Cell Bio

diffusion

movement across phospholipid bilayer (membrane) of cells

cations

positively charges molecules

anions

negatively charged molecules

membrane potential

charge that we measure across membrane

equilibrium

net movement of ions across the membrane is 0

forces that influence membrane equilibrium

concentration and charge

positively charged ion with semipermeable membrane and negatively charged magnet on one side

ions will stay towards the negatively charged magnet instead of moving across the membrane to balance concentration

losing resting membrane potential

means theres no response or action potentials

channel characteristics

proteins that penetrate cell membrane, only see size and charge, general movement via passive diffusion

phospholipid bilayer

2D array of lipid molecules hydrophobic tails and hydrophilic heads that allow tails to associate with each other

cholesterol decreasing cell membrane fluidity

restricts movement of acyl chains

cholesterol increasing membrane fluidity

prevents close packing of lipids

long acyl chains

more stiff membranes

short acyl chains

more flexible membranes

transverse diffusion

phospholipid will flip the sides that its on, very slow process

lateral diffusion

phospholipid will move over one place, very fast

integral proteins

membrane proteins, portion of structure is fully buried in lipid bilayer

peripheral proteins

loosely associated with membrane via interactions with lipid heads or integral proteins

proteins important for membrane transport

integral proteins like transporters, carrier proteins, and channels

simple diffusion

movement of molecule down it’s concentration gradient without the need for energy

simple diffusion requirements

lipid soluble and uncharged

passive transport diffusion

movement of a molecule down its concentration gradient with the assistance of a protein but without a need for energy

proteins involved in passive transport diffusion

carrier proteins, leak channels, gated channels, stretch channels

leak channels

membrane protein that is a permanently open channel for molecules to pass through

gated channels

membrane protein that will open and close to allow for flow of molecules

stretch channels

membrane protein that will stretch to allow for flow of molecules, and relax to close channel

active transport diffusion

movement of a molecule across a membrane with the assistance of a protein and the need for energy

secondary active transport diffusion

the movement of a molecule across a membrane with the assistance of a protein and this protein does not directly need energy, but the mechanism uses energy invested by another cellular process

voltage gated channels

open or close when there is a change in the charge (membrane potential) of the cell membrane

ligand-gated channels

channels open or close in response to the binding of a chemical messenger, such as a neurotransmitter (ionotropic or metabotropic)

sodium-calcium exchanger

an example of secondary active transport

glucose transporter

important carrier protein that facilitates blood glucose homeostasis

ATP/ADP translocase

facilitates the transfer of ATP produced inside the mitochondria to cytosol, and transfers ADP from cytosol into mitochondria by using proton motor force

cell-cell communication

the function of the organism requires that cells pass information to one another to coordinate their activities, endocrine and neural signaling

achieving action potential

the membrane must depolarize to threshold

depolarization

leads to action potential, excitation, membrane potential is closer to 0

hyperpolarization

makes it harder to accomplish action potential, inhibition, further from 0

nernst equilibrium potential

charge inside cell in which there is no net movement of ions, the electrical force required to equally oppose the chemical force

the more permeable the membrane is to an ion…

the closer the membrane potential moves to that ion’s equilibrium potential

cardiomyocyte special qualities

longer action potential bc of sustained calcium influx via secondary active transport diffusion (sodium-calcium exchanger)

high extracellular K+

nernst equilibrium potential for K+ becomes less negative, resting membrane potential depolarizes to this value

low extracellular K+

nernst equilibrium potential for K+ becomes more negative, resting membrane potential hyperpolarizes

hyper-parathyroidism

causes an increase in extracellular Ca2+ concentration

Ca2+ impact on membrane potential

inhibitor of voltage-gated Na+ channels, stabilizing the resting state and making channels less-likely to open (hyperpolarized)

sodium potassium pump

pumps 2 K+ into cell and 3 Na+ out for each ATP hydrolyzed, maintains concentration gradients and resting membrane potential

membrane potential of nerve cell

depends on concentration differences between Na+ and K+, opening and closing specific channels

nerve cell at rest

mostly K+ channels are open to trigger hyperpolarization

excited nerve cell

mostly Na+ channels are open to trigger depolarization and action potential

juxtacrine signaling

cell signaling to cell directly adjacent/next to other cell, directly connected via complementary proteins

paracrine signaling

secretory cell sends signal short distance to adjacent target cell

endocrine signaling

ling distance signaling through the blood supply

fat soluble ligand

bind to intracellular receptor

water soluble ligand

extracellular receptor

ion channel

ligand binds and the chennal opens allowing ions to move in or out, causing cellular response, common in nervous system

receptor enzyme

RTK is an example, when receptor binds activity is stimulated through dimerized RTK and then activated to carry out more signaling cascades

g-protein coupled receptor

most common in animals, when signal binds to receptor, activates a g-protein that will bind to intracellular receptor to cause signaling cascade

secondary messengers

small non-protein molecules that enact signal transduction within the cell

cAMP

cyclic AMP, secondary messenger that activates protein kinase A (PKA) to cause downstream effects

inositol phosphates

secondary messenger, phospholipids in cell membrane, there is IP3 that causes calcium release and DAG that activates PKC

ivermectin

binds to glutamate-gated chlorine channels of parasites to keep them in an open state, causes a constant influx of Cl- and hyperpolarization leading to nerve and muscle cell paralysis in parasite

insulin

binds to RTK (receptor tyrosine kinase) on muscle or fat cell, the activated RTK will phosphorylate other proteins that leads to the translocation of glucose transporters to cell surface so glucose can enter the cell and decrease blood glucose

epinephrine

binds to GPCR, causing g-protein dissociation and adenylyl cyclase activation, which results in cAMP production leading to downstream effects

ways to stopping signal at receptor

remove or degrade signal molecule, internalize or sequester receptor, inactivate or down regulate receptor

ways to stop signal inside cell

breakdown second messengers, inactivate signaling proteins, remove phosphate groups, degrade or inactivate key proteins

g-protein once receptor binds epinephrine

GDP is exchanged for GTP at the alpha-subunit and the alpha-subunit separates from the beta-gamma subunits and interacts with the target protein, adenylyl cyclase

activated glycogen phosphorylase

results in the breakdown of glycogen into glucose to provide energy

signal amplification

one small signal can cause a large cellular response to multiply the strength of the signal

glucagon

signal that targets GPCRs that result in activation of glycogen phosphorylase, leading to glycogen breakdown and ultimate increase in blood glucose

two steps in the cell cycle

interphase and mitosis (m phase)

parts of interphase

g1, s, g2, g0

g1

growth phase, duplicate cytoplasmic contents, metabolically active, sensitive to environmental cues

g0

quiescent, not really in cell cycle, maintains basal metabolism

s

dna synthesis phase, replicates all chromosomes, when cell is most sensitive to anti-cancer drug

g2

cell checks for errors, cell growth continues, cells getting ready for mitosis

two parts of m phase

mitosis and cytokinesis

mitosis

maintains the same number of chromosomes, cell duplicates into identical daughter cells, when

phases of mitosis

prophase, metaphase, anaphase, telophase

meiosis

gametogenesis, halves chromosome number, goes through 2 rounds of division

meiosis 1

goes from 2N → N

meiosis 2

N → N, the most like mitosis

source of genetic diversity in meiosis

independent assortment and crossing over events

non-disjunction

error in chromosome separation resulting in some gametes having extra chromosomes, or missing chromosomes

apoptosis

programmed cell death, is often a physiological event and requires ATP

necrosis

cell size increases, plasma membrane is disrupted which leads to inflammation, caused by external pathological event, and can adversely effect adjacent cells

general order of events for g-protein signaling cascade

signal binds to GPCR → g-protein → adenylyl cyclase → cAMP → PKA → response

what happens if 100 Na+ move into cell and 50 K+ move out of the cell?

the membrane potential is depolarized

spacial summation

two cells can send excitatory signal to nerve dendrite

temporal summation

a dendrite recieves 1 signal from 1 source and it summates

threshold

when reached, all voltage gated sodium channels open

conduction of action potential

action potential establishes circuit to bring next segment of cell membrane to threshold, fire an action potential, and so on, so the action potential travels across the membrane

T/F: action potentials can travel in any direction

FALSE; can only travel in one direction

refractory period

voltage gated Na+ channels close and cannot re-open until the membrane returns to resting membrane potential, channel is inactivated

steps for action potential generation

action potential propagates down axon via voltage gated Na+ channels → VG Na+ trigger VG Ca2+ → Ca2+ activate vesicles that hold NT → vesicle moves to snare proteins on axon membrane → NT released into synapse → NT binds to ligand gated Na+ channels → NMJ is depolarized and triggers VG Na+ channels on cell → action potential propagation

Na+ and K+ conductance

the ease of ion movement across a membrane, where 0 means no movement and high means ion is rapidly moving across membrane

conductance of Na+

depolarization

conductance of K+

hyperpolarization

Ca2+ conductance

sustained AP in cardiac muscle? (don’t quote me on that tho)

absolute refractory period

membrane cannot produce another AP because Na+ channels are inactivated

relative refractory period

occurs when voltage gated K+ channels are open, making it harder to depolarize

botox

impairs snare proteins, vesicles cannot release NT into synapse, muscle relaxes