Animal Physiology Exam 2

graded potential is diverse this means

can be generated by any ion channel

- voltage

- ligand

- mechanical

can graded potential travel long distance or short distance

travels only short distance (

decrease amplitude of graded potential with

increase distance from site of opened ion channel

what causes conduction with decrement in graded potential

leakage of charged ions.

electrical resistance of cytoplasm.

electrical properties of the membrane.

electrotonic current spread

denoting the direct spread of current in tissue by electrical conduction, without the generation of new current

can graded potential be excitatory or inhibitory

it can be both

what makes graded potential excitatory

(Depol.) Na+, Ca++ due to positive membrane potential

what makes graded potential inhibitory

(hyperpol.) K+, Cl- due to negative membrane potential

graded potential varies in

size ( amplitude) depending on the strength of stimulus that carries it

increase concentration of ligand will (in terms of GP)

open more ion channels- larger GP

higher concentration of neurotransmitter will open or close more channels

open

producing mroe depolarization

what is the general pathway of GP

NTM bind to ligand gated Na+ channel.

Na+ enters thru open channel.

Current spread thru cells.

Strength of signal decreases with distance.

Graded potentials are quicker or slower than action potentials

quicker, but travel shorter distance

(electronic current spread)

what is the presynaptic mechanism

1. vesicles load with NTM via active transport approach the active zone.

2. synaptobrevin binds to SNAP 25 and syntaxin.

3. when ECP hits nerve terminal action potential depolarizes.

4. VG Ca+ opens, Ca+ enters cell.

5. Ca+ binds to synaptictagmin on synaptic vesicle.

6. Ca+ bind changes configuration of core complex, makes fusion pore with vesicle membrane and presyn. memb.

what is the three protein complex

aka SNAPE proteins/core complex

-synaptobrevin

-SNAP 25

-syntaxin

irreversible binding until exocytosis

exocytosis

vesicle opens and flattens and becomes part of presyn. memb.

(NTM is released into synaptic cleft)

membrane re-uptake involves

1. recycling used vesicles

2. exocytosed vesicular memb. is coated with clathrin molecule that causes invagination/ endocytosis and reforms vesicle.

3. pinches off presyn. memb. and clathrin disperses.

4. Transported by multivesicular complex and refill with NTM or refuses with mult. complex.

Tetanus toxin and botulinum toxin B,D,F effect

synaptobrevin

botulinum toxin c effects

syntaxin

botulinum toxin A and E effect

SNAP 25

toxins that affect any of the core complex proteins does what

keeps vesicles from membrane and silence the synapse, cannot release NTM

NTM release mechanism

1. AP arrive at axon terminal

2. VG Ca++ chan. open

3. Ca++ enters cell

4. Ca++ binds to synaptictagmin on synp. vesicle

5. Ca++ depol. change conformation of SNARE proteins @ synaptic vesciles and PM

6. docked vesicles release NTM by exocytosis

7. NTM diffuses across the synp. cleft and binds to receptor on target cell.

Mitochondria

provides energy in the form of ATP

microtubules

deliver elements from cell body

multivescular complex

produce synaptic vesicles by budding

neurotransmitter

chemical messengers that cross the synaptic gaps between neurons

active zone

include docking proteins for vesicular release & voltage gated Ca++ ch.

ion channel

a pore in a cell membrane through which ions can pass

conotoxin

Blocks voltage-gated calcium channels

no Ca to bind to synaptobrevin

cone snail

cone snail

conotoxin

Blocks voltage-gated calcium channels

no Ca to bind to synaptobrevin

spinal motor neurons signaling

- signal reception: incoming signals are recieved and converted to a change in MP (GP)

- signal integration: change in MP initiated AP

- signal conduction: AP are conducted to the axon terminal (AP)

- signal transmission: NTM release transmits a signal to the target cell

how are NTM halted quickly

- diffusion of NTM --> slower

- enzymatic destruction --> quicker

- reuptake into surrounding cells --> quicker

what toxins affect VG Ca++ channels

conotoxins

What neurotoxins affect SNARE proteins

botulinus and tetanus toxins

ligand

A molecule that binds specifically to a receptor site of another molecule.

Receptor

- changes shape in response to ligand

- may be ligand gated ion ch (nicotinic ACHr)

- some have no built in ion channel: act. by effecting biochemical change (muscarinic ACHr or aldosterone rec)

-hydrophillic chem mess --> rec is integral membrane

- hydrophobic chem mess --> rec is located intracellulary

where are receptors for hydrophilic chem mess

integral membrane

in plasm membrane

where are receptors for hydrophobic chem mess

intracellularly

--> cytoplasm, nucleus, other organelles

Ligand-Receptor Interactions

only correctly shaped ligand can bind to each type of receptor

- exogenous ligands can mimic shape of natural ligands

--> drugs toxins

- agonist

- antagonist

exogenous ligand

can mimic the shape of a natural ligand

drugs and toxins from outside the body

agonist

a molecule that, by binding to a receptor site, stimulates a response

Antagonist

a molecule that, by binding to a receptor site, inhibits or blocks a response

every target cell has

specific receptors for chemical signaling molecules

receptors at postsynaptic membrane determine

whether or not the NTM will have an effect

specific nature of the effects

somatic nervous system

Division of the PNS that controls the body's skeletal muscles.

- single neuron carries signal

- target response to one AP is alwyas full exitation

- synaptic release of ACH is the only normal effector stimulus

only ligand and receptor in somatic nervous system

acetylcholine and nicotinic ACH receptor

Tetrodotoxin

Toxin from puffer fish that blocks voltage dependent sodium channels

--> sciatic nerve

--> gastronemius

mu-conotoxin

blocks voltage gated calcium channels of gastronemius

--> cone snail

muscle cells

contractile cells generate motion

- made of myocytes

- two main types : striated and smooth

myocytes

Muscle cells; contractile cell unique to animals

- contain myofibrils

- single cont. stretch of interconnected sacromeres

sacromere

contractile unit of a muscle fiber

myofibril

A long, filamentous organelle found within muscle cells that has a banded appearance

striated muscle cell

- thick filament (~300 myosin hexamers)

- thin filament (actin)

- troponin and tropomyosin

myosin

thick filament

actin

thin filaments

- troponin and tropomyosin

troponin

A protein of muscle that together with tropomyosin forms a regulatory protein complex controlling the interaction of actin and myosin and that when combined with calcium ions permits muscular contraction

tropomyosin

covers myosin binding sites on the actin molecules

Transverse tubules (T-tubules)

Transmit action potential through cell

Allow entire muscle fiber to contract simultaneously

Have same properties as sarcolemma

sarcolemma invaginnations

enchance AP penetration

sarcoplasmic reticulum

Organelle of the muscle fiber that stores calcium.

-- terminal cisternae: increase Ca++ storage capacity

terminal cisternae

increase Ca++ storage capacity

enlarged areas of the sarcoplasmic reticulum surrounding the transverse tubules

excitation-contraction coupling

1. somatic motor neuron release ACH at neuromuscular junction

2. Opening of VG Na+ channels allowing Na+ in --> depolirization

3. AP travels down the T-tubules

4. Ca++ enters thru L-type VG Ca++ channels and from outside the cell, and from SR thru RyR ch.

5. Ca++ binds to troponin allowing actin-myosin binding

6. muscle contraction

7. Sarcolplasmic CaATPase pumps Ca++ back into SR

8. decrease in [Ca++] causes Ca++ to unbind from troponin

9. tropomyosin recovers binding site --> relaxation

Acetylcholine (ACh)

enables muscle action

- found in PNS and CNS

- most abundant NTM in PNS

receptors for aCH

iontropic:

--> nicotinic ACHr

metabotropic:

--> muscarinic ACHr

iontropic receptors

receptors that are associated with ligand-activated ion channels

--> nicotinic ACHr

metabotropic receptors

receptors that act through a second messenger system and G prtoteins

- no ion channel

---> muscarinic ACHr

G protein

peripheral membrane protein

a protein coupled to a metabotropic receptor; conveys messages to other molecules when a ligand binds with and activates the receptor

Acetylcholinesterase (AChE)

the enzyme that breaks down acetylcholine in the synaptic cleft

ACH --> acetate + choline

what is ACH made of

Acetyl CoA + Choline --> ACH

symphathetic nervous system

the division of the autonomic nervous system that arouses the body, mobilizing its energy in stressful situations

- flight or fight

- NorEpi and Epi

Norepinephrine and Epinephrine

NTM involved in symp NS

Norepi and Epi Receptors

adrenergic receptor

- alpha-adrenergic rec

- alpha 1

- alpha 2

- beta-adrenergic rec

- beta 1 2 3

- all adrenergic rec are g protein coupled

- generally linked to 2nd messenger

- slow response @ all rec

- effects in flight or fight

- inc heart rate

alpha 1 adrenergic receptor

rec for NorEpi and Epi

activate by inc. [Ca++]

thru G protein and 2nd messenger

protein kinase C

increase protein phosphorylation and activate Ca++ binding proteins

alpha 2 adrenergic receptor

activate by dec. [cAMP]

protein kinase A

inhibitory

decrease protein phosphorylation

beta-adrenergic receptors

most present in heart

B1 B2 B3

B2: greatest affinity for Epi

activate by inc. [cAMP]

protein kinase A

increase protein phosphorylation

Mammalian and bird hearts

- 4 chamber

- 2 atria

- 2 ventricle

- valves

- atrioventricular

- semilunar

- veins

- sup and inf vena cava

- pulmonary

right atrium

Receives deoxygenated blood from the body

body --> sup and inf vena cava --> heart

left atrium

receives oxygenated blood from the lungs

lung --> pulmonary v --> heart

right ventricle

pumps deoxygenated blood to the lungs

left ventricle

pumps oxygenated blood to the body

atrioventricular valves

Valves located between the atrial and ventricular chambers on each side of the heart, prevent backflow into the atria when the ventricles are contracting.

atr-->vent

bicuspid and tricuspid

bicuspid valve

valve between the left atrium and the left ventricle.

tricuspid valve

valve between the right atrium and the right ventricle

Seminlunar valves

exit ventricles

pulmonary semilunar valve

heart valve opening from the right ventricle to the pulmonary artery

aortic semilunar valve

located between the left ventricle and the aorta

vena cava

One of two large vessels (superior and inferior) that return deoxygenated blood to the right atrium of the heart.

body-->heart

pulmonary veins

carry the oxygenated blood from the lungs into the left atrium of the heart

lungs --> heart

cardiac output

heart rate x stroke volume

intraventricular septum

separates the two ventricles

slow passage of electrical signaling

delay bw contractio

edema

puffy swelling of tissue from the accumulation of fluid

imbalance of P in circuits

sinoatrial node

pacemakers of the heart

amphibian heart

3 chambers (2 atria and 1 ventricle)

PMc in sinus venous

sinous venosus

pacemaker cells located in amphibians

systole

contraction phase of the heartbeat

Diastole

relaxation phase of the heartbeat

Valves open passively due to

pressure gradients

AV valves open when atrial pressure > ventricular pressure

Semilunar valves open when ventricular pressure > arterial pressure

p wave

atrial depolarization

SA node PMc contract and spread rapidly thru internodial pathway

delay of heart beat

depolirization thru bundle of his and purkinje fibers

QRS complex

ventricular depolarization

depol spreads up ventricles and ventricularmyocytes contract

t wave

ventricular repolirization and relaxation