regulate pain and feeling of reinforcement
30What does substance P do?
a. Involves sensitivity to
What does substance P do?
a. Involves sensitivity to pain
31What does neuropeptide Y do?
a. functions, esp
What does neuropeptide Y do?
a. Metabolic functions, esp eating
32What type of neurotransmitter is nitric oxide? What does it do? What is a clinical example?
a. neurotransmitter
b.Influences release of NT
c. = increases nitric oxides ability to blood vessels
What type of neurotransmitter is nitric oxide? What does it do? What is a clinical example?
a.RETROGRADE neurotransmitter
b.Influences presynaptic release of NT
c.Viagra = increases nitric oxides ability to RELAX blood vessels
33What do neurotransmitters bind to?
receptors called proteins.
What do neurotransmitters bind to?
Postsynaptic receptors called receptor proteins.
34How do neurotransmitters open ion channels?
a. Directly gating ion channels ( receptors)
b.Secondary messengers ( )
How do neurotransmitters open ion channels?
a. Directly gating ion channels (ionotropic receptors)
b.Secondary messengers (metabotropic)
35What are cation channels lined by? What do they allow to enter? What type of transmitters (excitatory or inhibitory) open?
a. Lined by change
b. Allow to enter
c. transmitters open them
What are cation channels lined by? What do they allow to enter? What type of transmitters (excitatory or inhibitory) open?
a. Lined by negative change
b. Allow positive charge to enter
c. Excitatory transmitters open them
36What are anion channels lined by? What do they allow to enter? What type of transmitters (excitatory or inhibitory)open?
a. Lined by charge
b. Allows
c. transmitters close them
What are anion channels lined by? What do they allow to enter? What type of transmitters (excitatory or inhibitory)open?
a. Lined by positive charge
b. Allows negative charge
c. Inhibitory transmitters close them
37What are the 6 ways that neurotransmitter release is manipulated?
a. Change in
b. rate
c. Alters
d. Alters
e. ( inhibitors)
f. Blocks and of receptors (mimics )
What are the 6 ways that neurotransmitter release is manipulated?
a. Change in synthesis
b. Storage rate
c. Alters release
d. Alters reuptake
e. Deactivates (MAO inhibitors)
f. Blocks and prevents attachment of receptors (mimics neurotransmitters)
38What is the structure of a G Protein-Coupled receptor? How does it work? Compared to ligand ion gated channels they are (slower or faster, shorter or longer lasting)
a. Has , , subunit
b. Opens channels, activates enzymes that synthesize
c. and
What is the structure of a G Protein-Coupled receptor? How does it work? Compared to ligand ion gated channels they are (slower or faster, shorter or longer lasting)
a. Has alpha, beta, gamma subunit
b. Opens ion channels, activates enzymes that synthesize secondary messengers
c. Slower and longer lasting
39How do secondary messengers function?
1.Opens or
2. Activation of
3. Activation of one or more
4. Activation of
How do secondary messengers function?
1.Opens channels or long time
2. Activation of cAMP
3. Activation of one or more intracellular enzymes
4. Activation of gene transcription
40How do neurotransmitters get removed from the synapse?
1.
2.
3.
4.
5.
How do neurotransmitters get removed from the synapse?
1. Diffusion
2. Enzymatic degradation
3. Recycling
4. Reuptake by glia
5. Uptake by the postsynaptic neuron
41What are M1 and M3 coupled with?
a.
What are M1 and M3 coupled with?
a. PLC
42What do M1 receptors promote?
Depolarization of (slow )
What do M1 receptors promote?
Depolarization of postganglionic autonomic (slow EPSP)
43What do M3 receptors do (3 things)?
a. Promote contraction of , increase secretion in , production
What do M3 receptors do (3 things)?
a. Promote contraction of smooth muscle, increase secretion in glands, NO production
44What are M2 receptors? What is the clinical correlation?
a. Are a that causes a decrease in , inhibition of voltage gated , and increasing (cause – slow )
b. M2 muscarinic receptors in heart act to
What are M2 receptors? What is the clinical correlation?
a. Are a Ga receptor that causes a decrease in cAMP, inhibition of voltage gated Ca2, and increasing efflux of K+ (cause hyperpolarization – slow IPSP)
b. M2 muscarinic receptors in heart act to slow heart to sinus
45The neuromuscular junction is related to what type of receptor?
a. receptor
The neuromuscular junction is related to what type of receptor?
a. Nicotinic receptor
46What is the effect of a decrease in M1 and M2?
, , and
What is the effect of a decrease in M1 and M2?
Memory confusion, hallucination, and decrease cognition
47What is Myasthenia Gravis? What makes better? Worse? What MOA is impacted? What remains normal and why?
a. Autoimmune disease at where there are antibodies against
b.Worse with , improves with
What is Myasthenia Gravis? What makes better? Worse? What MOA is impacted? What remains normal and why?
a. Autoimmune disease at neuromuscular junction where there are antibodies against acetylcholine
b.Worse with activity, improves with rest
48What MOA is impacted in Myathenia Gravia? What remains normal and why?
a. of : Antibodies against presynaptic voltage-gated prevent acetylcholine release
b. remains normal because it is related to receptor
What MOA is impacted in Myathenia Gravia? What remains normal and why?
a. MOA of Lamber-Eaton: Antibodies against presynaptic voltage-gated calcium channels prevent acetylcholine release
b. Papillary muscle remains normal because it is related to M3 receptor
49What does Beta 1 do? Beta 2?
a.Beta 1 = increased , Beta 2=
What does Beta 1 do? Beta 2?
a.Beta 1 = increased heart rate, Beta 2= bronchodilation