Phys Exam 1 Memory/Terms Flashcards
Depolarization
Decrease in membrane potential
Voltage difference between inside & outside of membrane is less
Hyperpolarization
Increase in membrane potential
More difference in voltage across membrane
Membrane Potential (Vm)
Difference in voltage across membrane
Resting membrane potential (Vr)
Voltage across membrane when cell is inactive
Capacitance
Membrane’s ability to store charge
Conductance (g)
ease of flow
Current (I)
Change in ion conductance
Equilibrium Potential of K+
-90 mV
Equilibrium Potential of Na+
+60 mV
Equilibrium Potential of Ca2+
+120 mV
Equilibrium Potential of Cl-
-70 mV
Ohms Law
V=IxR
Voltage = Current x Resistance
Contractility
Cardiac muscle’s ability to change force of contraction w/o changing muscle length
Occurs by change in Ca regulation
Activates sympathetic nervous system for increase of NE release
Gs (type of G protein-coupled receptor)
increase AMP | inhibit MLCK | stimulate SERCA
=relaxation
Gi (type of G protein-coupled receptor)
decrease cAMP | promote MLCK | inhibit SERCA |
=contraction
Gq (type of G protein-coupled receptor)
produce IP3 / DAG | Ca2+ release from SR | activates PKC
=contraction
Contraction Mechanism for Smooth Muscle
Ca2+ in | Calmodulin binds to Ca2+ | MLCK activated | phosphorylation of MLC | cross bridge formation | myosin flexibility =contraction
Relaxation Mechanism in Smooth Muscle
Ca2+ out of cell | decrease MLCK | dephosphorylate MLC | decrease myosin flexibility
= relaxation
Dystrophin & Role in Muscular Dystrophy
Binds sarcomere to outside of cell
Mutation = damage/wasting overtime with stretch (MD)
Order of Motor Unit Recruitment
Type I (slow/deep) –> Type II (fast/superficial)
Twitch
Muscle contraction from single action potential
Summation
combination of EPSPs & IPSPs which can form an Action Potential
Type I Motor Unit
Slow oxidative | Low myosin ATPase | Low SERCA | Lots mitochondria | Energy-conservative | Deeper | More excitable
“fine” motor control | fatigue-resistant | small neurons
Type IIA Motor Unit
Fast-oxidative | quick shortening | high myosin ATPase | medium SERCA | lots mitochondria
Type IIB Motor Unit
Fast-glycolytic | fastest shortening | high myosin ATPase | high SERCA | low mitochondria | fatigue common
Velocity of Muscle Fiber Contraction
Increase Myosin ATPase = increase velocity contraction
Determined by alpha motor neuron innervation
Power in Muscle Fiber
Greater velocity via Myosin ATPase = greater Power!
Force-Velocity Relationship in Muscle
Increase load = Decrease shortening velocity
Fastest contraction w/ 0 load
Active Force
F produced by actin-myosin cross-bridges
Passive Force
F produced by titin & connective tissue (elasticity, wants to go back to resting length)
Increase PF = increase muscle stretch
Optimal Length (Lo)
Where most active cross-bridges are formed in muscle to produce the maximum force
(in middle of how far sarcomere can be stretched)
Isotonic Contraction
eccentric (longer fibers) & concentric (shorten fibers)
Same load but change length
Isometric Contraction
No change in muscle length | Load changes
Increase Muscle in Series
Greater speed & shortening
Increase Muscle in Parallel
Greater force production
Contraction of Skeletal Muscle
Ach release | N1 receptors | Depolarization | Ryanodine pulls Ca2+ channel open | Ca2+ influx | Cross-bridge formation
=Contraction
Relaxation of Skeletal Muscle
SERCA pumps Ca2+ back into SR | Cross-bridge formation ends
=relaxation
Cross-Bridge Steps in Skeletal Muscle
Ca2+ binds to Troponin C | Troponin I cause conformational change | ATP binds to myosin | ATP hydrolyzed (at rest) | Myosin binds to actin | Phosphate released | Myosin head cocks = power stroke | ADP released
Troponin C
Binds to Ca2+ to uncover myosin-binding sites on actin
Troponin I
Causes conformational change so myosin can bind to actin
Troponin T
keeps tropomyosin in place
Tropomyosin
Covers myosin-binding sites on actin
Titin
Allows for elasticity of muscle
Stabilizes myosin | causes passive force
Tetany
Summation where plateau occurs | muscle cannot relax or “oscillate” at all = sustained contraction
Baroreflex Mechanism
BP = Cardiac Output x Peripheral Resistance
Up BP –> increase PSNS | decrease SNS = decrease BP
SNS (Sympathetic)
“fight or flight”
Dilate pupils | Increase HR | Decrease GI | Decrease saliva, Up viscosity
Short pregang | Long postgang
Thoracolumbar region
NT: NE
PSNS (Parasympathetic)
“Rest & Digest”
Constrict pupils | Decrease HR | Increase GI | Increase saliva, down viscosity
Long pregang | Short postgang
Craniosacral region
NT: Ach
Acetylcholine (Ach)
PSNS & SNS | Excitatory (EPSP)
Receptors:
Nicotinic (ionotropic/NSCC)
N1: NMJ - skeletal
N2: postganglionic fibers - autonomic neurons
Muscarinic (metabotropic) - smooth/cardiac
Glycine
Spinal cord | Inhibitory (IPSP)
Receptor: ionotropic (ligand-gated)
Cl- conductance
Location: spinal cord, retina, brainstem
GABA
CNS | Inhibitory (IPSP)
Receptors:
GABAa: ionotropic | Cl- conductance (hyperpolarization) fast
GABAb: metabotropic | K+ conductance (hyperpolarization) slow
Location: interneurons in brain
Jumping Frenchman Disease
Glycine (NT) Receptor mutation
Glutamate (Glu)
Brain | Excitatory (EPSP)
Receptors:
Ionotropic (NMDA | AMPA | Kainate)
Na, K, Ca flow | fast
Metabotropic (mGluR)
Na, K, Ca flow | slow
Norepinephrine (NE)
SNS (all postgang) | Excitatory (EPSP)
Receptors:
a-Adrenergic: metabotropic | more NE than E
a1: blood vessels (vasoconstriction)
a2: presynaptic terminals
B-Adrenergic: metabotropic | more E than NE)
B1: heart (up HR)
B2: lungs (bronchodilation)
B3: fat cells
Epinephrine (E)
SNS (adrenal medulla) | Excitatory (EPSP)
Receptors:
a-Adrenergic: metabotropic | more NE than E
a1: blood vessels (vasoconstriction)
a2: presynaptic terminals
B-Adrenergic: metabotropic | more E than NE)
B1: heart (up HR)
B2: lungs (bronchodilation)
B3: fat cells
Receptor Potential
Change in membrane potential at stimulus site
Synaptic Potential
Change in membrane potential at synapse when NT released
Tonic Receptor
Slow | AP maintained
Phasic Receptor
Fast | AP only when stimulus turned on/off
Ionotropic Receptor
fast | short | ligand-gated | NSCC | localized
Metabotropic
slow | long | G-protein coupled | widespread