Bio1 - Nerve & Muscle

• act as a permeability barrier that prevents the transport of protein molecules from the lumenal to basolateral side of the cell
• also hold neighboring cells together

a means for water-soluble molecules to pass from the cytoplasm of one cell to the cytoplasm of another cell

joins epithelial cell to the basal lamina; helps to anchor cell in place

made up of cells that secrete substances into the lumen through a duct

secrete substances into the blood

• E_m refers to the charge INSIDE a cell compared to outside
• generally the charge outside = 0 (as a reference)
• inside - outside charge

• at normal body temperature
• RT/zF • ln = 60mV/z • log
• R: gas constant (8.32 joules/mole • °K)
• T: the absolute temperature (in °K, ~37)
• z: ion valence (+1 in the case of K+)
• F: Faraday's constant (96,500 Coulombs/mole of + charge)

• E_K = 60mV/z • log [ion]_out/[ion]_in
• E_K = 60mV/(+1) • log (10/100)
• E_K = 60 • -1 / +1 = –60 mV

• if the denominator is greater than the numerator, then log(ion_out/ion_in) is negative
• if the numerator is greater than the denominator, then log(ion_out/ion_in) is positive

• actual E_K = -93 mV
• E_m = -70 mV
• [K⁺]_inside > [K⁺]_outside
• K⁺ wants to move OUT of the cell; this is down its electrochemical gradient
• moving out makes the inside of the cell more negative (b/c + charge is leaving), bringing the membrane potential CLOSER to that of K⁺ in equilibrium (E_K = -93 mV)
• the concentration gradient is directed OUTWARDS

• E_Na = 60mV/z • log [ion]_out/[ion]_in
• E_Na = 60mV/(+1) • log (100/10)
• E_Na = 60 • +1 / +1 = 60 mV

• actual E_Na = +65 mV
• E_m = -70 mV
• the concentration gradient is directed INWARDS
• when Na⁺ moves DOWN it's concentration gradient, the membrane potential inside the cell relative to outside the cell becomes more POSITIVE (b/c Na is a cation)
• this brings the E_m closer to E_Na

• E_Cl = -89 mV
• E_m = -70 mV
• higher concentration outside the cell; lower inside the cell (similar distribution as Na⁺)
• this concentration gradient drives Cl^- inside, making the inside of the cell more negative
• E_Cl is more negative than E_m; Cl^- wants to move into the cell (that's down its electrochemical gradient)

• K⁺: –93 mV
• Na⁺: +65 mV
• Cl^-: –89 mV
• Ca²⁺: +129 mV (extremely low inside the cell)

• Depolarization (upshoot): Na⁺ channels are open, K⁺ channels are CLOSED

- Na (+ charge) rushes into the cell, dePolarizing the membrane, making it more positive inside

• Repolarization (downshoot): K⁺ channels are OPEN, Na⁺ channels are closed

• to return the membrane to its normal (negative) resting potential, K (+ charged) exits the cell through open channels - too much leaves, causing hyperpolarization b/c K⁺ channels are slow to close

• P_Na: begins early & then inactivates
• P_K: begins more slowly & then does NOT inactivate

• inactivation of Na⁺ channels
• if the plasma membrane has been depolarized from an action potential, then another action potential cannot be generated until that membrane has once again reached its resting membrane potential
• b/c the Na⁺ channels become inactivated & the K⁺ channels take a while to close again after the action potential has occurred, there's a natural upper limit to the rate at which a nerve cell can generate action potentials

• conduction velocity is a function of the LENGTH CONSTANT
• an axon with a larger diameter has a lower internal resistance & therefore a LARGER length constant
• therefore conduction velocity by way of relation to length constant is related to axon diameter
• larger diameter axons conduct action potentials more rapidly

• increases the length constant → conducts action potentials more rapidly
• myelin is produced by oligodendrocytes in the CNS & schwann cells in the PNS

• voltage-dependent Ca²⁺ channels cause a prolonged action potential during which the heart muscles repeatedly contract to pump blood
• K⁺ & Ca²⁺ permeabilities exhibit a similar time course but have OPPOSITE effects on the membrane potential b/c they carry current in opposite directions → generates a plateau on the falling phase of the action potential during which K⁺ (out) & Ca²⁺ (in) currents are ~equal in magnitude but opposite in direction
• cardiac muscle APs last ~300 ms longer than those of skeletal muscle

• one that conducts a nerve impulse FROM the periphery TOWARD the CNS (periphery → CNS)
• otherwise known as a SENSORY nerve

• one that conducts a nerve impulse FROM the CNS toward the periphery (CNS → periphery)
• otherwise known as a MOTOR nerve

• nerve cell bodies & their dendrites
• makes up the outermost layer of the cerebrum (the cerebral cortex)
• more centralized in the spinal cord

• myelinated axons of the nerve cells
• centralized/lies beneath the cerebral cortex; peripheral in the spinal cord

• somatic nerves from CNS synapse DIRECTLY on effector organs
• ACh is the NT released at the synapse & it acts on nicotinic (N1) receptors on skeletal muscle cells at the NMJ

• an involuntary system that regulates all the “vegetative” functions of the body
• has afferent input from Visceral afferents (eg. arterial BP, visceral pain), Somatic afferents (eg. surface pressure & pain), and Special senses (eg. visual, auditory)

• the part of the peripheral nervous system that innervates ALL organs of the body & acts as a control system, functioning largely below the level of consciousness to control visceral functions
• it affects heart rate, digestion, respiratory rate, salivation, perspiration, pupillary dilation, micturition (urination), & sexual arousal
• can be divided into 2 subsystems: PSNS & SNS

• constriction of the Pupils & Bronchi
• increased detrusor muscle activity (bladder wall)
• reduced heart rate
• increased tear & saliva production
• increased GI peristalsis
• increased sphincter tone
• increased blood flow to the GI tract
• generally conserves energy & helps in the restoration of various bodily functions

are located in close proximity to the effector organs (the 1st neuron is LONG & the 2nd neuron is SHORT)

• dilation of Pupils & Bronchi
• reduced detrusor muscle activity
• increased heart rate
• constriction of blood vessels
• increased blood pressure
• reduced gastrointestinal peristalsis
• piloerection (goose bumps)
• “fight or flight”

form a chain, with divisions that occur closer to the spinal cord & farther from the end organs (1st neuron is SHORT & 2nd neuron is LONG)

• receive sensory information regarding pressure, hearing, ba0lance, & BP from the environment & pass that information to the nervous system
• respond to a change in their configuration

sense pain

detect cold & warmth

detect taste, smell, oxygen, carbon dioxide, hydrogen ions, & blood glucose levels

• when the generator potential & consequently the action potential frequency decline even though the stimulus intensity on a receptor is maintained
• as a receptor adapts sensory input to the CNS is reduced & the sensation is perceived as less intense

• whole muscle
• ↓
• Fasiculus
• ↓
• Muscle Fiber (myocyte) = muscle cell
• ↓
• Myofibril: very long chains of sarcomeres
• ↓
• Sarcomeres: contractile units of the cell; made of thin & thick filaments
• ↓
• Myofilaments: actin & myosin

• I band: light staining thin actin filament bisected by the Z line
• Z line: serves as an anchoring point for thin actin filaments (Z disk)
• Sarcomere exists from the dark Z line in one thin actin filament to the Z line in the next
• A band: dark staining THICK myosin filaments
• M line: line w/ proteins that reside in the middle of the A (thick myosin) band: hold the myosin together
• H band: slightly lighter area surrounding M line in the middle of the A (dark, myosin) band
• the bubbly/dotty stuff between myofibril striation = cell organelles (eg. mitochondria)

• muscle contraction is produced by actin & myosin filaments sliding past each other
• the Sarcomere overall shortens → a 'domino' effect of sorts that can cause the muscle to shorten by ~10% overall
• the Z-lines move CLOSER together
• neither the I nor A bands shorten (Z within the I band just moves)
• H band (surrounding M line) disappears - is filled in with thin filaments

• bipolar assemblies of multiple Myosin-II molecules, a double trimer made up of 2 intertwined heavy chains, two regulatory light chains, & two other “alkali” or “essential” light chains
• the heads of the heavy chains each can both bind to actin & have an enzymatic site for binding & hydrolyzing ATP
• the “alkali” light chain plays an role in stabilizing the head region
• the regulatory light chain regulates Myosin ATPase activity & is itself regulated by Ca²⁺-dependent & Ca²⁺-independent kinases

• in skeletal muscle this consists of Actin, tropomyosin, & troponin
• the filament itself is a double stranded helical polymer of Actin molecules
• has myosin-binding sites where myosin heads may bind
• F-actin is associated with 2 regulatory proteins: tropomyosin & troponin

• 2 identical helices that coil around each other & sit in the groove between the 2 wound actin filaments
• active state: makes myosin-binding sites on actin accessible to myosin heads
• resting state: covers the binding sites; it interferes with the binding of myosin to actin when the muscle is relaxed

controls tropomyosin by pulling it away from the myosin-binding site on actin filaments in the presence of Ca²⁺

responsible for generating the sliding movement of myosin along actin filaments that produces muscle contraction

0. Rest. ATP is bound to the myosin head, myosin head ISN’T bound to actin (ATP reduces myosin’s affinity for actin)

1. ATP attached to myosin head is hydrolyzed → ADP & Pi; conformational change occurs so that…

2. myosin head + ADP & Pi bind to actin filaments (as a result of conformational change)

3. hydrolysis products (ADP & Pi) are now released, causing the power stroke

4. the rotated & still-attached cross bridge is now in the rigor state

5. detachment occurs when a new ATP molecule binds to the myosin head

6. the ATP is hydrolyzed, activating the myosin head so it can rotate when [Ca²⁺] increases & again bind to actin

• the cyclic reactions will continue as long as there is an ATP supply & the Ca²⁺ concentration (what's activating it) is maintained
• ATP binding to the myosin head allows the head to dissociate from actin & rotate back to the resting state
• the energy of ATP hydrolysis is stored in the unbound “resting” myosin head
• Ca²⁺ promotes binding of the myosin head to actin; this releases the stored energy causing the cross bridge to rotate, forcing the filaments to slide over one another