PNB

coulomb’s law

opposite charges attract while like charges repel

chemical gradient

ions tend to move from higher concentration to low concentration

electrochemical gradient

combined effect of chemical and electrical gradient

electrical gradient

ions experience attraction or repulsion based on electrical charge

Potassium membrane potential

-93 mV

Chlorine membrane potential

-75 mV

Sodium membrane potential

60 mV

Calcium membrane potential

130 mV

unequal ion distribution

different concentrations of ions inside and outside the cell

unequal ion permeability

some ions cross the membrane more easily than others because ion channel

ion channels

allow ion flow at rest and contribute to resting membrane potential through passive facilitated diffusion

leak channels

allow ion flow at rest and contribute to resting membrane potential

voltage - gated channels

open or close in response to changes in membrane voltage

Na/K pumps

uses energy to maintain the concentration gradient required for electrical signaling

nernst equation

membrane voltage at which chemical and electrical forces acting on one ion are balanced

Vm = Ex

no net ion movement

Vm is more positive than Ex

ion moves out

Vm is more negative than Ex

ion moves in

GHK equation

takes into account the concentration gradient and relative permeabilities of multiple ions

steady state

unchanging state that remains so onlu by constant input/output

depolarization

Vm becomes more positive

hyperpolarization

Vm becomes more negative

repolarization

Vm returns towards resting potential from a depolarized or hyperpolarized state

influx

movements of ions in a cell

efflux

movements of ions out of a cell

action potential

potential change in the membrane to drive calcium mediated action out of the cell

resting potential

k leak channels dominate inside of neuron is negative

threshold

depolarization reaches the level needed to trigger AP

depolarization steps

voltage gated Na channels open quickly then Na enters and Vm becomes positive

repolarization steps

Na channels inactivate then slower voltage gated K channels open and K leaves

hyperpolarization steps

K channels remain open briefly and excess K leaves and Vm becomes more negative than the rest

returns to rest

K channels close, Na channels recover from inactivation and resting permeability is restored

absolute refractory

another AP cannot occur because Na channels are inactive

Relative refractory

another AP is possible but required a strong stimulus

nodes of ranvier

gaps in myelin where AP regenerates

saltatory conduction

AP jumps between nodes

graded potential

passive, decrease with distance and time, variable amplitude, duration and sign

electrical synapse

gap junctions, bi-directional, direct electrical coupling, fast/direct, connexon hemi channels

chemical synapse

neurotransmitters from vesicles, synaptic cleft, unidirectional

anterograde

forward direction between pre synaptic cell and post synaptic receptor

synaptotagmin

Ca sensor for neurotransmitter release

trafficking

vesicle moves towards the membrane

tethering

vesicle associates with the release site

docking/priming

vesicle prepares for fusion

exocytosis

vesicle releases neurotransmitter

endocytosis

membrane is recovered and vesicles are recycled

SNAREs

pre-synaptic membrane proteins involved in vesicle fusion

clathrin

Vesicle coating during recycling

dynamin

pinches off recycled vesicles

ionotropic receptors

ligand gated ion channels, fast response

metabotropic receptor

activates g-protein signaling, slower, longer lasting response

excitatory post synaptic potential (EPSP)

depolarizing (Na influx)

inhibitory post synaptic potential (IPSP)

hyperpolarizing (Cl influx or K efflux)

g-protein coupled receptor

slow synaptic transmission, opens/closes channels, metabotropic

ligand gated ion channels

fast, opens ion channels, ionotropic

spatial summation

multiple imputs from different locations add together

temporal summation

multiple psp adding up over time to recieve threshold

acetylcholine (ACh)

neurotransmitter at NMJ

muscarinic ACh receptors

metabotropic receptors that can indirectly activate K leak channels in the heart

myasthenia gravis

reduces functional nicotinic ACh receptors weakening neuromuscular transmission

TTX

blocks voltage gates Na channels

botox

interferes with SNARE mediated ACh vesicle release

skeletal muscle structure

muscle, fascicle, muscle fiber, myofibril, sarcomere, myofilaments

sarcolemma

muscle cell membrane

sarcoplasm

muscle cell sytoplasam

sarcoplasmic reticulum

stores Ca

t-tubule

carries action potentials deep into muscles

terminal cisternae

englarged SR regions containing Ca

triad

one t-tubule surrounded by 2 terminal cisternae

Z-disc

sarcomere boundary

M line

center of the sarcomere

A band

length of thick filaments

I band

thin filaments with out thick overlap

H band

thck filaments without thin overlap

during contraction

H and I shorten, z is closer, A stays the same

actin

thin filament

myosin

thick filament, generates force

troponin C

binds to Ca

tropomyosin

blocks actin binding sites at rest

titin

helps anchor myosin and provides elasticity (spring)

nebulin

helps align actin

smooth muscle

blood vessels, involuntary, no sarcomeres/striation, dense bodies instead of Z discs, Calmodulin not toponin C as Ca sensor

cardiac muscle

striated, short branches, intercalated discs have gap junctions/desmosomes, involuntary, troponin C for contraction

cardiac AP

depolarization Na influx, plateau Ca influx, repolarization K efflux

pacemaker cells

always depolarize to threshold

slow wave potential

fire AP when they reach threshold

motor unit

one motor neuron and its muscle fibers

henneman’s size principle

smaller motor units are recruited first then larger ones as more force is needed