ILS - 4 (Muscle Contractions)

Calreticulin and Calsequestrin

Calcium binding

DHP

Voltage-gated Ca2+ channel

T-tubule

Ryanodine receptors

Mechanically coupled to DHP

SR

SERCA pumps

Reuptake Ca2+

NCX

Expels Ca2+ using sodium gradient

Na+ - Ca2+ exchanger

PMCA

Plasma membrane Ca2+-ATPase

Expels Ca2+

Denervation Muscle Atrophy

Fasciculation or fibrillation (both uncontrolled contractions)

High ACh

Motor units enlarge and then muscle loss

Botulinum toxin

Cleaves SNARE proteins (vesicles)

ACh not released

Curare

Anatogonist of nAChR

Myasthenia Gravis

Antibodies attach nAChR

Duchenne’s Muscular Dystrophy

Muscle wasting

2-3 years

No sarcolemma stability

Becker’s Muscular Dystrophy

Later in childhood

Less dystrophin too

Malignant Hyperthermia

Gain of function for RyR1 > uncontrolled Ca2+

Central Core Disease

Loss of function for RyR1 > elevated Ca2+

Pax7

Transcription factor that regulates satelliteM

MyoD & Myogenin

Drives satellite to differentiate muscle cell

Cardiac Excitation

• Phase 0: depolarization

  • Na+ in

• Phase 1: small repolarization

  • K+ out

• Phase 2: plateau

  • Ca2+ in

  • K+ out

• Phase 3: repolarization

  • K+ out

• Phase 4: resting

  • K+ leaky

Smooth Muscle

No sarcomere

Calmodulin (binds to Ca2+ like troponin)

Myosin light chain kinase (allows cross-bridge)
Caveolae (membrane invagination for Ca2+ release)

Dense bodies (anchors for actin filament like Z disks)

Multi-unit smooth

No gap junctions

Ciliary, airways, arteries

Responds to ANS

Single-unit smooth

Electrically coupled w/ GJ

GI, bile, uterus

Responds to stretch, hormones