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122 Cards in this Set
- Front
- Back
Neurotransmitters: 3
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- do not get into blood
- act locally - can act as hormones/paracrines |
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Types of neurotransmitters based on structure: 7
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AcH
Monoamines Peptides Nitric Oxide ATP Carbon Dioxide Endocannaniulus |
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AcH is found in ______ and ______ between __________.
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AcH is found in CNS and PNS
between neuron and skeletal muscle, cardiac muscle and smooth muscle |
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Recepetors: 2
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Nicotene and Muscorine
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Nicotene and Muscorine are both ___________.
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isoforms of acH
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Nicotene receptor:
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gated (FAST)
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Muscorine receptor:
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G-protein (SLOW)
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Monoamines examples:
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Dopamine
Norepinephrine Epinephrin Histamine Serotonin |
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Catecholamines: 3
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Dopamine
Epinephrin Norepinephrin |
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Nitric Oxide:
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neurons can use NO as transmission
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Monoamines are synthesized from _______.
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precursor amino acids
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Monoamine example: 1. Serotonin precursor is _______.
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Tryptodin
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Serotonin is mostly synthesized where?
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outside of the CNS
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Serotonin is manufactured in the ________.
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Placenta
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Serotonin plays an important role in _______ and ______.
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Brain formation and synapses
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Serotonin can effect ________cells.
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Bone cells (osteoclasts and osteoblasts)
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Serotonin effects ______.
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sleep rhythms
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Day with ______ serotonin
Night with _______ serotonin |
Day HIGH
Night low |
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Nacrolepsy
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glitch in serotonin causes sleep paralysis
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Low levels of serotonin can contribute to _______.
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Abnormal pregnancy
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Abnormal pregnancies effected by serotonin low levels such as ______.
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SIDS
Irritable Bowel Syndrome Retardation |
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Serotonin as ____ receptors.
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15 --> all isoforms of serotonin
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Low levels of serotonin in synapse in : 5 conditions
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OCD
PMS SAD- seasonally associated depression Bipolar Panic disorders |
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What medications can increase serotonin levels?
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Prozac, Zoloft (reuptake)
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LSD acts as an ________ to serotonin because:
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LSD acts as an ANTAGONIST to serotonin because of hallucinogens that can eradicate(destroy) bad memories
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Monoamine example 2: Dopamine is metabolized by
___ to ____ to _____ to _____ and _____. |
tryposine -> doper-> DOPAMINE = epi + norepinephrin
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Dopamine relations:
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Schizophrenia
Reward muscle Parkinson's disorder Tourette's syndrome Alcholism Passage of Time Stuttering |
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Schizophrenia have ______ levels of dopamine.
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HIGH
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In Schizophrenia, the _________ are enlarged in the brain.
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Lateral ventricles
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Schizophrenia Tx: 2
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electroshock therapy
insulin shock therapy |
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Reward muscle is apart of what system? and where?
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Limbic system in dopanergic synapses
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Rewards muscle is:
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euphoric naturally reward for body giving off a high effect.
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In addictions, dopamine levels are _______ in limbic system.
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elevated
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ex of reward muscle drug
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Cocaine
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What happens with cocaine?
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Nucleus circumlens blocks synaptic fiber so dopamine can linger in synapse instead of being taken up resulting in a high
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However, with cocaine, neuron begins to produce dampening protein called ______.
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dynorphin
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Dynorphin produces to:
resulting in: |
reduce euphoric feelings making dosage of drug needed to increase to get high
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What releases dynorphin?
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CREB and Delta FosB
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Parkinson's disorder is due to gradual diminishment in _____ and _____.
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Brain and basal ganglia
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Parkinsons effects the :
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pathways from ganglia
o----< dopamine released: BASAL GANGLIA ---> l l (pathways) |
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Parkinsons TX
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replacement therapy but not with dopamine bc its too large to pass blood brain barrier therefore give doper
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Tourette's syndrome
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too many dopamine receptors
motor signals cannot be controlled in the descending pathways |
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alcholism
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too many dopamine receptors?
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Histamine precursor is _____
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histadine
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histamine works in which system?
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CNS and PNS
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Histamine in CNS:
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controls sleep
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Histamine in PNS:
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found in mast cells contributing to allergic reactions
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endocannabinoids effect: 3
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basal ganglia, cerebral cortex in cerebullum and hippocampus
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endocnnabinoids block:
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target neuron cells of cyclic-AMP 2nd msgers
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NT of endocannabinoids: 2
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Anandamide
2-arachidonyl glycerol |
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both NT bind to ____ and ____ receptors
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CB1 and CB2
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CB1
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neurons (g-protein)
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CB2
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immune and glial cells
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DSI (endocannabinoids)
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Depolarization Induced Supression Inhibition
-Neuron is turned off by inducing IPSP ex: GABA(IPSP) binds to receptor and is not inhibited. -excitatory transmittor comes in as GLUTAMATE and will bind to receptor causing depolarization bc of influx of Ca2+ (2nd msg) -Ca2+ will trigger release of endocannabinoids -Endo will then go back to CB1 on inhibitory neuron turning it on --> it stimulates the pre-synaptic ce;; turning it on |
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Amino acid NT:
a) inhibitory: 2 b) excitatory: 1 |
inhibitory: glycerin and GABA
excitatory: glutamate |
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GABAnergic synapse will yield a IPSP=
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hyperpolarization
meaning outside becomes more + than inside |
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Glial cells can communicate by using ____
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ATP
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How is nitric oxide used in communication?
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hemoglobin binds NO and when releasing allows blood vessels to dilate
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Argenine is what kind of transmission?
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retrograde transmission
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Nitric Oxide process
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-glutamate released and diffused across cleft. Binds to receptor on post synaptic cell
-non-NMDA and NMDA allow Ca2+ and Na+ ions leading to depolarization -Ca2+ acts as 2nd msger binding Calmoudin activating kinase to phosphorylate turning on enzyme: Nitric Oxide synthase -Nitric Oxide synthase generates NO -Argenine is generated then making NO go backwards (retrograde-LTP) |
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Argenine makes more _____ to be released from pre-synaptic cell
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glutamate
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Peptides
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cleaves large protein into seperate units
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What effects synaptic transmission?
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drugs
antagonist/agonist toxins autoimmune problems neuromodulators |
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Hebb's rule
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the ability to learn is based on synapse formation
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to increase synaptic strength=
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increase + of receptors on post synaptic cell
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How to increase # of proteins?
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genes must be activated specifically
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Physiology of receptor can be modified by ______
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phosphorylation
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How to turn genes on to affect gene expression and activation?
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-Ca2+ immobilized by NMDA receptors that can phosphorylate the Kreb (transcription factor) to get into the genome and modify genes
-cAMP activates Kinase that will phosphorylate and go to genome -PPI system -LTP |
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Which 2 proteins play a role in synaptic strength?
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alpha- synnuclein
thrombospondin |
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multinucleated name in myofibril?
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syncitium
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thin filament composed of
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actin
troponin/tropomyosin |
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skeletal proteins function as structure?
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connectins
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Why is the A band dark?(anysotropic)
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when polarized light interferes it becomes dark bc of large interference
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elastic proteins functioning as rebound for contraction and relaxation
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titin
nebulin |
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What is Ca2+ binding to while waiting(inactive) in the sarcoplasmin reticulum?
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Calciquestrin
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Binding site for Ca2+?
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troponin
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Myosin binds to ______ physically for contraction
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actin
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____ and ____ is needed for contraction
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ATP
ATPase linkage |
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What triggers sliding?
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Cell is stimulated with action potential and will release Ca2+ from SER
Ca2+ then binds to tropomysosin complex exposing actin to mysoin head ATP is split by ATPase releasing energy allowing for sliding. |
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ATP role in skeletal muscle 3
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-pumps SERCA relies on ATP
-detaches mylin crossbridge -sliding |
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rigor mortis
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crossbridges cannot break Ca2+ to relax
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EPP
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end plate potential
AP on endplate that is strong enough for AP to occur |
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EPP is ______ potential
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graded
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tetanic paralysis cannot move bc of ___ present and constant ______
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AcH and constant contraction
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______ breaks down AcH to relax muscle.
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Ach-esterase
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Curare causes _____ paralysis at ______
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flaccid paralysis at neuromuscular junctions
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Curare acts an an ______to the _______ receptor not allowing for AcH to bind causing relaxation
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antagonist
nicotene receptor |
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organophosphates ex: 2
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pesticides and mustard gas
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organophosphates cause ______ paralysis
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tetanic
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autoimmune disorder: eaton-lambert syndrome
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destroyed AcH receptor not allowing contraction
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autoimmune disorder: Mysathenia gravis
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destruction of nicotene receptors, fatal
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contraction definition:
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active force generated by muscles to convert chemical energy(ATP) to mechanical energy
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tension
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force of contraction exerted on an object
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load condition
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weight/mass as opposing force
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iosotonic contraction
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force of object allowing it to move by shortening muscle (can physically see it)
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iosmetric contraction
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muscles will not appear to change bc of load being too big
can see on molecular level |
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What determines the force muscle to contract? 3
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-# of contracting muscle fibers
-diameter of fiber -exercising muscle |
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What occurs during tetanus?
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Prolonged contraction period to a maximum resulting in fatigue
-Ca2+ increases: Ca2+ is surged out of SER bc Ca2+ did not have time to go back and relax resulting in pool of Ca2+ and more open binding sites for contraction. |
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Forced fatigue at level of muscles because of build up of _________
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lactic acid
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Lactic acid will _____ the pH of the cell
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lower
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primary energy source of muscle is ______
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glucose
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Fatigue reasons: 3
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-build up of lactic acid
-build up of K+ ion outside -build up of phosphorylate on inside |
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Why is the tension and length in difference?
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Crossbridge formation needs to be increased to increase the tension
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Stretching before exercise allows for maximum _______, _____ and _______
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crossbridges
tension and bindind sites |
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How is tension controlled in a muscle organ?
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-# of muscle fibers that are contracting
-increasing the degree of tension exerted by each muscle fiber that is contracting |
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How can # of muscle fibers in muscle control tension?
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-Motor units recruitment--> the more activated will cause more contraction
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How can tension of organ be increased on those cells that are contracting?
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-stretching
-summation |
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Muscle energy flow from:
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creatine phos to ADP to creatine kinase to creatine to ATP
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Muscle relies on other sources of energy once its exahisted such as :2
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oxidative phosphorylation
glycolysis |
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hypocalcemic tetany
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tetany that results from abnormally low calcium
-nerve will fire prematurely because Ca2+ levels are low |
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example of genetic anticipation disorder?
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myotonic dystrophy
gets worse passed on through generation bc gene enlarges |
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multiple sclerosis
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dymyelinates- velocity of conduction is slowed down
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What therapy can slow down MS?
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beta seron (betainteferon) therapy
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tx for myasthenia gravis?
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thymusectomy
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Poliomyelitis
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disease caused by RNA virus destroying neurons by motor end plate travelling up axon and destroyinh cyton
salt vaccine (1957) |
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SMA (spinal muscular atrophy)
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lack of protein made to connect muscle to spine
child loses posture, function of legs, vocal problems |
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SMA defected gene
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SMN2- multiple copies
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smooth muscle is controlled by the _______ nervous system
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autonomic
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Smooth muscle difference btw skeletal muscle
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-SER not as developed
-some smooth cells are myogenic(spontaneously depolarize and contracts on its own) -proteins: Calponin and Caldezmin Dezmin and Bimentin -No neuromuscular junctions -No end plate -No t-tubule |
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Autonomic Innervation with sympatethic is what NT?
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norepinephrine
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Autonomic Innervation with parasympatethic is what NT?
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AcH
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______are swellings where NTs are released.
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varicosities
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