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204 Cards in this Set

  • Front
  • Back

galvani

concluded that animal musles have electricity

conductor

channels/carriers ion pass through

capacitor

lipid bilayer preventing ions from passing (batter)

Vm

voltage=seperation of charge

charge made by movement of

potassium ions down conc gradient, while other ions stay similar

equilibrium potencial

equilibrium between electrical and conc gradient


(electrical potencial away from equilibrium)

nerst equation

equation for equilibrium potencial


E(x)=(58/2)log(Xo/Xi)


in mV


z=charge of ion (Na and k are +1 while Cl is-1)


x=conc outside and inside

E(Na), E(K), E(Cl)

Na=+58mv, K=-75mV, Cl=-59

Vm vs Ex

Vm is avg Ex of Na, Cl, K, with permeability wieghing some of them more

goldman equation

p=permeability, and concentration inside and outside


Vm=58log(PkKo+PNaNao+PClCli/PKKI+PNaNai+PclClo

inc permeability of one anion

Ex gets closer to = Vm and has a stronger effect on Vm

depolarization

dec in neg charge of Vm

repolarize

lower Vm to normal

hyperpolarize

Vm goes below normal

NT bind to were and what NT

to ligand binding cite were signal causes ion channels to open


Ca2+

Vm aproaches what after nueron ap and receptor opens

it approaches E(Na)

inhibitory post-synaptic potencial (IPSP)

inhibites nueron by hyperpolarization coming from nueron behind it

graded potencial

strenth decrease over space/time


ex of graded potencial

synapse and NT trans

excitatory post-synaptic potencial (EPSP)

flow of postive ions from postsynapse and makes nueron more likely to fire

soma

recieves EPSP and IPSPs and intergrates signals

axon hillock

base of axon, axon desides to fire or not

passive electrical signal

dissosiation of charge accross space and time (graded potencial)

active electrical signal

action potencial with no dissos of charge over space time

dirrection of action potencial

usually forward, some go backward

steps to firing ap

imput signal-->integration-->output signal

initial axon segment


-structure

input signal, initial intergration, starts ap


trigger zone aka


-lots of Na channels

activation gate

closes channel at resting potencial, help build up charge


-opens for depolarizing stimulis


-closes when inactivation gate closes

inactivation gate

closes Na channel and it coincides with peak of Vm graph

Na gates cycle

-gates swtich to orginal position=activation gate closed and inactivation gate open/resting


-initiation gate opens and Na comes in


-at peak Na inactiavation gate closes


-once repolarized they switch back to orgianal positions

na activation gate opens

when depolarization stimulus apears

congenative insensativity to pain

numbness due to Na channel insensativity

paraoxymal extreme pain disorder

increased channel function, occular pain increased

primary estryommelangia

constantly open Na channel for constant pain

mouse immune to scorpion

scorpion poison opens channels for extreme pain (Na), mouse has effect do opposite so channels make it numb

Na inactivator blockage

Na inc well beyond max and takes far longer to get K back to normal

no K channels effect

Na goes slightely beyond max (Vm) but takes very long time to get back ot normal repolarization

hyperkalemic peridic paralysis

incomplete closure of inactivation gate causeing Na to go beyond normal max and slower responces yield paralysis

Steps of firing ( for each part of cell)1ms, 1.5ms, 2ms, 2.5ms


1.resting potencial


2.depolarizing stimulus


3. Membrane depolarizes to threshold (channels open)


4.rapid na entry depolarizes cell


5. Na channels close, slower k channels open


6.k moves to ectracellular fluid


7. extra k leaves hyperpolarizing it


8.k channels close and k leaks out


9.resting potencial achieved

1ms: (1-5)


1.5ms: (6-7)(1-5)


2ms: (8)(6-7)(1-5)


2.5ms: (9) (8) (1-5)

myelenation

inc speed of tran 100x

myelentation speeds how

less na pumps, jumps around myelin to speed things up

node

space between myelin containing pumps

sultory condance

jumping form node to node between myelin

internode

myelin between myelinless nodes

cardic graph of Vm

slower na/Vm increase then platue till repolarization

plateu in cardiac graph

maintained depolarization due to opening Ca from outside channel

resting cardiac Vm

-90mV-->+15mV

graded potencials occur were

dendrties and cell body

ions of graded potencial

Na, Cl, Ca

initiation of graded potencial

entry ions via channels

ions involved of AP

Na and K only

type of signal of AP

depolarizing only

muscle fassicle

bundle of muscle fibers(cells)

motor unit

single nueron and all its connected fibers

char of muscle contractoni

all or nothing

inc size of muscle nueron

inc number of fibers assos

inc strenth of contraction by

inc number of motor units firing

dystinia

disorder with muscle contractions (stay contracted) , treated with botox (hard to target on fiber with botox)

synaptic knob

end of nueron, expanded for greater SA to connect with muscle

motor end plate

sarcolemna accross from synaptic knob, folded for inc SA

sarcolemna

cell membrane of staited muscle tissue

synaptic cleft

space between synaptic cleft and motor end plate

acetocholnestrase

enzyme that breaks down Ach in the synapse

Step 1-7 of Ach in muslce

mtor nueron apo

a-bungarotoxin

binds to Ach receptor and effects it

nondepolarizing blocker

puts Ach recetor in semiopen state


-desensitizes-->shuts down muscles

depolarizing blocker

binds to Ach receptor to keep it open and it shuts down sytem

sarcoplasm

muscle cytoplasm

sarcoplasmic reticulum

muscles smooth ER

transfer tubules

invagination of sarcolemma, helps transfer AP to DHP receptor

terminal cisternae

end of sarcoplasmic reticulum, part of triad


storage of Ca

in sarcoplasmic reticulum

triad

two ends of sarcoplasmic reticulum and t tubulue-->allows release of Ca

chain of action potencial--> Ca release in skel muscle

motor end plate-->t tubule-->DHP receptor-->opens RyR receptor-->Ca exits via RyR receptor

DHP receptor

in t-tubule, ap trigers it to activate and open RyR receptor from sarcoplasmic reticulum

after ca released form sarcoplasmic reticulum

ca goes to troponin and actin and myosin can power stroke

RyR receptor

Ca channel opener, signalled by DHP, DHP activation makes z-protein retract and it unplugs hole

z-protein

acts like plug in RyR receptor blocking Ca release from sarcoplasmic reticulum

excitable contraction coupling

converting electrical stimuli form nueron to muscle contracion

cardiac muscle Ca responce

uses L-type Ca channel to bring Ca in as well as DHP receptor

L-type Ca channel

AP-->L type channel opens-->Ca outside--> Ca inside

PMCA and NCX

cardiac muscle uses this to bring Ca back to outside after L-type Ca channel brings it inside


NCX:3 Na in and 2 Ca out

tube carriers

used to get Ca outside of cell (NCX and PMCA)

multiminocore disease

mutation in RyR1 and SEPN1 genes-->muscle weakness


-->muscle unable to contract without RyR receptor

Ca inc signals RyR

to release more Ca, positive feedback

malignant hyperthermia

anesthetic triggeres overheating by massive release of Ca by RyR receptor


-treated with edrophonium which stops RyR receptor

NMJ disorders

nueromuscular disorders

myasthenia gravis

autoimune respone to Ach receptor causes occular weakness and treated with edrophonium


-exersize makes it even worker

myasthete synapse

decrease Adh release, exersize helps resist weakness

Guillan bizzare

virus:attacks myselin, slows connections

Smooth muscle step 1

1. Ca outside cell-->inside, ca also released from sarcoplasmic reticulum


smooth muscle step 2

ca binds to calmodulin (CaM)

calmodulin (CaM)

in smooth muscle, when Ca binds to it activates MLCK

step 3 smooth muscle

Cam (w/ Ca) activates MLCK

myosin light chain kinase (MLCK)

activated by CaM (w/ Ca), it phosphorylates light chains in myosin head

step 4 smooth muscle

mlck phosphorylates light chains in myosin head


-results in myosin forming cross bridge with actin

steps of relaxation of smooth muscle

dec in Ca-->CaM unbinds Ca--> myosin phosphorylase removes phosphate form myosin

myosin phosphorylase

relaxation of smooth muslce


-low Ca Cam activates it


-removes phasphate from myosin light chains

smooth muslce signalling pathways

IP3, Ca, modular pathways

IP3

activated by ligands, helps releases Ca

modular receptors

activated by ligands, activates MLCK or myosin phosphatase


anesthetic mechanism

open K+ channels-->hyperpolarization

TTX

(zombies) enter trance cause it blocks Na channels in brain, nuerons cant fire

myofirbils

contain actin, myosin, ect, main part of sarcomere


many make up cell

thin miliment

f-actin=filamentous actin


+


g actin=globular in twisted string

thick filament

myosin head and tail

g-actin

globular proteins in twisted string, part of actin filament

f-actin

filamentous actin, wraps around g-actin

sarcomere

unit of muscle contractions between two z plates

h-zone

gap in sarcomere were thick and thin filamnet dont overlap

troponin

bound to tropomyosin, when Ca present it makes tropomyosin able to bind to actin

tropomyosin

string around myosin, connected to troponin, tropinin unblocks it when Ca present

muscle contraction steps

1. actin binds-myosin when atp attaches


2. power stroke ATP-->ADP(stays attached)+Pi (leaves)


3. ADP leaves


4. ATP binds-->cross bridge detaches


5.hydrolysis of ATP results in new cross bridge formation

shape fo smooth muscle

smaller than skeletal with longer actin/myosin wrapped around dense body

sarcoplasmic reticulum of smooth musle

less than skeletal

dense bodies

connect different strands of actin/myosin fiber

kinase

ATP-->ADP


-add P to protein and activates it

phosphorylase

ADP-->ATP


-removes P from protein and deactivates it

aortic aneurysm

smooth muscles around aorta relax and aorta expands

twitch

single contraction/relaxation cycle

tetanus

max tension period

central fatigue

CNS psychological fatuge, protective reflexes

peripheral fatigue

at NT junction and on

nueromuscular junction fatigue

nuerotransmitter release, receptor activation

excitation contraction coupling

change in musle membrane potencial

Ca signal fatigue

dec Ca, less interaction

contraction/relaxation theory

a theory of fatiuge, atp, glycogen depltion


-depletion theories

accumilation theories

a theory of fatige, H+,Pi, lactate accumilation

isometric contraction

tension<resistance, building up tension for lifting


-elastic fibers elongate while actin and myosin shorten

isotonic contrcaiton

tension>resistacne, object moves


-elastic fibers shorten and actin and myosin stay same

nebulin

helps align actin

titin

provides elasticity of muscle and stabalizes myosin

intercollated disks composition

gap junctions

autorythmic

able to gen contraction wihtout nerves (heart0

cardiac fibers lenth

short

cardiac controlled by

sympathetic and parasympathetic nervs

t-tebules found in what muscle

skeletal and cardiac only

controll of skeletal done by what chems

Ca and troponin

controll of smooth done by what chems

ca and calmodulin, with fibers electrically linked via gap juncitons

controll of cardiac done by

ca and troponin, fibers linked via gap junctions

spd of cardiac muslce

intermediate

graded potencial in what muscle

smooth and cardiac

epinephrine effects what muscle

cardiac only

initiation of contraction for each muslce

skeletal=Ach


Smooth=stretch/chem


cardiac=autoarythmic

type of nueron for each muscle tisuse

skeletal=somatic


smooth and cardiac=autonomic

facilitates integration

dendrites

missl bodies

rouph ER

axon hillock

were axon connects to cell body

axon collaterals

side branches of main axon

anaxonic nuerons

axon the same as dendritea nd branch in every dirreciton

unipolar nueron char

very long axon fused with dendrite


-not common in humans

bipolar nueron char

small, one dendtrite and one axonmu

multipolar char

abundant in humans


single long axon with mult dendrites

internueron

facilitate communication between sensory and moror nuerons


-are inhibitory

glia cells located where

both CNS and PNS


-half volume of Nervous system

size of glia

smaller than nuerons but ten times more abundant in number

char of glia

mitotic


-protect and noursish nuerons

four types of cells in CNS

astrocyte, ependymal cell, microglial cell, oligodendrocyte

astrocytes

protective=maintian blood-brain barrier


-scaffold=create 3D framework for CNS


-repair damaged nueral tissue


-control interstitial environment (clear potassium form inside)

devopment of astrocytes

glia develope before astrocytes

ependymal cells (type of cell)

ciliated cuboidal epithelial cells lining ventricles of the brain and spinal cord


-cilia used for circulating spinal fluid

purpose of ependymal cells

working with glial cells, it produces cerebral spinal fluid and form choroid plexus


-have stem cell like properteis

choroid plexus

clustering of ependymal cells making spinal fluid

microglial cells

small motile cells that remove debris via phagocytosis


-imp part of immune system

microglial cells char

are motile enabling them to undergo phagocytosis on cell debris anywere in CNS

oligodendrocytes

CNS only


-wrap themselves around axons like electrical tape around wire producing myelin


-1 cell can wrap multiple sections of myelin

glial cells of PNS

satellite cells and shwann cells (nuerolemmocytes)

satellite cells/amphicytes

aka amphicytes


-surround ganglia


-regulate environemtn around nueron

nuerolemmocytes/shwann cells

PNS only, wrap themself aroudnt he axons for myelin, 1 cell= one myelin sheath part

types of reflexes (ex)

-auditory, corneal (light touch of cornea causes eye to blind)


-cough, gag, pupillary (light causes eyes to constrict), muslce (stetching), movement(walking)

reflex occurs were

bypasses brain, goes to spinal cord or to brain stem

cranial reflex

integration of reflex occuring in brain

automatic responce char

happens same way every time

somatic reflexes

contraction of skeletal muscles


-includes superficial and stretch reflexes, muscle contractions

autonomic (visceral) reflexes

involuntary, smooth muscle, glands

ways to get reflex

innate and learned

ganglia

nueron cell bodies collected in spinal cord

PNA nueroglia

satellite cells and schwann cells

PNS grey/white matter

grey=ganglia=collection of cell bodies in PNS


white=nerves=bundles of axons in PNS

sensory nuclei

in posterior horns of spinal cord


contain internueron cell bodies of somatic sensory and visceral sensory nuclei

motor nuclei

in anterior horns of spinal cord


-contain somatic motor nuclei

autonomic motor nuclei

found in lateral horns of spinal cord

order of nuclei in spinal cord form anterior to posterior

somatic>autonomic>visceral>somatic


sensory motor

reflex arc

nueral wiring of single reflex


-begins at receptor in PNS-->CNS-->peripheral effector

reciprical inhibition

when one muslce is reflexed to contract the antagonist gets hyperpolarized so it stays relaxed

reflix is a ___system

feedback or feedforward


-stress-->receptor-->controll center-->effector-->return to homeostasis


-feedforward=anticipate change and prevent it

proprioreceptors of somatic muscle reflexes

found in skeletal muslce, joint capsules, and ligaments


-carry imput sensory nuerons to CNS.


-effectors are muscle

alpha motor nuerons

carry output signal in somatic motor responce

proprioceptor structure

muscle spindles and golgi tendon organs


=sensory receptors of muscles

extrafusal muslce

part of muscle that contracts-->leads to responce of proprioreceptor

muscle spindle

senses stretch change in muscle and if hits trigger point then it tells CNS of problem

central region of proprioreceptor

lacks myofibrils, full of tonically active sensory nuerons for detecting stretch

steps to muscle spindle firing

1. Extafusal muscle fibers at resting lenth


2. sensory nueron is tonically active


3. spinal cord integrates funciton


4. alpha motor nuerons recieve tonic imput from muscle spindles


5. Extrafusal muscle fibers maintain a certain level of tension at rest (spindles fire even at rest)

alpha-gamma coactivation steps

muscles both working, muscle tone


1.alpha motor nueron fires and gamma motor nueron fires (antagonist muslces)


2. Muscle contracts


3.stretch on centers of intrafusal fibers unchanged, firing rate of afferant nuerons will remain constant alpha

golgi tendons

nerve endings located near a muscle-tendon junction


-prevents damage by turning off muscle if too much tension

char of golgi tendon vs. muscle spindle

polysynaptic, spindle wasn't polysynaptic

were are muscle spindles in comparison with golgi tendon organs

in series with them, their muslce spindles are connected to golgi tendon organ

how golgi tendon reflex works

nuerons fire to hyperpolarize motor nueron so it relaxes


-prevents damage from excess loads

flexion reflex/crossed extensor reflex

when u walk on something painful


2. primary sensory nueron enters spinal cord and diverges


3.a one collateral activates pain and changing center of gravity


b.withdrawel reflex pulls foot away from painfull stimulus


c. crossed extensor reflex supports body as wiehgt shifts away form painfull stimulus


brain stem

posture, hand eye movement

motor areas of cerebral cortex

planning and coordinating complex movement


-recieves info from thalamus


-sends info to mid and hindbrain

cerebellum

monitors output signals form motor areas and adjusts movements


-revieves info from spine, cerebral cortex


-sends info to brani stem, cerebral cortex


thalamus

connects relay nuclei that moduclate and pass messages via cerebral cortex

basal nuclei

motor planning