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