Talbot Flashcards
Homeostasis
ability to maintain internal environment w/n narrow limits; ex: BP, pH
Sensory receptor
detects deviations of a specific parameter that moves out of its normal range of function
Integration or control center
receives info from the sensory receptor and decides if there should be a response
Effector
induces the change that brings the parameter back towards set point
Negative feedback
response generated by the effector acts to oppose/remove the stimulus
Positive feedback
response reinforces stimulus; ex: labor
Steady state
rate of influx is equal to outflux
Equilibrium
no net flow into or out of system
Is homeostasis more of a steady state or equilibrium?
steady state!
Tonic activity
maintenance of some level of activity at all times
Antagonistic control
two different control mechanisms that induce opposite effects
Diffusion
movement of a solute suspended or dissolved in an aqueous solution down its concentration gradient
Osmosis
movement of water from a lower solute concentration to a higher solute concentration
When would a cell be in an iso-osmotic solution?
with urea and ethanol
Change in solute concentration will lead to
osmotic water gain/loss
Hypertonic environment
NKCC or NHE transporters are activated to let Na, K and Cl into cell
Hypotonic environment
efflux pathways and KCC transporter is activated to move K+ and Cl- out of cell
What are the 3 major body compartments?
Interstitial 66%
Vascular 25%
Intracellular 8%
What does structurally polar mean?
in microtubules, the minus ends are oriented towards the center of the cell and the plus ends are oriented towards the cell periphery
Kinesin
walk towards plus end (periphery) of microtubules;
have a binding site on opposite side of feet for membrane bound organelle or another MT
Dynesin
walk toward the minus end; larger, more complex and faster than kinesin
Facilitated diffusion
spontaneous passage of molecules or ions down their electrochemical gradient across membranes with the use of an integral transmembrane protein
Simple diffusion
diffusion across the lipid membrane
Carriers
solute physically binds to transport protein; can be active or passive
Channels
solute moves through an aqueous pore; can be ligand-gated, phosphorylation-gated, voltage-gated or mechanically gated
Uniporter
one solute, one direction; ex: Ca ATPase
Symporter
2+ solutes in the same direction; ex: Na+/glucose cotransporter
Antiporter
“opposite” 2+ solutes exchanged between compartments; ex: Na/H exchanger
Primary active transport
uses cellular energy (ATP); drives solute against electrochemical gradient; transporters are pumps or ATPases
Secondary active transport
uses potential energy; drives active transport of a different solute; always coupled with transporters
Polarized cell
two distinct membrane domains; presence of specific protein that allow cell to have a unique function
Transepithelial transport
movement of substances across epithelium; across apical and basolateral membranes in series
Movement of ions across membrane is influence by both their:
chemical gradient and electrical gradient (electrochemical gradient)
Nernst equation
allows you to predict which direction an ion will move across a membrane
Na+ moves
into the cell; down its electrochemical gradient
K+ moves
out of the cell so Vm would become more negative
Cl- moves
out of the cell making the Vm less negative
Ca2+ moves
into the cell
Membrane potential
source of potential energy that can be used to drive a variety of transport processes; real value measured by using GHK EQ
Equilibrium potential
the membrane potential that will exist when ion x is at equilibrium; theoretical value
Time constant
time it takes the membrane to reach 63% of final voltage
Length constant
distance needed before the Vm decays to 37% of its peak value
Amplitude of the voltage deflection is
variable and dependent upon the stimulus intensity
Action potential
induced by a depolarizing stimulus of sufficient intensity
Resting state
all voltage-gated Na+ and K+ channels closed
Depolarizing
all voltage-gated Na+ channels open
Repolarizing
all voltage-gated Na+ channel inactive and K+ channels open
Hyperpolarizing
all voltage-gated K+ channels slowly closing and Na+ channels inactive –> closing
Refractory
unresponsive membrane due to inactivation phase of voltage-gated Na+ channels
Absolute
no AP can be generated; most Na+ inactivated
Relative
smaller than normal AP can be generated from larger stimulus; some Na+ channels capable of opening
Dynamic instability
microtubules are constantly growing at + end and shrinking at - end
Acting
globular monomer bound to ATP
Microtubules
13 protofilaments made up of alternating dimers of alpha and beta tubulin
Monomer binding (or sequestering) proteins
promote growth often of new actin filaments
Nucleating proteins
promote rapid depolymerization
Cross-linking proteins
help form a web like structure
End-binding (or capping) proteins
one version specific for plus end, another for minus end; prevent assembly and/or disassembly at the respective capped off ends
Side-binding/stabilizing proteins
help stabilize the filament and prevent depolymerization
Motor proteins
myosin walks along all types of actin filaments
Binding proteins
help arrange actin filaments in stable, parallel structures
Myosin I subfamily
monomeric myosin; ATPase head interacts w/actin filament
Myosin II subfamily
muscle myosins; bi-polar thick myosin filament
Muscular disease
muscular dystrophy - dystrophin is an ABP that helps link muscle actin to plasma membrane
Neurological diseases
synaptic function is dependent upon synaptic morphology which is dependent upon proper functioning of actin filaments; ex: Alzheimer’s, Parkinson’s, Huntington’s
Immunological diseases
impaired regulation of actin cortical filaments in autoimmune diseases
Cancer
migratory cells become less dependent upon attachment dependent proliferation
Excitable cells
capable of developing action potentials
Nebulin
actin stabilizing protein
Titin
set length of thick filament and helps pull sarcomere back to its resting length
Myomesin
stabilizes sarcomere (M-line)
