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33 Cards in this Set
- Front
- Back
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Brain stem
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regulates vital functions
site of action for barbituates |
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Cerebellum
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controls movement and posture
site of action for ethyl alcohol |
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Hypothalamus
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integrates involuntary nervous system (eat, sleep, temp, emotion, sex)
limbic system controls emotion/reward |
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Subthalamus
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a motor system
dopamine deficient region in Parkinson's |
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Lobes of the cerebral cortex
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frontal- conscious thought
parietal- body sensations temporal- touch/smell occipital- vision |
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Steps of synaptic transmission
Synthesis/vesicle loading |
1. production of NTs from precursors
2. loading of NTs into vesicles 3. quality control (degrade NTs that aren't in vesicles) |
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Steps of synaptic transmission
Vesicle fusion/receptor binding |
1. AP causes vesicle fusion
2. negative feedback on presynaptic neuron 3. NTs bind to postsynaptic receptors |
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Steps of synaptic transmission
Termination of transmission |
NT reuptake or breakdown
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4 common targets of neuroactive drugs
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ion channels (ionotropic)- open pore
g-protein coupled (metabotropic)- second messenger carrier/transporter- pump against [gradient] enzymes- involved in breakdown of NT |
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Properties of receptor-ligand interactions
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molecular switch- conformational change
reversible binding modulated signal intensity (# and time bound) specificity |
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What are NTs?
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- synthesized in neurons
- present & release from presynaptic neuron - exogenous application mimics normal action - have specific mechanisms for removal |
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Pyramidal system
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controls VOLUNTARY motor movements
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Extrapyramidal system
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controls INVOLUNTARY motor movements
includes cerebellum and corpus striatum |
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Cerebellum
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organizes muscle contractions into useful sequences
problems w/ it cause inability to walk in straight line |
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Corpus striatum
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AKA basal ganglia
highest level of organization in extrapyramidal system |
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Parkinsonism
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neurodegenerative disease associated with hypodopamanergic state caused by loss of DA neurons in substantia nigra
DA falls to 20% of norm, lose 80-90% of DA neurons in SN |
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Clinical symptoms of Parkinsonism
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bradykinesia- slowness of movement
muscle rigidity- (cogwheel) jerkiness resting tremor- (pill rolling) stops during voluntary movements impaired postural balance |
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Goals of therapy
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increase DA levels
DA agonist block DA metabolism prevent DA neurons from dying |
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What crosses BBB?
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small lipid-soluble nonpolar molecules
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Levodopa
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precursor to dopamine
administered orally and rapidly absorbed/converted to dopamine (1-5% of dose crosses BBB) 95% converted to dopamine peripherally, causes nausea & orthostatic hypotension |
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COMT
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catechol-O-methyltransferase
converts levodopa, dopamine and DOPAC to inactive metabolites |
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AAD
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aromatic L-amino acid decarboxylase
converts levodopa to dopamine |
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MAO-B
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monoamine oxidase type B
breaks down dopamine into DOPAC |
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Carbidopa
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inhibits AAD
can't cross BBB so reduces peripheral DA by 75%, reducing side effects but keeping CNS function |
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Sinemet
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levodopa + carbidopa
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Tolcapone
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COMT inhibitor
crosses BBB, acts centrally and peripherally to decrease breakdown of levodopa enhances effects of levodopa and reduces 'wearing off' phenomenon |
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Entacapone
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COMT inhibitor
doesn't cross BBB, acts peripherally to decrease breakdown of levodopa enhances effects of levodopa and reduces 'wearing off' phenomenon |
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'Wearing off' phenomenon
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initially, levodopa has a strong effect, over time, the effect decreases and symptoms fluctuate dramatically between doses (levodopa has short 1/2 life)
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Ways to stop 'wearing off' phenomenon
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increase dose of levodopa
decrease time between doses add COMT inhibitor use SR Sinemet |
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Adverse effects of levodopa
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metabolism of levodopa produces free radicals which can cause death of DA neurons
?if oxidative stress kills neurons, neuroprotective drugs could be more helpful in preventing disease? |
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Pramipexole and Ropinirole
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DA receptor agonists
don't depend on DA producing neurons useful in early stages b/c of less damage useful in late stages b/c don't require dopamine have high affinity for D3 receptors and less 'wearing off' than levodopa side effect of falling asleep at the wheel |
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Selegiline
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MAO-B inhibitor, keeping dopamine levels high
has neuroprotective effect, use early metabolized to amphetamine (CNS stimulant) which increases DA release |
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Non-pharm Parkinson's treatments
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prevent cell death in SN
- surgical electrode placement - gene transfer techniques (GDNF) important b/c of reduced drug effect over time |
