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40 Cards in this Set
- Front
- Back
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contents of cranial nerves
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cranial nerves, spinal nerves
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effectors
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glands, adipocytes, muscles
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interneurons
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20K million, coordinate input and high energy function
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sensory neurons
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10 million, balance, temp, pain
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motor neurons
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0.5 million, muscles, glands, adipocytes
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what are axons and dendrites?
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axons: propagate AP; dendrite: receive signal
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what is soma and synaptic terminals?
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soma: axon and dendrite fxs and large peptide NT created there; synaptic terminal: small peptide NT created and stored there. All NT released there.
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telodendria
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branches at end of axon
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what are unipolar and multipolar neurons common to?
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unipolar: sensory; multipolar: motor and interneurons
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what is an infection of motor nerves and how does it manifest?
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rabies; manifest by sensory nerves (shingles, cold sores)
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what are multiple axons and cell bodies called in CNS and PNS
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axon CNS/PNS: tract/nerve; cell body CNS/PNS: nucleus/ganglia
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what is the name for a mixed nerve
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sciatic nerve
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difference between neurons and neuroglia
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neurons (10%) fx cells, neuroglia (90%): supporting cells - fx with CSF
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definition of synapse? give quantity of neurons in brain and synapses per neurons
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junction between 2 cells that propagate an electrical impulse; 100 billion neurons; 100-1000 synapses per neuron
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AA NT are in which nervous system
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Glutamate, Aspartate, Glycine (all CNS)
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AA derivatives are in which nervous system
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GABA (glutamate-CNS), serotonin (tryptophan-CNS), Histamine (CNS/PNS), EPI-CNS/NOR/DOP-CNS (tyrosine)
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which tyrosine derivative is found in the CNS/PNS?
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norepinephrine
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which peptides fall into which nervous system
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opioids (CNS), substance P/neuropeptide Y-most atoms (CNS/PNS)
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what more commonly just neuromodulators
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peptide and gas molecules
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monoamines
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Serotonin, Histamine, Epinephrine, Norepinephrine, Dopamine
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what do noradrenergic and adrenergic neurons release?
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Noradrenergic release noradrenaline and norepinephrine; adrenergic release adrenaline and epinephrine
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basic NT release
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AP activate VG Ca+ channels, Ca2+ in stimulates vesicles stored with NTs to dock and release NTs, NTs drift to receptors
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what is the slowest part of neural signaling
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time needed for Ca2+ influx and vesicle docking. More synapse = slower signal.
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vesicle dysfunction: overstimulation
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black widow spider toxin (latrotoxin); much docking and NT release in PNS: much ACh = rigidity
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vesicle dysfunction: understimulation
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clostridium botulinum bacteria toxin (botulinus toxin) inhibit docking and NT release in PNS: neurons can't release ACh = paralysis
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negative synapse regulation (located on presynaptic membranes)
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enzymes breakdown NTs, reuptake transporters, autoreceptors (negative feedback by released NT)
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negative or positive regulation (located on postsynaptic membranes)
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heteroreceptors - double dipping, infleunce by receptors that bind other molecules.
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AChE
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inactivation of ACh by hydrolysis, postS, degrade 50% b/f rec, other 50% 20mSec after binding. Choline recycled in preS terminal
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inhibitors of AChE
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irreversible = toxins, insecticides, Sarin nerve gas; reversible: meds - Aricept for Alz.
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reuptake transpoters located on presynaptic neuron
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CHT, SERT, NET, DAT
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which reuptake transporter is blocked straterra? paxil?
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NET, SERT
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reuptake transporters located on glial cells
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excitatory amino acid transporters - ex. transport glutamate
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MAO
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inactivate NT by oxidation, preS, degrades monoamines, increase MAO (more NT) = depression, less MAO = rage, maori, depression tx
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COMT
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inactivate NT by methylation, preS/astrocytes, degrade catecholamines, increase COMT = schizo, decrease COMT = agressive/parkinsons tx
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which enzymes can be used to degrade catecholamines?
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COMT and MAO
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autoreceptors
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preS, respond to same NT released by synapse, decrease syn and release of NT
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examples of autoreceptors
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Glutamate: NMDA receptors, NE: alpha 2A or 2C; ACh: muscarinic 2 or 4
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heteroreceptors
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preS that respond to NM, NT, NH by influencing intracellular Ca2+ levels
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presynatic inhibition of heteroreceptors
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GABA can decrease release of ACh, NE can decrease release of ACh, ACh can decrease release of NE
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presynaptic facilitation of heteroreceptors
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serotonin can increase release NTs, ACh release decreased by NE binding to noradrenergic receptors (alpha 2A, 2B or 2C) on cholinergic synapses
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