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SDSU / OTHER / Bio 336 / What is the problem with sodium layers?

What is the problem with sodium layers?

What is the problem with sodium layers?

Description

Lecture #1: Membrane Potential 


What is the problem with sodium layers?



● Phospholipid Bilayer

○ Phosphate head = polar, hydrophilic

○ Fatty Lipid tail = nonpolar, hydrophobic

● Muscle cell

○ Extracellular Fluid (ECF): blood, sweat, tears, water

○ Intracellular Fluid (ICF)

● Na+/K+ Pump

○ Integral membrane protein

○ 2 K+ pumped into ICF and 3 Na+ pumped out to ECF

○ High concentration of Na+ in ECF

○ High concentration of K+ in ICF

○ Creates voltage

● Problems with Sodium levels

○ Hypernatremia: high concentration

○ Eunatremia: healthy level (135-145 mmol)

○ Hyponatremia: low concentration

■ Can get this from drinking too much water


What are the problems with potassium?



● Problems with Potassium

○ Hyperkalemia: high concentration

○ Hypokalemia: low concentration

● Practice Questions

○ 1. Why does the bilayer form this way? Don't forget about the age old question of layer of hard keratin that coats the hair

■ Answer: The lipid tails are hydrophobic so they are not soluble in water which is why they are on the inside.

○ 2. How does the Na+/K+ ATPase work?

■ Answer: ATP - Adenosine Triphosphate

○ 3. What is the Resting Membrane Potential?

■ Answer: -80 mV

Lecture #2: Action Potential/ Neuromuscular Physiology 

● Hodgkin and Huxley conducted experiments about ACtion Potential ○ Did 3 things

■ 1. Measure the resting membrane potential

■ 2. Measure action potential


What is a muscle cell?



■ 3. Action potential conduction

● 1. Measure the resting membrane potential (RMP)

○ Giant axon of the squid

○ Axon 1mm in diameter

○ Every cell has a voltage between -60 and -80 mV

○ Negative on the inside at rest, positive on the outside

○ Action potential occurs at -50 mV

● 2. Measure Action Potential

○ Vocab:

■ Threshold: cell must reach this point in order for an action potential to occur

■ Depolarization: brings cells closer to 0 mV

■ Repolarization: brings cells back to RMP We also discuss several other topics like math 115 towson

■ Hyperpolarization: more negative than RMP / VGK+C closwes here (@ -90 mV)

○ At +30 mV, cell is positive on the inside, negative on the outside

○ Action Potential = change in polarity

○ Integral Membrane Proteins - no channel closes at -80 mV

■ A. Voltage Gated Sodium channel (VGNa+C) - opens first

● Electrical volts open the gate

○ Voltage will change if channel is gated

● Protein is designed to only allow solium in

● VGNa+C is completely closed at -60, -70, and -80 mV

● Opens at threshold for 1ms

● Depolarization and overshoot is due to opening of VGNa+C

● Closes at the top of overshoot

● Novacaine and Lidocaine block VGNa+C

● Tetrodotoxin (TTX) from pufferfish binds to VCNa+C --> no action potential --> flaccid paralysis

■ B. Voltage Gated Potassium Channel (VGK+C)

● Stays open for 2ms

○ 1st second: repolarizes

○ 2nd second: makes cell more negative -->

hyperpolarization

● Action potential diffuses out of the cell We also discuss several other topics like cse 535 asu

● Causes repolarization

● 3. Action Potential Conduction

○ Conduction: action potential moves forward along the tissue of a muscle ■ Does not go backwards

■ Hyperpolarization prevents action potential from going backwards ○ Conduction Velocity: speed (meter / second)

■ Unmyelinated neuron: 1m/s

■ Myelinated neuron: 100 m/s

○ Myelinated Neurons:

■ Almost all neurons are myelinated

■ Myelin quickens action potential

■ Myelin blocks any conduction from occurring so the action potential jumps ■ Myelin does not affect the inside of a cell

○ Demyelination Diseases

■ 1. Multiple Sclerosis

● Produces antibodies to oligodendrocytes

● Muscle weakness We also discuss several other topics like math 125 uic

■ 2. Guillain-Barré Syndrome

● Damages myelination of Peripheral Nervous System

● Lead can cause this disease, so can heavy metal such as mercury

○ C.O.P.S.

■ Central Nervous system (CNS)

● Oligodendrocytes cause myelination in CNS

■ Peripheral Nervous System (PNS)

● Schwann Cells cause myelination in PNS

○ Neurons:

■ About 87 billion in the human body

■ Dendrites of one neuron do not touch terminal button of another neurons ● Area between dendrite and the terminal button is called the We also discuss several other topics like anthropology 102 final exam

synapse

■ No neurons touch each other

■ Action Potential can NOT jump the synapse

■ Levels of nerves: pain (smallest), temperature, touch, motor (biggest)

Lecture #3: Synaptic Transmission / Neuromuscular Junction 

● How it Works

○ 1. Nerve action potential comes down collateral to the terminal button ○ 2. Voltage gated Calcium Channel opens at +30 mV

■ VGCa+C only in terminal button

■ (a) once VGCa+C is open, Ca++ rushes in

■ (b) 2 Ca++ bind to synaptotagmin We also discuss several other topics like cmps111

● Synaptotagmin keeps vesicles from fusing to the T-Snares unless

they have action potential

○ 3. Synaptotagmin changes shape and V-Snares bind to the T-Snares --> vesicle fuses to the terminal button

○ 4. Ach vesicle exits terminal button vis calcium induced exocytosis

○ 5. Ach binds to the Nicotinic Acetylcholine Receptors (NAchR) which are on the motor end plate

○ 6. NAchR opens for 1ms which allows for Na+ to diffuse into the muscle --> cell reaches threshold (-50 mV)

● Problems with Channels

○ Clostridium Botulinum

■ Anaerobically grown

■ Produces a toxin to destroy snares protein

■ Causes Ach to not be able to perform exocytosis out of the cell causing flaccid paralysis

○ Botox

■ Destroys V-Snares and T-Snares

■ Vesicles are not docked --> cannot have Ca++ exocytosis --> flaccid paralysis

■ People get small minute amount to make their muscles relax which can make them look younger

■ 1 kilogram can kill millions of people (it is a biohazard)

○ Black Widow Spider Venom (latrotoxin)

■ Forms pores in terminal button that allows Ca++ to flood in causing

spasmodic paralysis

■ Pore is highly specific to Ca++ only

○ Curare

■ Ach antagonist

■ Used in poisonous darts

■ Looks like Ach but not enough to open the NAchR causing flaccid

paralysis

■ Only lasts 15 minutes

■ Used in general anesthesia

○ Banded Krait (snake)

■ Venom called alpha bungarotoxin

■ Blocks NAchR --> permanently causes flaccid paralysis

● There is no anecdote

■ Rat receptors are different so the snake can still eat the rat after it has been bit

○ Lambert-Eaton Syndrome

■ Antagonizes VGCa++

■ Body produces antibodies that bind to VGCa++C and keeps it from

opening

■ No Ca++ induced exocytosis --> flaccid paralysis

● Cholinesterase: breaks down Ach down into acetic acid and choline then receptor closes ○ Receptor only needs to be open for 1ms to reach threshold

■ Terminal button reuptakes acetic acid and choline for recycling

○ Cholinesterase Inhibitors:

■ Sarin Gas

● Causes spasmodic paralysis

● Twitching is a symptom

● Used in Tokyo Subway Massacre

■ VX Gas (more potent)

● Does not allow cholinesterase to break Ach down

● Causes spasmodic paralysis

Lecture #4: Nervous System 

● Lobes

○ Frontal: motor cortex, motor activity starts here, upper motor neurons are here ○ Temporal: auditory cortex, used for hearing, aphasia: inability to speak

○ Parietal: sensory cortex

○ Occipital: visual cortex

● Structures:

○ Precentral Gyrus: contains upper motor neurons

○ Grey Matter: contains cell body, dendrites, terminal button, axon hillock ○ Corona Radiata: type of white matter, fibers continue as the internal capsule ○ Internal Capsule: ends at the start of the midbrain

○ Longitudinal Fissure

○ Thalamus

○ Lentiform Nucleus

● Cranial Nerves (12 pairs, know 3)

○ CN III: Oculomotor Nerve

○ CN VII: Facial Nerve

○ CN XII: Hypoglossal nerve

○ All cranial nerves decosate at the level of the cranial nerve

● Spinal Nerves (31 pairs, know 4)

○ C5: innervates bicep

○ C7: innervates tricep

○ L3: innervates quadricep

○ S1: innervates gastrocnemius

○ All spinal nerves decosate at medulla pyramids

Lecture #5: Central Nervous System 

● Structures of Spinal Cord:

○ Ventral Medial Sulcus: indentation on the ventral side of spinal cord

○ Corticospinal Tract (CST): the location where upper motor neurons exit after traveling down the spinal cord

■ Nerves that go to the arm exit the CST on the medial side

■ Nerves that go to the leg exit the CST on the lateral side

○ Ventral Horn: where dendrites and cell bodies of lower motor neurons are located ● Types of Lesions and their Effect

○ Lesion at C2: quadriplegia, cannot breathe

■ C2 innervates the diaphragm

○ Lesion at C4: quadriplegia, no activities of daily living

○ Lesion at C6: ability of elbow flexion

○ Lesion below C5: can accomplish most things

○ Lesion below C7 and above L3: paraplegia (arms are okay, legs do not work) ● Destruction of Motor Neurons

○ Polio:

■ Destroys lower motor neurons

■ Arm, leg, and respiratory paralysis

■ Lesions would be in the ventral horns

○ Amyotrophic Lateral Sclerosis (ALS)

■ Also known as Lou Gehrig’s Disease

■ Disease / destruction of upper AND lower motor neurons

■ Lesion would be in the ventral horns & CST

● The Brain

○ 2% of your body weight

○ Receives 20% of blood flow

○ Lack of blood flow to the brain --> tissue starts to die within minutes

○ Main source of blood flow to the brain: carotid artery

○ Anterior Cerebral Artery: takes blood to medial aspect of precentral gyrus and to the frontal lobe

○ Middle Cerebral Artery: takes blood to the superior and lateral aspects of the precentral gyrus

● Strokes

○ 1. Ischemic Stroke

■ Arteries become too narrow

■ Thrombus blocks vessel and there is no blood flow further down the vessel

● Thrombus = blood clot

■ Can be given a thrombolytic (tPA) to minimize the damage

● tPA: breaks thrombus down, allows blood flow, must be

administered within 4 hours of showing symptoms

○ 2. Hemorrhagic Stroke

■ Vessel ruptures --> no blood flow further down the vessel because blood is going out of the ruptured area

■ Can NOT be given a tPA

● tPA makes a hemorrhagic stroke even worse by possibly

increasing the bleeding / damage to the brain

○ How to tell the difference between the two strokes:

■ Cat / CT Scan (unit Hu)

■ Blood is hyperdense (will be white on scan)

● More dense than brain tissue and neurons

■ Ischemic stroke: blood vessel will be when then abruptly turn dark (no blood flow) --> administer tPA

■ Hemorrhagic stroke: large, white, hypersense regions around the brain --> NO tPA

Lecture #6: Muscles Part 1 

● Types of Proteins:

○ Contractile: actin, myosin

○ Structural: actinin- holds actin parallel to myosin

○ Regulatory: tropomyosin, troponin, SERCa

● How a muscle contracts:

○ 1. Crossbridge

○ 2. Power stroke

○ 3. Detachment

○ 4. Recovery (myosin head goes from 45 degrees to 90 degrees) - slowest step ● Titin: largest protein

● Troponin: smallest protein --> first protein to enter the bloodstream

● Myosin + ADP = myosin head in high affinity for actin

● Myosin + ATP = myosin head in low affinity for actin

● Myosin ATPase: enzyme that breaks down ATP

● Dead --> rigor mortis (stiffening of body) --> ADP --> myosin attaches and power strokes, but can NOT detach (step 3) because there is no ATP

● Myasthenia Gravis: give small amount of sarin gas or VX gas (a cholinesterase inhibitor)

Lecture #7: Muscles Part 2 

● Contracted Muscle

○ Sarcomere gets shortened

○ I-Band disappears

○ A-Band does NOT change size when muscle contracts

● How Steric Hindrance if Removed

○ 1. Muscle Action Potential travels down the sarcolemma --> reaches T-tube ○ 2. M.A.P. goes down T-tube and get to DHP receptor --> DHP receptor moves and binds to the Ryanodine Receptor (RyR) and opens it

○ 3. Ca++ diffuses/releases out for the Sarcoplasmic Reticulum (S.R.)

○ 4. Ca++ binds to Troponin and causes Tropomyosin to move - removing the steric hindrance

○ 5. Muscle contracts

● Proteins:

○ 1. Sarcoplasmic Reticulum Calcium ATPase (SERCa)

■ Allows muscle to relax

■ Pumps Ca++ into S.R. and causes Ca++ ions to accumulate in the

terminal cisternae

■ Located in the longitudinal S.R.

■ No SERCa --> muscle as a hard time relaxing

○ 2. Ryanodine Receptor (RyR)

■ Closes once no more M.A.P. travels down

■ Located in the terminal cisternae of S.R.

■ RyR antagonist: Dantrolene

● Used for relieving muscle spasms

● Responsible for the release of Ca++ from the terminal cisternae

○ 3. DHP Receptor

■ Located on T-Tube

■ Moves and binds to RyR to release Ca++

● Triad: 2 Terminal Cisternae, and T-Tube

● Calcium Cycling

○ 1. M.A.P. travels down

○ 2. DHP receptor binds with RyR

○ 3. RyR opens and releases calcium

○ 4. Calcium binds to troponin

○ 5. Muscle relaxes --> Ca++ into S.R.

● Two Types of Muscle

○ 1. Fast twitch fibers (pale / white)

■ Time to peak tension: 50 m/s

■ Contracts and relaxes rapidly

■ Fast isoform of Myosin ATPase

■ 4% fiber is S.R.

■ Fatigues rapidly

○ 2. Slow twitch fibers (dark / red)

■ Time to peak tension: 200 m/s

■ Contracts and relaxes slowly

■ Slow isoform of myosin ATPase

■ 2% fiber is S.R.

■ Does NOT fatigue rapidly

○ Humans have both fast twitch and slow twitch fibers in all muscles ■ Called mosaid muscles

■ Greater diversity

■ Most people have 50:50 ratio

■ Genetics can affect the ratio

● We use ~100 lbs of ATP every day

○ Muscles only have ~6 seconds of ATP

○ Two ways to remake ATP

■ 1. Glycolysis

● Faster (4x faster)

● Anaerobic

● Fast twitch fibers

■ 2. Mitochondria

● Slower

● Aerobic

● Slow twitch fibers

Lecture #8: Muscles Part 3 

● 2 ways to Remake ATP

○ 1. Glycolysis

■ Carbs get broken down in the ICF in 10 steps

■ Does NOT require oxygen

■ Leads to pyruvic acid

○ 2. Mitochondria

■ End product: H2O, CO2

■ Can train body to have more mitochondria

● Live at high altitudes

● Important for distance runners

● Motor Unit

○ All fibers in a motor unit are fast twitch OR slow twitch fibers ○ Small twitch = small motor unit

○ Fast twitch = big motor unit

● We can recruit motor units to lift heavier things

○ Start with the smaller ones then move to the larger ones ● Hypertrophy: gain muscle (increase # of myofibrils) ● Atrophy: loss of muscle (decrease # of myofibrils) ● Hyperplasia: increase number of muscle fibers

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