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What is the difference between neurotransmitters and neuromodulators and hormones?
ex. of neuromodulator?
Which is longer lasting? Which two act at synpase? Do hormones affect neurons?
Neurotransmitters - chemicals released from presynaptic axon terminal that serves as basis of communication between neurons
Neuromodulators - not transmitters, rather affects release of transmitter or response of neuron to transmitter
Hormones - chemicals secreted by endocrine gland (not at synapse) that is transported in blood. Slower and longest-lasting
- Hormones, then neuromodulators. Neuromodulators and neurotransmitters.
In neurotransmitters what are there few of? What are there many of? How are receptors diversified?
- 1. Signals
- 2. Receptors
- 3. Evolutionarily
Define the following:
4. Inverse agonist
- 1. Ligand - molecule that binds to receptor molecules
- 2. Agonist - a substance (drug) that binds receptor molecule initiating response like that of another molecule (NT)
- 3. Antagonist - a molecule (drug) that interferes with or prevents action of NT
- 4. Inverse agonist - a molecule that binds to receptor causing it to do the opposite of what it normally does
What type of hormone is:
9. Hypothalamic releasing hormones
- 1. Ach = quaternary AMINE
- 2. Vasopressin = peptide
- 3. Oxytocin = peptide
- 4. 5. 6. Ne, Ep, dopamine are catecholamines --> monoamines.
- 7 & 8 are indoleamines --> monoamines
- 9. Peptides
Name the quaternary amine we should know?
Name the five monoamines we should know? Which are catecholamines?
What are the peptide hormones we should know? (3)
- 1. Ach
- 2. Catecholamines: NE, Ep, dopamine. Other monoamines: serotonin & melatonin
- 3. Vasopressin (ADH), oxytocin, hypothalamic releasing hormones.
What is the main difference between amine, amino acids, gases VS. neuropeptides/peptides?
No genes encode amines, amino acids, and gases (amino acids are from diet. Gases and amine NTs are synthesized. There are genes for synthesis of gases and amines, but no specific gene for these NTs.
Neuropeptides & peptides --> genes do directly and specifically code for these NTs.
Name pathway of catecholamine synthetic pathway - what does this demonstrate?
What are the two important enzymes? Which is rate-limiting?
Tyrosine --> L-dopa --> Dopamine --> Norepinephrine --> Epinephrine
Demonstrates that these monoamines are synthesized from a substrate - not made from scratch like peptides/neuropeptides.
Tyrosine hydroxylase: Tyrosine --> L-dopa (Rate-limiting!)
Dopamine B-hydroxylase (dopamine --> NE).
Where do epinephrine and norepinephrine play an important role? 2
In the peripheral nervous system (autonomic)
What is the difference between a cell synthesizing NE for release and a cell synthesizing dopamine?
In the second cell, what would you see instead?
A cell synthesizing NE will express both tyrosine hydroxylase and dopamine B-hydroxylase
A cell synthesizing dopamine will only express tyrosine hydroxylase
Enzymes leading to degradation
What is the major NT of the autonomic nervous system?
Which cells are cholinergic? (4) Draw the first few
- 1. Pre-ganglionic cells of sympathetic pathway
- 2. Pre AND 3. Post-ganglionic cells of parasympathetic pathway
- 4. All motor neurons innervating skeletal muscles are cholinergic (peripheral NS)
Where are cholinergic nerve cell bodies located? (2,1) - function?
Where do they project to? (2) - function?
1. Basal forebrain (medial septal nucleus) to hippocampus (memory), cortex, and amygdala.
2. Pedunculopontine --< basal ganglia (coordination of movement) and motor neurons and widespread arousal
What are the two main receptors for Ach?
1. How are they named? What specifically?
2. Ionotropic or metabotropic?
3. Predominant in PNS or CNS?
What receptor works with certain poisons? (2)
1. Two functions
2. Found in?
Nicotinic: nicotine, ionotropic, PNS
Muscarinic - muscarine, metabotropic, CNS.
Nicotinic - works with (1) Botox - cosmetic product smoothing skin by causing paralysis; botulism (damaged cans) causing paralysis & death. Antagonist to Ach.
(2) Curare - antagonist to Ach, blocks nicotinic Ach receptor causing quasi paralysis (poison dart frogs).
What happens when there is widespread loss of cholinergic neurons?
Why does blocking nicotonic receptors cause paralysis?
Because it blocks projection to basal ganglia/motor neurons which are important for movement.
What are the two major pathways of dopamine?
and what is each pathway associated with? 1-1
Which is associated with schizophrenia? When?
Are these ascending or descending projections?
1. Mesostriatal: substantia nigra (midbrain - mesencephalon) --< striatum in basal ganglia.
2. ventral tegmental area (VTA)
-------< limbic system (nucleus accumbens - reward), amygdala, hippocampus
------< cortex (frontal lobe, emotional responses, decision making)
Excess dopamine causes schizophrenia due to mesolimbocortical system.
Why is substantia nigra called that?
Because it contains melanin (dark pigment) found in primates
Which dopaminergic system projects to more places?
mesolimbicocortical (projects to nucleus accumbens, amygala, hippocampus, frontal lobe) vs. mesostriatal which only goes to striatum (basal ganglia)
What are the receptors of dopamine? (5)
Are these receptors metabotropic or ionotropic?
Through what mechanism do these receptors work through?
What are the two classes? Which receptors belong in which class? (2,3) and how do they affect cAMP?
Metabotropic - secondary messenger
D1-like (D1, D5) and D2 like (D2,3,4).
D1-like increases cAMP activity while D2-like decreases cAMP activity
What causes Parkinson's disease? What can't they produce? What are the two causal factors?
Treatment? How does it work? What is the problem with this? What can excess treatment cause and through which pathway?
Cells in substantia nigra die, damaging the the mesostriatal dopaminergic pathway (substantia nigra can't project to striatum). Can't produce L-dopa.
Genetics and environment.
L-dopa is the precursor to dopamine, allowing cells in substantia nigra to keep trying to make dopamine to project to the striatum.
The problem is that it can only stimulate live cells to create dopamine - if most cells are dead, will be limited.
Schizophrenic results through mesolimbocortical pathway
1. What happened with the frozen addicts?
2. What did the bad heroine contain?
3. What did it interact with? In which cells? What did it produce?
4. How did this toxin affect the dopaminergic system?
5. What does this tell us? How did this same rxn affect rats?
- 1. Bad heroine batch made young adults come in with Parkinsons-like symptoms
- 2. MPTP (contaminant)
- 3. Combined with MAO (monoamine oxidase - degrades monoamines) in monoaminergic cells producing MPP+
- 4. Melanin caused MPP+ concentrated in cells causing mesostriatal system to degrade.
- 5. Tells us that mesostriatal system is susceptible to environmental toxins. Rats only had transitory effects.
How does cocaine affect reward/addiction? (1) In what pathway? Amphetamines? (3)
Which drug causes faster tolerance? Through what mechanism?
1. Both cocaine and amphetamines affect mesolimbocortical system (VTA --< nucleus accumbens - reward system).
- 2. Cocaine blocks monoamine transporters (reuptake) that remove dopamine from synapse
- 3. Amphetamines block reuptake of dopamine, decrease degradation and increase release of dopamines (all catecholamines)
- 4. Amphetamines cause faster tolerance, but both decrease the number of postsynaptic receptors.
Draw the sources of norepinephrine (2) and their projections (6)
What are the functions of this? (2)
Arousal and contact-dependent sensory responses
Ach (peduculopontine also leads to widespread arousal)
1. What are the receptors for norepinephrine? (4)
2. Are they ionotropic or metabotropic?
3. What is a common drug that affects NE receptors?
- 1. A1,2 and B1,2
- 2. Metabotropic (and highly specific)
- 3. Caffeine
1. How does pre-synaptic cell detect amount of NT released?
2. What drug competes with noradregenic receptors? How?
3. Define drug tolerance in equation form. What is the most important part?
- 1. Negative feedback: autoreceptors bind to adenosine (NT) released. Increased binding decreases secretion.
- 2. Caffeine binds to autoreceptors on pre-synaptic cell, so less NT binds, so cell think its producing less than it actually is, increasing NE released.
- 3. Drug tolerance = upregulation of autoreceptors and downregulation of post-synaptic receptors (esp this downregulation part).
1. What is the shorthand name for serotonin?
2. Where is it produced? Where does it project to? What four areas specifically
3. What's important to note about its source?
4. Why is this system difficult to target pharmacologically?
- 1. 5HT
- 2. Raphe Nuclei (reticular formation) ----< everywhere, affecting everything - namely thalamus, hypothalamus, basal ganglia and cortex.
- 3. The raphe nuclei are part of the reticular formation, so important for arousal, sleep and rhythms.
- 4. because it has lots of targets and receptors - has at least 15 type of receptors mostly metabotropic including autoreceptors with both inhibitory and excitatory effects
How do SSRIs work?
Prozac - increases serotonin concentration in synapse.
But it takes 2-3 weeks to see effect on depression even though serotonin reuptake is affected immediately.
What type of NT is glutamate?
2. What are its two types of receptors? Describe their characteristics and what ions they bind to.
3. When will the second type open? Under what conditions? What is it important for activating? What does this affect? What is the ultimate change?
- 1. Amino acid
- 2. AMPA (ligand-gated - Na+) and NMDA (ligand and voltage gated Ca2+)
- 3. When Mg2+ is bound AND membrane potential exceeds level of depolarization (usually under a lot of glutamate release and opened AMPA receptors) --> lots of depolarization, causing MG2+ to discharge. Mg2+ is blocking channel.
Because of its trait and because its permeable to calcium, NMDA receptor can activate secondary messenger cascade (Ca2+=secondary messenger) --> genomic action potential
--> learning & neuron plasticity.
What are diseases associated with glutamate systems? Specific term?
What drug acts through GABA receptors? How?
- 1. Seizures due to overactivity of glutamate synapses.
- 2. Excitatoxicity - result of overactivity of glutamate receptors --> brain damage.
Valium - inhibits overall action of nervous system --> calms anxiety
Describe characteristics of GABA receptors?
1. Ionotropic vs. metabotropic//excitatory vs. inhibitory
2. Impact which type of channels?
3. What is special about this?
- 1. Both ionotropic and metabotropic; inhibitory
- 2. Impact Cl- channels
- 3. Produced by 5 subunits - cell can then mix and match subunits to create large number of receptor types with variable impacts on post-synaptic cell.
How do receptors for glutamate and GABA differ?
1. Glutamate has excitatory effect on post-synaptic cell, while GABA is inhibitory.
Both can be ionotropic - glutamate works with Na+ and Ca2+, while GABA receptors works with Cl-.
1. What are the two important peptide NTs we're talking about?
2. What's similar about these? How do we know? (2)
3. Where are they produced? What actions do they have? (2)
4. What type of receptors do they use? What impacts do they have at post-synaptic cells?
- 1. Oxytocin and vasopressin
- 2. Evolutionarily related - both 9 AAs long with only one substitution.
- 3. Hypothalamic cells - hormone actions when released in blood and NT activity when released at synapses.
- 4. metabotropic - variety of impacts
What is the function of oxytocin? (1-3, 2-2)
What is the function of vasopressin? (1-1, 2-2)
What receptors are implicated in runner's high?
1. Smooth muscle contraction (uterus during childbirth, milk letdown during lactation, orgasm) and social behaviors (social memory and pairbonding)
2. Increases BP when released in blood supply, social behavior (aggression and pair bonding)