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Ionotropic (Directly-Gated) channel
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binding of neurotransmitter causes conformational change in proteins, opening up the channel-fast synaptic responses
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K channels
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4 polypeptides, each with 6 membrane-spanning segments -S4 segment is voltage-sensitive-S5 and S6 are connected by hydrophobic region called a pore loop, which determines the K specificity -blocked by TEA and 4-aminopyridine
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spatial summation
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arrival of multiple signals at the trigger zone at the same time
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slow anterograde transport
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0.5-5 mm/day-for soluble proteins
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multiple sclerosis
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-women more than men, usually between 20-40-unknown cause-affects white matter of cerebellum, spinal cord, corticospinal tract projections and basal ganglia-autoimmune demyelination (and degeneration)sx: numbness and weakness in limbs, often unilateral; visual loss or other sx; tremors, ataxia; fatigue, dizzinesstx: symptomatic, but no cure
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voltage-gated Na channel
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long polypeptide with four domains, each containing 6 membrane-spanning helices (S1-S6)-S4 segment is voltage-sensitive-S5 and S6 are connected by hydrophobic region called a pore loop, which determines the Na specificity - can be blocked by tetrodoxin and local anesthetics (lidocaine) which bind to the outside pore of the channel
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fast anterograde transport
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100-400 mm/day-depends on microtubules and requires kinesin-moves propeptides
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Inhibitory post synaptic potentials
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inhibitory signals caused by GABA or glycine in CNS
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endocytotic budding process
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-retrieves synaptic vesicle membrane after NT release
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terminal boutons
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overlie the motor end plate, which contains the postsynaptic junctional folds and has nicotinic cholinergic receptors (ionotropic), which are Ach-sensitive
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acetylcholinesterase
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inactivates Ach present in synapse so that receptors don't stay open too long-made in neuron and transported to synapse by axonal microtubules
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synaptotagmin
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protein on vesicle membrane-binds with Ca can causes the vesicle membrane to fuse with the presyn terminal membrane
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clear-core vesicles
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package for small molecule neurotransmitters
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chemical synaptic transmission
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action potential reaches presynaptic area and stimulates the release of vesicles containing neurotransmitters into active zones of the presynaptic terminal
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cholestrum toxins
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botulism and tetanus-affect NT release by disabling vesicle fusion with membrane, so prevents release
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neuropeptide neurotransmitter synthesis
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-necessary enzymes synthesized in RER-neuropeptide NTs synthesized as pre-propeptides in cell body-packaged into vesicles as propeptides along with enzymes and moved to axon terminal by fast axonal transport on the microtubules via motor proteins (kinesins, require ATP)-converted to neuropeptides (instead of pro) at terminal and packed into dense-core vesicles-inactivated by degradation in cleft, NOT reuptaken
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rectifying synapse
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current can go in only one direction
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dense-core vesicles
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house only two small molecule neurotransmitters- norepi and serotoninpackage for neuropeptide NTs
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Lambert Eaton Syndrome
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-assoc. with small cell carcinoma lof lungs, which contain voltage-gated channels - body develops antibodies against these- these antibodies are also active against Ca channels in presynaptic membranes of NMJ - so less Ca in, and so less Ach releasedsx: autonomic sx and muscle weaknesstx: increase Ach release; exercise is good bc increases amount of Ach released bc more needed
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small molecule neurotransmitter synthesis
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-enzymes synthesized in the neuronal cell body and transported via cytoskeleton to axon terminal-precursors are taken up by presyn terminal from the syn cleft-synthesized and stored in small vesicles until action potential in nerve terminal leads to Ca influx and exocytosis-inactivated by degradation or reuptake by presyn terminal
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Charcot-Marie-Tooth Disease
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demyelination (and thus degeneration) of Schwann cells in peripheral nervous systemsx: hyporeflexia, foot weakness, foot drop, neuropathic pain
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Excitatory post synaptic potentials
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excitatory signals caused by glutamate in CNS-make membrane potential more positive (bringing closer to threshold for AP)
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Acetylcholine
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common small molecule, excitatory NT in CNS and PNSsynthesis:-glc is taken into terminal by faciliated diffusion, eventually forms acetyl CoA-choline is transported from synaptic cleftcholine and acetylCoA combine and ACH is stored in vesicles removal:-AChE in synaptic cleft hydrolyzes into componentslocation:-found in basal forebrain (basal nucles of Meynert) - Ach involved in learning and memory-found in dorsolateral tegmentum of pons- Ach involved in forebrain activity during cycles of sleep and wakefulness
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Neuromuscular junction
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consists of the terminal portion of the motor neuron, which has lost its myelin sheath and gives off many branches, which have terminal boutons and contains Ach
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Myasthenia Gravis
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autoimmune disease which causes decreased amount of nicotinic ACh receptors at postsyn membrane of NMJ-muscle weakness, eye muscle weaknesstx: rest (NOT exercise); drugs to reduce AChE activity (to increase ACh) ex: neostigmine
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non-rectifying synapse
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charge can pass bidirectionally
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Metabotropic (Indirectly-Gated) channel
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neurotransmitter receptor and ion channel are separate-requires 2nd messengers (uses G proteins)-slower response system
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electrical synaptic transmission
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rare; only for synchronous activation of neurons-occurs via gap junctions between neurons, which allow charge to spread quickly from one neuron to the next
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fast retrograde transport
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50-200 mm/day-from axon terminal to cell body-moves vesicle membrane recovered from cleft-can carry nerve growth factors back to the CNS to stimulate nerve growth-many viral diseases also use this
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End plate potential (EPP) magnitude
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determined by:1) #EPPs 2) probability of channels opening 3) conductance of each open channel 4) driving force of the ions-overall, higher current for Na, so depolarization occurs and AP occurs, which gets propagated along muscle, causing contraction
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temporal summation
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arrival of multiple signals at the trigger zone at different times
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Synaptobrevin and syntaxin
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proteins associated with vesicles and presyn terminal membrane, respectively-form a complex that brings the two structures close togethers
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Guillain-Barre Syndrome
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inflammatory demyelinating disease of PNS-can progess rapidly-sx: ascending motor and sensory losses affecting limbs, face, trunk, and/or diaphragm; absent reflex arcs of deep tendon reflexes (arcflexia)-tx: gamma globulins to prevent antibodies from attaching
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when a nerve impulse reaches the boutons...
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it depolarizes their membrane, opening Ca channels-the Ca influx promotes fusion of Ach vesicles with the membrane and Ach released into cleft-Ach acts on nicotinic receptors, opening the channel (Na and K permeable), causes a current (EPP)
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graded potentials
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produced when a neuron is stimulated in CNS-brief local changes in membrane potential that occur in neuronal dendrites and cell bodies, but not in axons (which only carry APs)-travel through cell body to the trigger zone (axon hillock in efferents), where if they are strong enough to reach the threshold, they generate an AP...otherwise they do nothing
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