Human Phys Exam 1

rate of diffusion

• inc w shorter distance solute has to travel

• inc w surface area of mem that solute is diffusing across, more holes to pass thru

osmosis

• diffusion of water from low osmolarity to high osmolarity

osmolarity

• number of solute particles per liter

• 1 M NaCl = 1 mol Na and 1 mol Cl = 2 Osm

active transport

• membrane carrier ptn ATPase

• breaks down ATP to release energy

• moves molecules against conc gradients

coupled transport

• doesn’t need atp itself but requires gradient from previous transporter

• molecule 1 moves down conc gradient

• couples energy of molecule 1 to co-transport molecule 2 against gradient

• ex: Na+ down gradient coupled w glucose against

cholera

• disease of mem transport

• excess transport of contents of intestine

• Cl forced out by toxin

  • Na+ and K+ follow bc of excess negative charge

  • water dragged out of cell since high Osm outside

nernst equation

• equilibrium potential in mV for a single permeant ion

• (61 / charge) x log ([ion]_out / [ion]_in)

equilibrium potential

• voltage at which electrical force balances chemical force

membrane potential

• V_m

• approaches equilibrium potential of most permeable ion

• V_m close to E_K since most permeable ion

• at resting, x is weighted average of all equilibrium potentials

goldman equation

• finds compromise membrane potential accounting for each permeant ion

skeletal muscle

• muscle attached to bones by tendons

• contract when stimulated by somatic efferent nerves (motor neurons)

• allow for conscious movement of limbs

fascicles

• fibrous connective tissue from tendons covers and divides x of muscle

• made up of striated myofibrils (fused muscle cells)

myofibrils

• divided into sarcomeres

• make up fascicles

• made up of myofibers

z-discs

• at either end of sarcomere

I band

• area of thin filaments

A band

• overlap of thin filament and thick filaments

H zone

• center of thick filaments

M line

• disc in center of sarcomere

• joining thick filaments

titin

• elastic filament running through center of thick filaments

sliding filament

• shortening of myofibrils caused by shortening of sarcomeres

  • distance btwn z discs is reduced by sliding of myofilaments

  • produced by asynchronous power strokes of myosin cross bridges

    • pull thin filaments over thick

• A bands same length but pulled closer to origin of muscle

• I bands btwn A shorten

• h bands shorten

• area of overlap gets bigger

max shortening

• when there is no more thin filament to pull on

length-tension relationship

• more overlap = more force can be generated

• if muscle rlly stretched out or shortened, can’t generate much/any force

• sweet spot

actin/myosin sliding model

• Ca2+ binds to troponin on actin and exposes myosin-binding sites

• ATP binds to myosin head and gets hydrolyzed to ADP

  • myosin head in high-energy state

• myosin head binds to actin

• during power stroke, myosin drops ADP and pulls on thin filament

  • thin moves toward center of sarcomere

• ATP binds to myosin to cause myosin to release actin and restart cycle

• cycle continues until Ca2+ pumped back into sarcoplasmic reticulum or ATP runs out

actin

• make up thin filaments

• wrapped w long fiber tropomyosin

  • has troponin on it

• has specific sites where myosin can grab

• when relaxed, tropomyosin covers binding sites

• Ca2+ binds to troponin which causes tropomyosin to move and reveal sites

muscle contraction

• requires myosin in high-energy config (ADP bound)

• requires Ca2+ bound to troponin/actin to reveal myosin-binding sites

• no energy required for ADP to stay on myosin and myosin to attach to actin

  • cocked myosin has chemical attraction to actin once binding sites uncovered

  • breaking down atp was used to bring myosin head into high energy

• Ca2+ can leak from sarcoplasmic reticulum for thin filament binding

muscle relaxation

• replace adp on myosin w ATP to cause myosin to release actin

• remove Ca2+ by pumping back into sarco

  • requires atp-fueled pump

• requires energy from ATP

rigor mortis

• no circ/breathing after death so no cellular resp/atp production

• muscles contract but no energy for relaxation 4-12 hrs after death

• 48-72 hrs after lactic acid builds up in muscle cells during anaerobic resp

  • drop in pH causes tissue damage

  • muscle fibers relax as filaments degrade

neuromuscular junction

• motor neuron innervates one group of muscle fibers (motor unit)

• motor neurons release ACh onto x

• ACh binds to nicotinic receptors (ligand-gated Na+ channel)

  • let Na+ into cell

  • cause muscle APs across entire muscle fiber and down thru t-tubules

• AP opens voltage-gated Ca2+ channels

  • Ca2+ release from sarcoplasmic

  • rise in Ca2+ causes muscle contraction

• Ca2+ ATPase pumps transport from cytoplasm back into sarcoplasmic

• Cholinesterase degrades ACh, terminates chem transmission

motor unit

• one group of muscle fibers innervated by a motor neuron

bungarotoxin

• binds tightly to nicotinic ACh receptor at NMJ

• krait and cobra snake venom

• irreversible competitive antagonist

• no matter how much ACh in cleft, can’t bind to receptors

• can’t contract, paralysis

curare

• binds weakly to ACh receptor w/o activating

• muscles fully relaxed and unable to move bc ACh can’t bind to nicotinic receptors

• reversible competitive antagonist

• can get contraction w enough ACh

botulism

• blocks release of ACh from motor neuron

• muscle receives 0 signal to contract

• severe experience breathing failure and paralysis

sarin

• cholinesterase inhibitor

• inc ACh in synapse that continuously binds to muscle receptors

  • immediate, violent muscle twitching and convulsions

  • results in locking muscle membranes in permanently depolarized state

    • can’t reset or fire

    • suffocating paralysis

tetanus

• blocks release of inhibitory NTs (gaba and glycine)

  • supposed to tell motor neurons to stop firing

• motor neurons fire uncontrollably

• constant overlapping muscle contractions

• lockjaw

GABA

• primary inhibitory nt

• opens Cl- channels and lowers Vm

• hyperpolarizes

• enzyme GAD to convert glutamate to x

glutamate

• primary excitatory nt

• opens ion channels that let in Na+ and K+

• depolarizing

• simple, get from diet

  • no synth pathway

tyrosine hydroxylase

• marker for catecholamine neurons

• rate-limiting

  • how fast enzyme converts tyrosine

cathecholamine pathways

• tyrosine → dopa via tyrosine hydroxylase

  • all have tyrosine hydroxylase

• dopa → dopamine via decarboxylase

• dopamine → norepinephrine via dopamine B-hydroxylase

• norepinephrine → epinephrine via PNMT

neuropeptides

• small chains of aa

  • 4-100 aa

• coded for by genes, synthesized by ribosomes in neurons

• directs x into ER, golgi, and into secretory vesicles

• released w classical NTs by neurons

• serve as hormones secreted by glands into blood

• act on GPCRs, slow, long-lasting effect on target

• may act as modulators of NTs

GPCR

• NT binds to receptor ptn

• activates G-ptns

  • can interact w ion channels to change Vm

  • can activate 2nd messenger systems to raise cAMP lvls for slower intracellular signaling

  • can be stimulatory (G_s) or inhibitory (G_i)

nicotinic receptor

• ion channel receptor

  • primary receptor at NMJ

• curare, ACh, and nicotine can act on

muscarinic receptor

• GPCR

• atropine, muscarine, and ACh act on

  • atropine is antagonist

G ptn activation

• when mem receptor is unbound, g-ptn subunits aggregate and alpha binds GDP

• when ligand binds receptor, alpha releases GDP and binds GTP

  • allows alpha to dissociate from beta-gamma subunits

• alpha or beta-gamma units move thru mem and bind to membrane effector ptn (ion channel or enzyme)

• deactivation of effector ptn caused by alpha subunit hydrolyzing gtp to gdp

• allows subunit to reaggregate and bind to unstimulated receptor ptn (no longer bound to regulatory ligand)

electrical synapse

• couples neurons or muscle cells

• connexin ptns form gap junctions which ion currents move thru

  • continous cytoplasm

• no delay in AP moving btwn cells

  • bidirectional transmission

Ca chem synapse

• AP causes voltage-gated Ca2+ channels to open

  • Ca2+ enters presynaptic nerve terminal

• causes vesicles to fuse w presynaptic mem

• NT released into synapse by exocytosis

ttx

• blocks voltage-gated Na+ channels

• no APs