________ and Botox are paralytics bc they block the ability of ACh to bind to the muscle- antagonists.
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Alzheimers Disease
________- shrinkage in the hippocampus, tau protein chains start to disintegrate and break, neurons die or retract; plaque forming in synapse makes it hard for ACh and glutamate.
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lipid solubility
Some ________- pretty much everything has to have an active transport system (glucose, amino acids, vitamins, hormones)
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loss of coordination
Alcohol (agonist)- ________ and balance (cerebellum)
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external environment
Autoreceptors:: a way of giving feedback to the neuron about the status of the ________; guides overall production in Cell A.
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Axons of motor neurons
________ synapse onto receptor proteins that form clusters on various muscles throughout the body.
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Nicotine
________- agonist, causing brain fog because ACh receptors are being removed.
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Therapeutic Index
________ (TI):: difference between ED and LD can have wide or narrow variability.
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Parkinsons
________- tremors, inability to initiate movement, DA neurons in substantia nigra are dying and cant stimulate the basal ganglia in the mesostriatal pathway- treat w /a dopamine agonist (L- Dopa)
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Tryptophan
________:: essential amino acid (foods high in protein- wild game, seeds /nuts, cheeses, seafood /fish, meat)
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Diffusion
________- they float away where they have no effect (automatic)
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Acetylcholine
________ works on skeletal muscles, tissue, internal organs.
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Schizophrenia
________- delusions and hallucinations, flight of ideas, disorganized behavior, overstimulation of dopamine in mesolimbocortical pathway- treat w /a dopamine antagonist (anti- psychotics)
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release
Blocking ________ interferes w /ability of presynaptic cell to affect postsynaptic cell.
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THC
________- pain relief, lower BP, relief of nausea, decreased eye pressure in glaucoma, immunosuppressive actions (Schedule I drug)
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Glial cell help
________- astrocytes pull excess NTs and safely give to cell A.
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Wellbutrin
________- dopamine reuptake inhibitor, helps people w /depression.
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Agonists
________:: increase effectiveness of the NT targeted.
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Phenylanine
________ and tyrosine part of our diet- essential amino acid, foods high in protein (soy based products, eggs, nuts /seeds, seafood, meat)
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Some lipid solubility
pretty much everything has to have an active transport system (glucose, amino acids, vitamins, hormones)
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Circumventricular organs
not protected by the BBB
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Area postrema
neg
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molecules coming into brain and brain stem
the first poison detection center, causes vomiting/diarrhea
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Glucose, lactate, acetate
brain uses more sugar than any cells/organs
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1st NT discovered by Otto Loewi (1921)
acetylcholine using frog hearts
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Ionotropic receptors
open ion channels
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Metabotropic receptors
2nd mess, metabolic change occurs
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Slow, long lasting (30ms
s, m, etc.)
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Autoreceptors
a way of giving feedback to the neuron about the status of the external environment; guides overall production in Cell A
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Diffusion
they float away where they have no effect (automatic)
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Degradation
degrade/fall apart over time (automatic)
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Transporters (reuptake)
presynaptic, reabsorb the NT and recycle it so it can be used again
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Glial cell help
astrocytes pull excess NTs and safely give to cell A
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Type I
excitatory
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Type II
inhibitory
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PSD
pre or post synaptic density
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Agonists
increase effectiveness of the NT targeted
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Antagonists
decrease effectiveness of the NT targeted
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Pharmacologists need to know Effective Dose of potential drugs
start w/animal models
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Therapeutic Index (TI)
difference between ED and LD can have wide or narrow variability
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GABA
gamma-aminobutyric acid
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Alcohol (agonist)
loss of coordination and balance (cerebellum)
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Makes GABA
in every cell in our body, but very specialized in neurons
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Alcohol (antagonist)
loss of memories (hippocampus), poor decisions (PFC)
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If turned up too high, can become neurotoxic
kills other neurons
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Acetylcholine (ACh)
highly tied to learning and memory (hippocampus and basal ganglia); fast acting at the neurotransmitter junction and degrades very quickly
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Acetylcholinesterase (AChE)
enzyme, breaks down ACh
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Curare, Botex, Sarin/Soman/Tabun
neuromuscular junction
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Curare and Botox are paralytics bc they block the ability of ACh to bind to the muscle
antagonists
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Sarin/Soman/Tabun
nerve gases and AChE-I agonists
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Nicotine
agonist, causing brain fog because ACh receptors are being removed
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Alzheimers Disease
shrinkage in the hippocampus, tau protein chains start to disintegrate and break, neurons die or retract; plaque forming in synapse makes it hard for ACh and glutamate
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Monoamine NTs
Catecholamines
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Cocaine, methylphenidate
dopamine agonists and block reuptake
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Adderall, amphetamines
dopamine agonists and increase release of DA
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MDMA
at low doses releases DA
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Wellbutrin
dopamine reuptake inhibitor, helps people w/depression
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SNRIs (Effexor, Remeron, Cymbalta, Meridia)
good for mild/mod depression
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Mainly in body, small amounts in brain
aka "adrenaline rush"
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Phenylanine and tyrosine part of our diet
essential amino acid, foods high in protein (soy based products, eggs, nuts/seeds, seafood, meat)
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Monoamine NTs
Indoleamines
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SSRIs
Prozac, Paxil, Lexapro, Celexa, Zoloft
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Ecstasy
MDMA
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Opioid receptor activation
inhabit VTA GABA neurons and increase DA activity
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THC
pain relief, lower BP, relief of nausea, decreased eye pressure in glaucoma, immunosuppressive actions (Schedule I drug)