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310 Cards in this Set

  • Front
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homeostasis

a dynamic process that maintains relatively stable physical and biochemical conditions in the internal environment

why is it critical to maintain homeostasis in a living environment

otherwise cells can become damaged and die; need to maintain health

Define interstitial fluid, blood plasma, and extracellular fluid and explain how they are related

interstitial fluid is the fluid that bathes every cell - cells get their nutrients from this fluid and dump their waste into it




blood plasma is the fluid circulating in the blood vessels - interstitial fluid gets nutrients from here (coming from organs) and dumps waste here (which goes back to organs)




together they make up the extracellular fluid which is our internal environment (in which tissue cells, with intracellular fluid, exist)

Identify the features of a homeostatic mechanism

Stimulus: Fluctuation in variable measuring


Sensor: Detects Change


Control Center: Receives one or more signal and sends appropriate response


Effector: makes change happen


Response: from effectors, helps return variable to homeostasis

Afferent pathway in homeostasis vs efferent pathway

Afferent - pathway from sensor to control center; info input




Efferent - pathway from control center to effector; info output

Features of a control center

-has a set point


-looks for error signals


-responds by controlling the effector

steady state

feature of homeostasis - no net change occurs


-requires continual energy input into system (compared to equilibrium)

Which of the following requires continual energy input into a system?




-equilibrium


-steady state

steady state

Set Point

Feature of homeostasis; steady state value maintained by homeostatic control




Instead can have a range

Feedback

info compared to the set point

Error signal

Any different between the set point and feedback information

Negative Feedback

Initial stimulus creates an error signal; a response is created to correct the error signal and return to set point

Positive Feedback

Initial stimulus creates response that amplifies the stimulus, which amplifies the response and so on.

How does a positive feedback loop stop?

Requires outside factor to shut the cycle off

What is positive feedback useful for?

For helping drive processes to completion - ex childbirth

Explain the positive feedback loop in childbirth

-Baby dropping into uterus causes cervical stretch


-This stimulates oxytocin release


-Leads to contractions


-Pushes baby against uterus


-Causing more stretching


and so forth...

How can set points change? List several examples

Under certain circumstances: such as Circadian Rhythm - cyclic alterations in metabolism, under control of biological clock




Feedforward information: anticipates internal changes and changes the set point; ex: salivating at sight/smell of food, increased heart rate before athletic activity

circadian rhythm

causes variations in set point


cyclic alterations in metabolism


under control of biological clock



Feedforward information

Changing set point in anticipation of internal changes




ex: salivating in response to sight/smell of food


ex: increased heart rate before athletic event

thermoregulation

process by which animals maintain their body temperature within a normal range

what temp must most cells be between?

0 and 40 degrees celsius; but most organisms have a much narrower range and have evolved thermoregulatory adaptations to stay within the range

Why are temps outside 0-40 C generally incompatible with life

Under 0 -> ice crystals form


Over 40 -> Proteins begin to denature

What is Q10?

The factor by which an enzymatic reaction or metabolic process increases with a 10 degree increase in temperature; describes temperature sensitivity

Formula for Q10

Q10 = (R2/R1)^(10/(T2-T1))

Stipulations for T2 and T1 in Q10 equation

T2 must be greater than T1

What are most biological values of Q10?

Between 2 and 3

Classify animals based on source of heat for thermoregulation (and give examples)

Ectotherms: body temp is determined primarily by external environment (reptiles, fishes, amphibians, and most invertebrates)




Endotherms: body temp is regulated by producing heat metabolically (mammals and birds)




Hectotherms: Can behave as endotherms or ectotherms (hibernating animals)

What are the four processes by which heat can be lost by an animal

1) Radiation: Emission of infrared radiation by all objects warmer than absolute zero




2) Convection: Transfer of heat by movement of air or water past a surface (even occurs in stagnant rooms because heat rises)




3) Evaporation: Removal of heat from the surface of a liquid that is losing some of its molecules as gas (sweating, panting, etc)




4) Conduction: Direct transfer of heat between two objects in contact with each other

Energy Budget

The balance of heat production and heat exchange




metabolism + Rabs = Rout + convection + Conduction + Evaporation




Heatin = Heatout

Classify the main types of adaptations for thermoregulation (which are reflected in an animals energy budget)

1. Behavioral responses


2. Insulation


3. Circulatory Adaptation


4. Cooling by Evaporative Heat Loss


5. Adjusting Metabolic Heat Production




6(ish). Morphological Adaptations - in endotherms

Examples of behavioral adaptations for thermoregulation




Types of animals using this

Lizard seeking shade when hot


nest construction


Putting sweatshirt on




Both endotherms and ectotherms use

Insulation - how used for thermoregulation




In humans, how used

Reduces flow of heat between an animal's body and the environment - from hair/feathers or fat layers formed from adipose tissue


-Thick layers of air trapped in hair/feathers reduces heat loss to surroundings




humans primarily rely on fat; but also get goosebumps (leftover from ancestors who fluffed hair/feathers up to trap heat in) - hair rises

Circulatory Adaptations - how used for thermoregulation

Controls blood flow to the skin




Vasoconstriction: Constricts blood vessels - shunt redirects blood from skin; results in less heat loss




Vasodilation: Dilate (increases diameter) of blood vessels near skin surface (capillary vessels) - shunt constricts to force blood into capillary veins; results in heat loss




Countercurrent Heat Exchanger: Arterial blood flowing away from heart warms up cooler venous blood heading toward the heart (since arteries and veins run parallel to each other)


-a passive process for recovering heat from blood traveling to extremeties

How does cooling by evaporative heat loss work? Types in terrestrial animals. Examples. Downsides

Water absorbs heat when it evaporates - this heat is carried away from body surface with the water vapor




Terrestrial animals lost water by evaporation across skin AND respiratory surfaces:


-bathing and sweating - moistens skin ---> increased evaporation on skin


-panting ----> increased evaporation from lungs




Panting and sweating dissipate heat BUT at a cost:


(1) Water loss is problematic - dehydration, etc.


(2) Are active processes that require energy --> also generate heat

What type of animals adjust metabolic heat production metabolically?

Endotherms AND some ectotherms

How do some ectotherms adjust metabolic heat?

Some insect contract flight muscles to "warm up"


Chemical reactions accelerate in the warmed flight motors, enabling insects to fly when it is cold

How to endotherms produce heat metabolically?

Shivering Thermogenesis: Muscle activity such as moving or shivering


-muscles contract, ATP is converted to ADP -> heat is released




Non-shivering Thermogenesis: Mostly occurs in brown adipose tissue:


-Uncoupling Protein 1 (UCP-1) uncouples ATP production from fuel oxidation --> no ATP is produces but heat is released.

Brown Adipose Tissues features - found in; contains

-Found in hibernating mammals and small rodents


-Also find lost in newborn humans


-Find some in human adults too - may play role in obesity (less brown fat = more obese)






-Rich in mitochondria


-Highly vascularized

Metabolic Rate - definition. Where does the energy come from?

The sum of all energy an animal uses in a given time interval




(animals use chemical energy harvested from the food they eat to fuel metabolism and activity)

Measuring metabolic rate

Measure rate of O2 consumption or CO2 production

What most increases metabolic rate

Altered skeletal muscle activity (i.e., exercise)

Basal Metabolic Rate

Metabolic rate of a resting animal at a temperature within the thermoneutral Zone



Thermoneutral Zone

A narrow range of environmental temperatures where the metabolic rate of endotherms are at low levels and independent of temperature

How to measure BMR

Animal at rest, with empty stomach, not stressed, not pregnant, not lactating, etc.

What is meant by the metabolic cost of living?

The BMR - which is the rate at which resting animal is consuming just enough to carry out minimal body functions

How does BMR correlate to body size; explain some possible explanations behind these correlations

-Large animals have higher BMR




-Small animals have higher BMR/gram of tissue


--possible explanations for this:


-as animals get bigger, have smaller ratio of surface area to volume (heat production is related to volume but heat dissipation is related to surface area) - so larger animals may have evolved lower BMR to avoid overheating


-larger animals have a greater proportion of support tissues which aren't as metabolically active as other tissue

What bounds the thermoneutral zone

Upper critical Temp: above which animal expends energy to lose heat (sweating, panting, etc.)




Lower critical Temp: below which animal expends energy to produce metabolic heat




Within TMZ, thermoregulatory responses don't use much energy

Two rules for morphological adaptations in endotherms

Bergmann's Rule: Larger mammals and birds in colder climates and smaller in warm climates


-decreased surface area to volume ratios for large animals - better at retaining heat; and vice versa for small animals




Allen's Rule: Protruding body parts are shorter in cold climate animals than in warm climate animals


-decreased surface area to volume ratios for large animals - better at retaining heat; and vice versa for small animals

Example of Bergmann's and Allen's Rules

Bergmann's - Polar bears; large and compact




Allen's - Jack Rabbit ears; long and thin

What is the homeostatic control center for temperature. What does it do?

Hypothalamus. Several functions:


1) integrates sensory information


2) establishes set points for body temperature


3) regulates physiological thermal responses

Hyperthermia and hypothermia; examples

Hyperthermia: Unregulated elevated body temp.


-Exercise is most common cause - retention of internal heat generated by exercising muscle




Hypothermia: Unregulated decreased body temp


-two main types of regulated hypothermia: topor and hibernation

Topor vs. hibernation (and arousal)

Both are regulated hypothermia with decreased metabolism and body temp - e.g., decreased set points:




Topor - decrease occurs at night to prevent overnight starvation (daily resetting)


-ex: bats and hummingbirds reduce their set points




Hibernation: decrease occurs for days or weeks


-arousal occurs when set point returns to normal and begins with a large rise in metabolic heat production, followed by body warming

Fever vs hyperthermia

Fever is a regulated elevated body temp; hyperthermia is unregulated

What is a fever?

An adaptive response to help body fight pathogens - rises body temp set point

What is a rise in body temp caused by

Pyrogens - molecules that cause body to respond by increasing body temp


-can be exogenous (bacteria, viruses, etc.) or endogenous (produced by immune system in response to infection)


-local synthesis and release of prostaglandins within he hypothalamus causes a resetting of the temperature set point

Value/danger of fevers

Moderate fevers help body fight infection but extreme fevers can be dangerous




-decreases microbial growth and increases functioning of immune system

what happens at the onset of a fever

Set point increases above your body temp


So, you feel cold


So, your body starts to increase its body temp - vasoconstriction and shivering

What happens when your fever breaks

Your body temp is above your new set point


So, your body starts to decrease its body temp - vasodilation and sweating

what is meant by gas exchange and transport?

O2 suplied for cellular respiration, and CO2 disposed of

How are gases exchanged with the environment?

Passive diffusion through respiratory surface with the environment

how does gas diffusion occur?

passively




driven by partial pressure differences

calculate partial pressure of air at sea level

P(O2) = X(O2) x P(atm)




= 0.209 x 760 = 159 mm Hg

what happens do O2 and CO2 partial pressure at altitude?


O2 - mole fraction same (20.9%)


but total air pressure decreased


so O2 is greatly impacted




CO2 - not greatly impacted - because PCO2 is so low at sea level, always have a large concentration gradient

Frick's Law of Diffusion

Describes diffusion rates of respiratory gases:




Q = DA (P1 - P2)/(L)




A = area over which diffusion occurs


D = diffusion coefficient


P1 and P2 = partial pressure of two locations


L = path lengths between mediums


Q = rate at which gas diffuses between two locations

Adaptations to maximize Gas Exchange (and examples)

1) Increase Surface Area:


ex: alveoli in lungs, trachea, gills, etc.




2) Increase partial pressure gradient


-minimize L (Thin tissues in lungs and gills)


-ventilation = increase contact between external medium and external side of respiratory medium (ex: breathing - exposes surfaces to fresh respiratory medium with max O2 and min CO2)


-perfusion = increase contact between internal medium and internal side of respiratory surface (Ex: blood transports CO2 to surface and O2 away)

How do gills maximize gas diffusion

Increase P1 - P2 = Constant water flow maximizes PO2 on external surface (ventilation)




Decrease L = thin lamina of gills

How does countercurrent flow in fish maximize gas exchange

Maximizes PO2 gradient - allowing for more complete transfer of O2 to the blood




Blood flows across lamellae in direction opposite the flow of water over the lamellae

Anatomy of human lungs - from top (nose/mouth) to bottom (alveoli)

(1) Air enters through oral cavity or nasal cavity


(2) Cavities form pharynx


(3) Below pharynx, esophagus directs food to stomach and the trachea conducts air to the lungs


(4) Larynx is beginning of trachea - the voice box, houses the vocal chord


(5) Trachea branch to 2 bronchi - one leading to each lung


(6) Bronchi branch repeatedly


-after ~4 branchings - bronchioles appear


-after ~16 branchings - alveoli appear


-after ~6 more branchings - end in clusters of alveoli

lungs are suspended in the ____, which is a ________, bounded by the _______, which is a _______

-thoracic cavity - a closed compartment

-diaphragm - sheet of muscle at bottom of thoracic cavity



Membranes of thoracic cavity/lungs, how work together

2 pleural membranes - one covers lungs, other covers thoracic cavity




move along each other well, fluid in between them

What is between the ribs; what do they do

Intercostal muscles




-external intercostals - expand thoracic cavity by lifting ribs up and out


-internal intercostals - decrease volume of thoracic cavity by pulling ribs in and down

alveoli

site of gas exchange; small thin-walled sacs

keys to diffusion in alveoli

Small diffusion path




Surfactant - coats alveoli; a detergent that lowers surface tension and prevents alveoli from collapsing, to make alveoli easier to inflate

anatomy of alveoli

Minimize path length:


-covered by thin epithelial layer


-run right next to capillaries - which also have very thin cells




-allows O2 to diffuse into capillaries and CO2 to diffuse out of capillaries into alveoli

where does gas exchange occur inside of our bodies

between alveoli and capillaries

in humans, list 3 ways Q can be affected

1) Emphysema - walls of alveoli break down, and may alveoli merge to form larger alveoli (A is decreased)




2) Pneumonia - accumulation of fluid in alveoli (L is increased)




3) Supplemental O2 - patient breathes in 100% O2 vs 20.9% O2 (P1 increases, so P1 - P2 increases)

What is the guiding principle behind how lungs are ventilated?

Negative pressure breathing

List steps of inhalation

1) Diaphragm contracts


2) thoracic cavity expands - causing thoracic wall and attached pleural membrane to move outward


3) causing suction (more negative pressure) in the pleural cavity


4) causing second membrane to be pulled along (lung is attached, so moves as well)


5) lungs expand, so dos their interior gases


6) expanded air in lungs has lower pressure than outside air - so air flows in

List steps of exhalation

1) Diaphragm relaxes --> causing elastic recoil


2) Thoracic cavity contracts


3) intrapleural pressure becomes less negative


4) lungs contract and gases are expelled

How does air move?

Passively




From regions of higher to lower pressure

Pressure in alveoli and intrapleural cavity

-inhalation - alveoli pressure is below that of atmosphere (air rushes in)




-exhalation - pressure in alveoli becomes above that of atmosphere (air expelled)




-intrapleural cavity pressure always negative w.r.t atmosphere


--more negative during inhalation (suction), and returns to original value during exhalation

tidal ventilation

in lungs; breathe in and out through same tube, so oxygenated and deoxygenated air mixes (decreases partial pressure of air)

tidal volume

volume of air inhaled and exhaled in total breath

vital capacity

maximum capacity if take really large inhalation and fully exhale

vital capacity =

= tidal volume + inspiratory reserve volume + expiratory reserve volume

inspiratory capacity =

= tidal volume + inspiratory reserve volume

residual volume/capacity

amount of air that remains in lungs after forcefully exhalation




always have some of this dead space/air in lungs

functional reserve capacity=

= expiratory reserve volume + residual volume

define circulatory system

-muscular pump + fluid + series of conduits (blood vessels, etc.)

purpose of circulatory system

blood transports respiratory gases (through perfusion)

2 types of circulatory systems

Open - hemolymph leaves vessels and flows through tissue




Closed - blood flows through closed vessels and exchanges with interstitial fluid

Evolution of circulatory systems

-becoming more separated




fish (unidirectional flow) -> lungfish (partial separation) -> amphibians (3 chamber heart - still have blood mixing) -> reptiles (start to separate 2 systems) -> mammals (2 separate systems)

Key features of mammal heart

4 chambers


-two atrium (right and left)


-two ventricles (right and left)




two circuits - pumonary and systemic

Advantages of mammal heart

1) Systemic circuit reserves blood with higher O2 content




2) gas exchange is maximized (blood with lowest O2 and highest CO2 sent to lungs via pulmonary circuit)




3) circuits can operate at different pressures

Arteries

vessels AWAY from heart

Veins

vessels going TOWARDS heart

High level summary of blood flow through body

Right heart -> lungs -> left heart -> body

DETAILED summary of blood flow through the body

1. Deoxygenated blood is in right atrium


2. Goes into right ventricle via an AV Valve (atroventricular valve)


3. Flows through pulmonary arteries to capillaries in lungs via a semilunar valve (the pulmonary valve)


4. Undergoes gas exchange in lungs ----> now have oxygenated blood


5. Oxygenated blood comes back to the heart via the pulmonary veins (on both left and right lungs)


6. Pulmonary veins dump off into left atrium


7. Blood goes to left ventricle via another AV valve


9. Goes through Semilunar valve (the aortic valve) which pumps blood into the aorta


10. Aorta branches off in both directions - towards head and toes (2 branches)


------down -> goes to capillaries of abdominal organs and hind limbs


------up -> goes to capillaries of head and forelimbs


11. Aorta deliver oxygen to sites (up and down)


12. Deoxygenated blood travels back to right atrium


------ via the inferior vena cava for the branch going down to toes


------ via the superior vena cava for the branch going up to head



Purpose of valves in heart

prevent backflow and make sure blood goes in correct directions

valves in heart

AV Valves -> atrium->ventricle


-tricuspid valve = right AV valve


-mitral valve = left AV valve




Semilunar Valves > ventricles-> arteries or aorta


-pulmonary valve = right ventricle ---> arteries


-aortic valve = left ventricle ---> aorta

Name for contraction and relaxation

Contraction - systole




Relaxation - diastole

Describe how the heart pumps blood

1. Atrial and ventricular diastole - blood returning from veins flows into atria and then into ventricles (in both circuits)


---- AV valves open, semilunar valves closed


2. Brief atrial contraction -> Atrial systole and ventricular diastole (in left and right atrium)


-----so get all blood from both atrium into ventricles


3. Ventricles contract and blood pumps to arteries -> ventricular systole and ventricular systole


-----AV Valves closed, semilunar valves open

How are heart sounds caused

by valves shutting




-"lub" = AV valves close (beginning of systole)


-"dub" = Aortic and pulmonary valves close (end of systole)

Which ventricle faces more resistance, why?

Left Ventricles;




left has to pump to entire body (right just pumps to lungs)


-cardiac muscle is thicker here

Blood pressure

Normal = 120/70




systolic value = min pressure that restricts blood flow




diastole value = min pressure that allows flow

Pacemaker Cells

can initiate action potentials without input from nervous system

Sinonatrial (SA) node

Main pacemaker of heart (wall of right atrium)

where does impulse from SA Node travel

Rapidly due to cardiac muscles being in contact via gap junctions;




impulses also pass to atroventricular node (AV Node) between right atrium and right ventricle which delays impulse before spreading to walls - delays impulse before spreading to walls of ventricles to ensure that the atria completely empties before getting ventricular systole

How does SA Node cause constant pumping

1) fires action potentials


2) leading to contraction of both left and right atrium




also


1)sends impulse to AV node


2) which sends signal to Bundle of His


3) then to Purkinje fibers

Electrocardiogram (ECG/EKG)

-can record electrical events in cardiac muscle (by recording impulses traveling through muscle)


-electrodes on skin measure voltage differences


-wave patterns represent particular events

Events portrayed in wave patterns of ECG

P = Activation of atria


-beginning = SA Node fires


-end = signal travels to bot atria




between -- atria to ventricle




QRS = Activation of Ventricles


-impulse spreads through rest of heart (ventricular contraction)




T = Recovery Wave


-ventricles relax

Describe how Pressure gradients ensure that O2 travels where needed

P (atm) > P (alveoli) --> O2 enters alveoli


P (alveoli) > p (blood from tissues -> lungs) ---> O2 enters blood


P (blood from lungs -> tissues) > P (tissues) --> O2 leaves blood and enters tissue

hemoglobin

transports respiratory gases through blood; in red blood cells

makeup of hemoglobin

4 subunits - each with 1 heme group (which each bind 1 O2)

when does hemoglobin bind O2

when P O2 is high; releases it when Pressure is low

Positive Cooperativity of hemoglobin

subunits increase O2 affinity after first O2 binds, but after 3 bind, takes greater P O2 to get 100% bound ===> sigmoidal relationship

what causes positive cooperativity of hemoglobin

probability phenomenon - as more subunits are bound, it's less likely O2 will find somewhere to bind

what is meant by hemoglobin reserve oxygen

Blood returning to heart is only 75% oxygenated; blood leaving is 100%




thus reserve of 75% is held - to release in tissues with low P O2

How does carbon monoxide affect us?

Has higher affinity for hemoglobin than O2, so binds to hemoglobin so O2 can't bind (we're starved of O2)

How does myoglobin affect our body's oxygen levels?

has higher affinity for O2 than hemoglobin


so binds to O2 and contains an oxygen reserve




-useful for contracting muscles which squeeze (interrupting blood flow)

How is CO2 transferred in the body

Via the bicarbonate ion - it is converted to bircabonate, keeping P CO2 low in cells and blood plasma (facilitation diffusion away from tisues)

What rxn occurs between CO2 and Bicarbonate?

(1) CO2 moves from body tissue to blood plasma (where pressure is lower)


(2) CO2 in blood plasma is hydrated - by carbonic anhydrase, leading to Carbonic Acid, which diffuses into red blood cell


(3) Carbonic Acid dissociates - get H+ and bicarbonate


(4) Bicarbonate enters plasma in exchange for Cl- (thus P CO2 is lowered in plasma)




-- process is reversed in lungs

elastic recoil

rebounding of lungs caused by diaphragm relaxing

venules

very small veins; collect blood from capillaries

how do you measure blood pressure?

sphygomomanometer - cuff connected to column of mercury next to a graded scale

neuron basic anatomy

cell body = contains nucleus and organelle


dendrites = receives info


long axon = carries info away from cell body


axon terminals = relay signals to target cells


axon hillock = integrates many signals and transmits the integrated signal

snyapse

junction between axon terminal (of presynaptic cell) and target cell (postsynaptic cell)

Types of synapses

1) Chemical synapse (most common)


-electrical signal arrives at axon terminal and causes release of chemical signals (neurotransmitters) which diffuse to receptors on postsynaptic cell)




2) Electrical synapse - electrical signal passes directly from pre to post synaptic neuron via gap junctions


-very fast, for stereotyped and quick responses

Glia Cells

Support cells; outnumber neurons 10-fold


-don't generate action potentials

Types of glia cells

1) Oligodendrocytes


2) Schwann Cells


3) Astrocytes


4) Microglia

Oligodendrocytes

type of glia cell




produce myelin that covers the CNS


-has many projections that wrap around many axons, forming concentric layers of plasma membranes (a single cell wraps around many neuron cells)

Schwann Cells

type of glia cell




produce myelin that covers the PNS




single cell wraps around

Myelin

covering produced by schwann cells and oligodendrocytes; mostly lipid




-provides insulation - increasing speed of conduction and preventing signals from going where not intended

astrocytes

type of glia cell




form blood brain barrier = restricts entry of most substances to the brain (by making tight junctions on capillary)




takes up and releases neurotransmitter at synapse (clean up)




store glycogen - can be used for fuel




repair/regenerate neurons




signal changes in blood composition




nourishes neurons

tripartite synapse

special type of synapse = astrocyte connections + pre + post synaptic neurons

microglia

type of glia cell




provide nervous system with immune defenses




are phagocytic cells that ingest and break down waste products and pathogens in CNS

Membrane potential

the electrical charge difference across a neuron's membrane

Resting potential

membrane potential of unstimulated neuron






typically -60 to -70 mV

How to measure membrane potential

using electrodes - filled with conducting soln, attached to voltmeter - measures magnitude of charge separation in vs out of cell

what generates membrane potentials?

ion pumps and channels as well as ion concentrations (particularly Na+ and K+)

Channels

-allow ions to pass through passively


ions will flow down their concentration gradient

Sodium potassium pumps

Uses energy of ATP hydrolysis to actively transport Na+ out and K+ in (3 Na+ for every 2 K+)

Concentrations of Na+ and K+ in neurons; and why

More Na+ out of cell and more K+ out of cell


-because of sodium potassium pumps

Why is a neuron negatively charged

Because have more "leaky" K+ channels - which cause K+ to flow down its concentration gradient and out of the cell ---> thus the negative charge

Net ion movement depends on....

concentration gradient (wants to move where have lower concentration and electrical gradient (attracted to opposite charge) ---> combine and is called the electrochemical gradient



Equilibrium Potential for a particular ion (Eion)

Magnitude of the membrane voltage at equilibrium for a particular ion




Calculate using Nernst Equation

Goldman Equation; why the need for

If calculate E K+ using Nernst, find that it is too negative - because resting potential relies on other ions as well.




Goldman calculates membrane potential using all ions, as well as the relative permeability of the membrane to each ion

Patch Clamping

Can see how ion channels open/close and how ions move

-electrode suction removes membrane patch with ions intact


-ion movement, and opening/closing of gates can be measured as electric currents

Types of Gated Channels

-voltage gated channels


-chemically gated channels


-mechanically gated channels

how do gated ion channels alter membrane potential?

Resting Potential = Only K+ channels are open


Depolarized = Inside neuron becomes less negative (Na+ flows in)


Hyperpolarized = inside neuron becomes more negative (K+ efflux increases, etc.)

Graded membrane potentials

Changes to membrane potential from resting;




depolarization or hyperpolarization

how do graded membrane potentials function

-can only transmit signals short distances


-strength of stimulus determines magnitude of charge

Action Potential - when caused

-when graded depolarization reaches particular voltage, threshold potential, respond with an action potential in the axon

Features of action potential

-All or nothing depolarization


-sudden, transient, and large change in membrane potential


-once triggered is stereotyped


-generated by action of Na+ and K+ channels

Types of gates on voltage gated channels

On voltage Gated K+ channel

-Activation Gate - closed at rest, opens slowly in response to depolarization (and stays open longer)




On voltage gated Na+ channel


-Activation Gate - opens rapidly in response to depolarization


-Inactivation Gate - open at rest, closes slowly in response to depolarization

Course of an action potential

1) Resting Potential


-K+ channels leaky (but no movement)


-gated channels closed




2) Threshold


-some Na+ channels open as depolarizing stimulus arrives (brings membrane potential to threshold)




3) Depolarizing Phase


-If depolarization reaches threshold, additional Na+ voltage gated channels open


--Na+ rushes in and interior becomes more positive until reaches its peak




4) Falling Phase


-At peak, 2 processes happen simultaneously:


----many Na+ voltage gated channels' inactivation gates close


----Gated K+ channels open


-this causes membrane potential to become more negative (and towards resting)


---undershoot = brief hyperpolarization; because more K+ channels are open now than ever




5) Refractory Period


-Neuron insensitive to depolarization - sets limit on max frequency with which action potentials can be generated.


-Two causes:


---1) Undershoot due to K+ channels


---2) Refractory period of Na+ channels - because inactivation gates reopen after activation gates close

How does an action potential spread; general principles

-Self-regenerating


-spreads to adjacent membrane regions, without loss of signal magnitude


-Na+ entering cell creates depolarizing electric current on neighboring region

How does an action potential travel along an axon?

1) Generated as Na+ moves into the cell


2) Depolarizing current spreads down axon


3) Causing more Na+ channels to open if threshold is reached

Why can't action potential reverse?

Refractory period




-Na+ channels refractory upstream


-voltage gated K+ channels open - so hyperpolarized

Factors affecting action potential speed

1) Axon Diameter - longer = faster transmission


-ex: giant squid axon


-not possible for vertebrates (because have so many axons wouldn't have room)




2) Myelenation - speeds up action potential

Explain how myelenation speeds up an action potential

-Voltage gated channels are concentrated in gaps called Nodes of Ranvier


-Action Potentials "jump" from node to node - called saltatory conduction

Main 3 Steps to Chemical synaptic transmission

1) Action potential arrives at axon terminal - causing release of neurotransmitter






2) Postsynaptic membrane responds to neurotransmitter




3) Response is turned off by clearing neurotransmitter

Chemical synaptic transmission - explain how step 1 happens:


1) Action potential arrives at axon terminal - causing release of neurotransmitter



a) Action Potential arrives at axon terminal


b) depolarization is caused by Na+ channels opening


c) Depolarization causes voltage-gated Ca2+ channels to open


d) Ca2+ rushes into cell, causing ACh vesicles to fuse with presynaptic membrane


e) when ACh vesicle fuses, causes ACh to diffuse across synaptic cleft

Chemical synaptic transmission - explain how step 2 happens:


2) Postsynaptic membrane responds to neurotransmitter

a) ACh binds to its receptor - a chemically gated cation channel, which allows Na+ and K+ to flow in


b) response depends on neurotransmitter/receptor combo, but for ACh - Na+ flows in, depolarizing membrane


c) (for ACh) - depolarization spreads, firing action potential by opening voltage gated Na+ channels further down membrane

Chemical synaptic transmission - explain how step 3 happens:


3) Response is turned off by clearing neurotransmitter

a) Acetylcholinesterase (an enzyme) breaks down ACh (into AcetylCoA and coline), causing channels to close


b) Coline is taken back up into synaptic terminal for resynthesis into Acetylcholine (Ach)


c) synaptic vesicles are recycled via endocytosis of membrane and then refilled with ACh and ready for another round

How does the pufferfish toxin kill?

Binds to voltage gated Na+ channels - so can't open


-neurons can't fire action potentials - paralyzing muscles (including respiratory muscles)

What does the postsynaptic cell do at the axon hillock?

Sums excitatory and inhibitory signals - because each neuron has many dendrites that can synapse with different axons (so many possible signals), but only 1 output (action potential

Excitatory and inhibitory signals

Excitatory - always between motor neurons and muscle cell; depolarizing




Inhibitory - frequently between neurons; hyperpolarizing

types of summing in axon hillock

Spatial Summation

Adds up simultaneous influences of synapses at different sites on postsynaptic cell




Temporal Summation


Adds up potentials generated at the same site on postsynaptic cell in rapid sequence

Types of receptors (on synapses - which respond to neurotransmitter)

Ionotropic Receptors: Ion channels themselves -> neurotransmitter binds and causes change in ion flow (fast and short lived)




metabotropic receptors: induce signaling cascades via G-proteins, effectors, and second messengers that lead to either a) ion channels opening or b) further signaling cascade leading to other changes (slower and longer lived)

Drug types affecting synaptic interactions

Agonists - mimic or potentiate the effect of a neurotransmitter


-ex: morphine is agonist at endorphin receptor (blocking pain)




Antagonists - blocks the action of neurotransmitter


-ex: propranolol is antagonist of certain adrenic receptors (decreasing anxiety and panic attacks)

Central Nervous System

Site of most information processing, storage, and retrieval




Brain + Spinal Cord

Peripheral Nervous System

How CNS communicates to cells and organs of the body




Peripheral nerves = bundles of axons that work together to transmit information through nervous system

Pathways through which PNS and CNS communicate

Afferent Pathway (TO) = PNS Input (sensory receptors) ---> CNS




Efferent Pathway (AWAY) = CNS ----> PNS Output (Autonomic Nervous System or motor neurons)

Autonomic Nervous System

Division of PNS; consists of




Parasympathetic Division = "rest and digest"


Sympathetic Division = "fight or flight"




-work opposite one another

3 regions of the brain

1) Forebrain


2) Midbrain


3) Hindbrain

2 Regions of Forebrain

1) Diencephalon


2) Telencephalon

Diencephalon

of forebrain;




contains:


-thalamus (sensory info to cerebrum)


-hypothalamus (regulates homeostasis)


-epithalamus

Telencephalon - major parts

of forebrain; majority of human brain




-cerebrum: controls sensory, perception, memory, and conscious behavior; includes cerebral cortex


-basal nuclei


-limbic system





Cerebral Cortex

of telencephalon (in cerebrum)


-involved in higher order info processing


-increased surface area due to gyri (folds) and sulci (valleys)


-two hemispheres - right and left


---left mostly serves right side of body and vice versa


---not symmetrical


-Divided into 4 lobes:


---frontal = planning, personality, motor control


---parietal = touch/pressure, attending to complex stimuli


---occipital = visual info processing, translates visual experience into language


---temporal = auditory info processing, image recognition, naming


-------facial recognition - lower region of temporal lobe


-different body parts have different innervation amounts to the lobes



Parts of Midbrain

Mesencephalon


part of brainstem


-integrates info from different senses and coordinates motor responses

Hindbrain parts

Metencephalon = cerebellum (coordinates muscle activity) + pons




Myelencephalon = Medulla




-medulla and pons --> physiological regulation (e.g., breathing)

Limbic System

core of forebrain




-controls physiological drives, instincts, emotions


-hippocampus = transfers short term memory into long term memory


-amygdala = controls fear memory and response

How is brain studied

-damage - ex: Phineas Gage; construction accident - frontal lobe damage




-imaging - Positron Emission Tomography (PET); Magnetic Resonance Imaging (MRI)

primary motor cortex

region of frontal lobe; motor control

primary somatosensory cortex

region of parietal lobe; touch

motor end plate

large formation by which axon of motor neuron establishes synaptic contact with skeletal muscle fiber

sensory reception

detection of stimulus by sensory cells




stimulus can be outside the body (heat, light, pressure, or chemicals) OR inside the body (blood pressure, limb position etc.)

Stretch receptors

detect muscle stretching (type of sensory reception)

Sensory transduction

conversion of stimuli to changes in membrane potential of a sensory receptor




-sensory reception causes ion channels to open or close depending on the stimulus


-opening/closing of ion channels creates an altered membrane potential (receptor potential)


-receptor potential generates action potential


--either by directly triggering action potential in receptor cell


--or by causing receptor cell to release neurotransmitter to post synaptic neuron (inducing it to generate an action potential); amount of neurotransmitter released depends on strength of stimulus


-rate of action potentials is determined by magnitude of stimulus

sensory transmission

sensory information as action potentials are transmitted to CNS for processing and interpretation

perception

info is processed in brain (as action potentials arrive) which forms interpretations (colors, sounds, etc.)

how do our brains distinguish between stimuli

by the path along which the action potential arrives

Amplification

strengthening of sensory signal during transduction




ex: amplification of signal between outer and middle ear

Adaptation

receptors undergo decreased responsiveness upon continued stimulation




-action potentials slow down or cease


-allows animals to ignore background info and be sensitive to changes and new information

sensory pathway

1) Stimulus is detected through Stimulus Reception


2) Stimulus is converted to changes in membrane potential of a sensory receptor = sensory transduction


3) Sensory transmission = sensory information as action potentials are transmitted to CNS for processing and interpretation


4) Perception = Info is processed in brain

Sensory Organ

assemblages of sensory receptor cells with other types of cells (ex: eyes, ears, etc)

Sensory system

Includes sensory cells, their associated organs, and the neural networks that produce the information

Types of metabotropic receptors

Chemoreceptors = receptor proteins that detect quality and quantity of a molecule which binds to the receptor (and triggers cascade inducing ions to flow through channels), detect chemical stimuli, pheremones, etc.




Photoreceptors = detect light - which causes cascade leading to Na+ gates opening, hyperpolarizing the cell

Types of ionotropic receptors

Mechanoreceptors = detect physical deformation caused by pressure; plasma membrane of receptor distorts, causing ion channels to open


-ex: touch and balance mechanoreceptors




Thermoreceptors = temperature sensitive cation channels




Electroreceptors = voltage gated channels

nociceptors

pain receptors

pheremones

a specialized type of chemical signal used for communication between individuals of the same species

Receptors more likely and less likely to adapt

More = touch mechanoreceptors


Less = nociceptors, balance mechanoreceptors

_________ of receptors in connective tissue affects type of energy that stimulates them

location




deeper down - strong pressure


closer to skin surface - pain, temp, gentle pressure

how does bending of stereocilia cause depolarization in the organ of corti?

Mechanoreceptors on stereocilia bend in response to pressure




-waves of pressure bend the stereocilia


-ion channels close


-stops flow of neurotransmitter, leading to no action potentials

3 basic parts of the ear

Outer ear


middle ear


inner ear

Outer ear anatomy

Pinnae = funnel of the ear -->


Auditory Canal = where sound is amplified ->


Tympanic Membrane (aka eardrum)= receives waves of pressure moving down canal, and vibrates in response to pressure waves

Middle ear

Air filled cavity beginning on other side of tympanic membrane; transmits vibrations from tympanic membrane to oval window via the ossicles

Ossicles

in middle ear


Three bones which vibrate on each other and then ultimately on the oval window


-malleus "hammer"


-incus "anvil"


-stapes "stirrup"

Oval Window

thin membrane under stapes that makes contact with the cochlea




movement of oval window imparts pressure changes to fluid in inner ear

Inner ear

fluid filled cavity, receives vibrations from oval window - movement of oval window imparts pressure changes to enclosed fluid

enclosed fluid of inner ear

perilymph

2 sets of canals in inner ear

Cochlea = auditory system

Vestibular system - semircular canals


Cochlea

---3 Parallel canals - vestibular canal, cochlear canal, and tympanic canal


---at end of tympanic canal, have round window


---canals are separated by 2 membranes: vestibular membrane and basilar membrane


---organ of corti - sits on basilar membrane and transduces pressure waves into action potentials

How does inner ear transduce pressure waves into action potentials?

1) Stapes pushes on oval window

2) pressure wave (aka a flexion) displaces fluid in vestibular canal


3) different pitches of sound flex the basilar membrane in organ of corti at different places, activating difference set of hair cells (due to variation in basilar membrane thickenss)


4) Action potentials occur where basilar membranes flex

How does hair bending in organ of corti cause action potentials?

-Hair cells in organ of corti have stereocila which bend when fluid is displaced


-Stereocilia are attached to basilar membrane, and connect at top to the tectorial membrane


-when at rest: stereocilia not bent, ion channels open (some neurotransmitter released, thus constant action potentials)


-when stereocilia bend one way --> ion channels open (more neurotransmitter released, depolarizing cell, causing increased frequency of action potentials)


-when stereocilia bend other way --> ion channels close (less neurotransmitter released, hyperpolarizing cell, causing decreased frequency of action potentials)

What determines sound volume?

wave amplitude - more vibrations means more stereocilia bending and more action potentials firing

What determines sound pitch?

Where basilar membrane flexes - which is determined by thickness of basilar membrane




-basilar membrane is narrower at base (Better at high pitch sounds) and thicker at apex (better for low pitch sounds)

types of hearing loss

Conduction deafness = loss of function to middle ear (tympanic membrane and or ossicles); caused by recurring middle ear infections and aging




Nerve deafness = damage to inner ear or auditory pathway - hair cells become flattened; caused by loud sounds

Vestibular system

consists of vestibule and canals - 3 semicircular canals




detects body movement, position, and balance




-the vestibule and canals each have stereocilia which bend to maintain balance and detect movement

Vestibule

Bony chamber containing saccule and utricle (membranous structures) - fluid filled (with endolymph)

semicircular canals

of vestibular system




fluid filled (fluid is called endolymph)

How does vestibule detect movement and momentum?

-In sacule and utricle, stereocilia tips are in contact with otoliths = membranous structures containing crystals of calcium carbonate


-when head accelerates forward or backward, momentum of otoliths causes stereocilia to bend - opening/closing ion channels in a direction indicating direction of movement

otoliths

membranous structures in saccule and utricle (of vestibule) that contain calcium carbonate crystals


their movement causes stereocilia to bend

How do semicircular canals detect head turning and help with balance?

At base of each canal is capula = gelatinous projection encasing a cluster of stereocilia


when head moves, endolymph moves, pushing capula and stereocilia


-this causes graded membrane potential in hair cells' plasma membrane - neurotransmitter released, and sensory neurons fire action potentials in vestibular nerve

Anatomy of the eye - from front to back

Sclera (cornea in front) -> Choroid (iris in front; pupil is the opening) -> lens -> retina

Sclera

tough connective tissue layer of eye


plays role in maintaining shape


forms cornea at front

cornea

front of sclera - transparent, through it light passes

choroid

thin pigmented layer of eye that forms colored iris

iris

controls amount of light entering pupil (using ligaments and muscles)

lens

makes fine adjustments to image - focuses image on the photosensitive layer, the retina

retina

photosensitive layer in back of eye where image falls (contains nerves and photoreceptors)




*Energy is converted from light to action potentials that ultimately travel along optic nerve from the retina

pupil

central opening of iris, under neural control


-bright light - iris constricts, pupil small


-dim light - iris relaxes, pupil large

photoreceptor sensory cells

On back of retina, contain light absorbing pigment molecules (in their discs) that detect light. Also have outer segment, cell body, and synaptic terminal (synapses with neuron)




two types - cones and rods

Rods

photoreceptor, more sensitive to light


allow night vision


can't distinguish colors

Cones

Less sensitive to light, detect high acuity color in high light

Where are most cones located

in fovea = region of retina that receives light from center of visual field

Types of cone

3 - red, blue, and green




-each contains different opsin proteins


-each has optimal absorption at different wavelengths

Photoreceptors _______ in the dark and _______ in the light

DEPOLARIZE in the dark and


HYPERPOLARIZE in the light


(opposite of most other neurons - which depolarize with stimuli)

Describe why photoreceptors are depolarized in the dark

Cyclic GMP (cGMP) is bound to Na+ channels, so Na+ enters the cell


Thus the cell is depolarized and continually releases neurotransmitter (to the bipolar cells which either depolarize or hyperpolarize)

How does light hyperpolarize photoreceptor cells

1) Light activates rhodopsin pigment = light absorbing pigment located in plasma membrane of photoreceptors


---does this by activating it - turning it from 11-cis retinal (bent and inactive) to all-trans retinal (straight and active)


2) Active rhodopsin activates multiple transducin molecules (a G protein)


3) Transducin (which has high catalytic capabilities) activates many phosphodiesterase (PDE) enzymes


4) PDE hydrolyzes cGMP - turning it into GMP


5) This causes Na+ ion channels to close


6) This hyperpolarizes the cell - shuts off release of neurotransmitter


-hyperpolarizes a depolarized bipolar cell or


-depolarizes a hyperpolarized bipolar cell

How does light flow through layers of neurons in the retina

Photoreceptors > Neurons > optical nerve > brain




1) light enters eye and photoreceptors absorb wavelengths


2) cones and rods' membrane potentials change - changing release of neurotransmitter


3) info is processed through bipolar cells - membrane potential changes, causing change in release of neurotransmitter


4) info goes through ganglion cells - fire action potential to optic nerve




Also have horizontal and amicrine cells - interneurons that communicate laterally across retina to change illumination and sharpen image

Amacrine Cells

internuerons of eye;




focal connections between bipolar and ganglion cells

horizontal cells

interneurons of eye




synapse with photoreceptors and bipolar cells

cause of temporary blindness when move from bright area to dark

rhodoopsin remains active and response in rods becomes saturated completely (takes a while to regain responsiveness)

how does light travel from ganglion cells through optic nerves to brain (aka TRANSMISSION)

-Have 2 optic nerves, each with 10 million axons - some of which crossover at optic chism




-Each eye has right and left visual field


--in left eye -> axons with info from left visual field cross over chism and enter right side of brain but axons with info from right visual field don't cross over and enter left side of brain (and vice versa for right eye)




Thus, sensations from left visual field of both eyes go to right side of brain and vice versa




-also, lens projects upside down image, and our brain flips it

How does our eye focus?

Using suspensatory ligaments and circular ciliary muscles




Near vision = lens thickens and round


-muscles contract (pull border of choroid towards lens)


-ligaments relax




distance vision = lens flattens


-muscles relax (border of choroid moves away from lens)


-ligaments pull against lens

Type of receptor for gustation

chemoreceptors

5 receptor types for gustation

sour


salty


sweet


bitter


unami

anatomy of taste cell

-each taste cell contains a single receptor type


-found on taste buds - each taste bud contains multiple taste cells, of ALL 5 receptor types


-taste buds are located on papillae of tongue

how do taste buds function

have microvilli with large surface area, and generate action potentials - releasing neurotransmitter, causing sensory neurons to depolarize and send signals to CNS

tastant

stimulus for gustation (causing sensory neurons to depolarize)

how do taste and smell interact?

have separate pathways




BUT interact during perception

Type of receptor in olfaction

chemoreceptors

how many odorants can we detect?




how does this affect or genome

over 10,000.




each odorant has its own odorant receptor and each receptor has its own gene


--comprises 3% of the human genome

anatomy of olfactory receptors

-Olfactory receptors are embedded in epithelial tissue of upper portion of nasal cavity


----very close to brain; so axons extend directly to olfactory bulb of brain


-is a sensory neuron with cilia

what happens to olfactory receptors when have cold

odorants get trapped in mucus and can't make it to receptor

odorants

molecules that bind to and activate olfactory protein receptors

Steps that occur during olfaction

1) Odorant binds to receptor


2) G-Protein is activated


3) Which activates an enzyme that causes increase of second messenger


4) Second messenger binds to and opens cation channels


5) Influx of Na+


6) action potential fires

Knee Jerk Response; and role of different neuron types

1) Mallet tap stretches tendon


2) receptors detect stretch


3) Sensory Neurons - convey info to spinal cord (convert stimuli to electrical impulses)


4) Sensory neurons branch into 2:


--one branch - directly synapses to motor neuron - causes contraction


---other branch - synapses with interneuron first, which then synapses to motor neuron and inhibits it (thus can relax hamstring)

pathogens

harmful organisms and viruses that cause diease

three stages of a defensive response:

1) Recognition phase: distinguish self from non self


2) Activation phase: mobilization of cells and molecules to fight disease


3) Effector Phase: cells and molecules destroy invader

features of the lymphatic system

lymph: contains WBC and platelets; fluid derived from blood and other tissues, and accumulates in extracellular spaces


thymus: site of T cell maturation


spleen: filters blood


bone marrow: site of B cell maturation (T cells also start here then mature in thymus)


Lymph Ducts: conduct lymph


lymph nodes: filters lymph; lymphocytes (type of WBC) are found here and inspect lymph for pathogens

blood plasma

liquid component of blood, contains RBCs WBCs and platelets

types of WBCs

Lymphocytes: smaller than other WBCs, aren't phagocytic, "get the job done"


-B cells and T cells




Phagocytes: phagocytic, holding site often for non-self so B cells can come make antibdies or T cells can come and kill;


some are granulocytes = contain numerous granules (vesicles containing defensive molecules)

compare and contrast the two types of defense systems

INNATE = nonspecific and rapid


-first line of defense = skin, toxic molecules, microbiota


-second line = cell-derived: inflammation, phagocytosis, natural killer cells, complement system, interferons




ADAPTIVE = specific, slow and longer lasting


-humoral --> B Cells produce antibodies


-cellular --> cytotoxic T cells

describe first line of innate defense

Barriers


skin


saltiness and dryness of skin


microbiota




Chemical Defenses


mucus


lysozomes - enzyme produced by mucus, causes cells to lyse open (found in tears, etc.)


defensins: another class of toxins

describe second line of innate defense

Cell derived defense (triggered by self not non self) ----- types:




Cell-signaling Pathways


-PAMP recognizing PRR, and triggering defensive protein production




Inflammation


coordinated response to infection; isolates injured area




Other Cell-derived defenses


complement system, inteferons, phagocytes, natural killer cells, dendritic cells

PRRs

Pattern Recognition Receptor




found on macrophages, dendritic cells, and natural killer cells




One key type: toll-like receptor: activate transduction pathways important in both innate and adaptive systems

PAMPs

Pathogen Associated Molecular Patterns




Recognized by PRRs, molecules on bacteria etc. (basically are antigens)




ex: lipopolysaccharide

How do Toll-Like Receptors Work

1) PAMP binds to PRR


2) triggers protein kinase signaling cascade


3) NF-KB is activated


4) Causes transcriptional factor to be altered


5) causing gene expression


6) which causes gene to produce defensive proteins to target the invader

complement system

complement proteins = series of proteins that work together in a cascade to lyse a cell


also found in inflammation

interferons

signal (or cytokine) that increases resistance to infection

phagocytes

phagocytic, recognizes pathogen, engulfs it, breaks it down

Natural killer cells

initiate apoptosis

can recognize self from nonself

dendritic cells

phagocytic; act as messengers between innate and adaptive immunity

describe steps of inflammation

1) Mast Cells release signals - histamine, Tumor Necrosis Factor, Prostaglandins, etc.


2) Histamine - diffuses into blood vessels and cause them to dilate and become leaky (so other factors can leave blood vessels). TNF = kills target cells and initiates immune response. Prostaglandins - widens blood vessels


3) complement proteins leave blood vessels and attract phagocytes which target pathogens (complement proteins can also lyse)


4) Growth factors and platelets heal wound

What happens to inflammation after bacteria has been cleared

mast cells stop producing histamine




pus may accumulate = mix of leaked fluid and dead cells - bacteria, neutrophils, and damaged body cells

What happens if inflammation does not stop

Can lead to fever and then ultimately sepsis: blood vessel dilation throughout the body, causing decrease in blood pressure (can be lethal)

List several proteins that are key to cell-cell interactions as well as cell-pathogen interactions to provide defense for our body

Antibodies


Major Histocompabilitiy Complex


T Cell Receoptors


Cytokines

Antibodies

Bind specifically to certain substances identified by body as non-self = antigens


Antigen-antibody complexes make easier for body to recognize and attack


-prdoduced by B cells

Major Histocompatability Complex (MHC)

protein that displays antigen on surface of self cells so can be detected by antibodies and immune system cells

T Cell receptors

Membrane proteins on surface of T Cells; recognize and bind antigens presented by MHC on surface of other cells

Cytokines

soluble signaling proteins released by many cell types


-bind to specific cell surface receptors and alter behavior of target cells


-activate or inactivate T cells, macrophages, B cells

4 key features of adaptive immunity

1) Specificity: antibodies and T cell receptors bind to specific nonself substances - epitope = specific binding site on antigens; each T Cell and antigen is specific for a single epitope


2) Distinguishing Self from NonSelf: using clonal selection, clonal deletion, and TReg cells


3) Diversity: human body can respond to 10 million antigens (due to mutation and different gene arrangements)


4) Immunological Memory: faster response to subsequent exposures

Clonal Selection

Antigen binding "selects" a particular B or T cell for proliferation




-innate immune system presents antigen (on surface of antigen presenting cell)


-antigen binds to specific B or T cell, activating it, and causing it to proliferate

Clonal Deletion

early in differentiation of B and T cells; immature B and T cells that mount an immune response against self antigens undergo apoptosis




---doesn't always work perfectly --> autoimmune diseases

Immunological Memory

Activated T and B Cells produce two types of cells:




-Effector Cells = attack antigen and only live a few days. Effector B cells = plasma cells (prudce antibodies); effector T cells = release cytokines and other molecules that initiate killing of nonself


-Memory Cells: longer lived and can divide on short notice to produce more effector and memory T and B cells - to allow immune system to remember antigens for years

primary immune response

when body first encounters antigen, previously unexposed B and T cells recognize it and proliferate

Secondary immune response

on subsequent exposures to a known antigen, memory cells bind to antigen and proliferate faster and more powerfully

vaccination

introduction of antigen to body in form that doesn't cause disease (but still elicits primary response by first producing effector and then memory cells)

how to alter antigen in vaccine so doesn't cause disease

1) inactivation of pathogen - kill with heat or chemicals


2) attenuation - decrease virulence by repeatedly infecting cells in lab to get mutated avirulent stain


3) recombinant DNA technology - produce peptide fragments which bind to and activate lymphocytes without having harmful part of protein toxin

immunity

ability to avoid disease when invaded by pathogen by deploying various defense mechanisms

what did rat vaccine experiment show?

1) vaccines are capable of protecting


2) vaccines must be specific

key features of Humoral Response

-B cells secrete antibodies which travel freely in blood and lymph


-antibodies react with antigens

How do B cells produce antigens via the humoral response (the first time infected)? List the steps

First, Activation Phase:


1) Antigen Presenting Cell takes up antigen by phagocytosis and breaks it into fragments (by fusing antigen with lysosome)


2) a Class II MHC protein binds to antigen fragment and presents fragment on cell surface of APC


3) Thelper cell recognizes antigen fragment on class II MHC protein and binds to the protein


4) Interlukin-1 (a cytokine) are released from the APC and activates TH cells


5) Activated TH cells produce their own cytokine, which stimulate their proliferation




Next, Effector Phase:


6) B cells have IgM receptors specific for present antigen, and the antigen binds to the IgM receptor and engulfs it and breaks it down (by fusing it with lysosome)


7) Fragments attach to MHC Class II proteins and present on surface of B cell


8) Thelper cell recognizes it and binds to MHCII on B Cell


9) Causes Thelper cell to produce cytokines


10) these cytokines cause B cells to proliferate into memory and effector cells


--Plasma B cells are more of a "flagging" mechanism so that they can later by engulfed by macrophages, etc.

Antigen Presenting Cell

A cell that ingests and digests antigen and then exposes fragments of the antigen outside of the cell (bound to proteins in the cell's plasma membrane)

Immunoglobins

Class of protein that antibodies belong to

basic makeup of antibodies

4 polypeptide chains - held together by disulfide bonds


-2 light chains and 2 heavy chains


-each chain has variable region (antigen binds here, determines specificity) and a constant region (determines Ig class)

Ig Classes

IgG - most abundant antibody in primary and secondary immune responses


IgM


IgD


IgA

how are macrophages part of both innate and adaptive immune systems

innate = engulf and kill


adaptive = present antigen that will bind to antibdy

how do antibodies lead to killing of antigen

"flag" them and bring them together in a clump to be killed by other cells

How is diversity of immunoglobins created?

Shuffling of variable regions (both of light and heavy chain)




-V D J regions of heavy chain (just V J of light) - in immature B cell, have 100V, 30D, and 6J -- in mature, each gene is arranged to take just 1 of each, creating a supergene - each heavy chain is made up of two supergenes (light chains function similarly)

Class Switching

Splicing occurs in constant regions of Ig transcription, causing Ig class (of B cells) to change - start outs IgG, after splicing different constant region is closest to variable region and that determines Ig class

T Cells overview

-use gene reshuffling to create diversity


-contain a glycoprotein receptor which binds to antigen presenting cell


---receptor has 2 chains - alpha and beta; each chain has variable (site of antigen binding) and constant (anchors receptor to T cell membrane) region

Antigen Presenting Cells example

Major Histocompatability Proteins (MHC)


Presents antigen on cell surface and then binds directly with T cells

Classes of MHC

Class I MHC - present on ALL nucleus containing cells = enable Tc cells to recognize virus infected cells (with help of CD8 protein)




Class II MHC - mostly on B cells, macrophages, and other APCs = enables Th cells to recognize antigen fragments (with help of CD4 protein)

Types of T cells (and functions)

Cytotoxic T Cells = recognize virus infected or mutated cell and kills by lysis (via cellular response) by producing perforin


T Helper Cells = Stimulates both cellular and humoral responses


T Regulatory Cells = binds to self antigen, causing release of interleukin-10 which supresses T cells and leads to apoptosis of Tc and Th cells (thus ensuring immune system doesn't attack self cells)

Features of the cellular response

-destroys infected cells via cytotoxic T cells


-directed against antigens established within host cell


-critical for response against viruses

List steps of cellular response

First, Activation Phase:


1) Antigen enters a cell (becomes infected)


2) Antigen is broken down into fragments


3) MHC I binds to fragment and presents in to cell surface


4) Cytotoxic T Cell Receptors recognize antigen bound to MHC I and binds to complex (with help from CD8)


5) This binding activates Cytotoxic T cells, causing them to proliferate




Next is the Effector Phase:


6) Tc cells recognize MHC I complexes on other infected cells and bind to the complexes


7) This binding causes Tc cell to release perforin


8) Perforin causes cells to lyse