| 1. large, mylenated n that originate from s.c
2. nerve endings branch after entering muscle belly
3. each nerve ending makes juction-> one junction per m fiber | summary of skeletal m |
| 1. motor end plate= whole region where nerve invaginates m. surface
2. synaptic trough/gutter= invaginated membrane
3. synaptic cleft/space= spce b/w terminal & m fiber
4. subneural clefts= @ bottom of synaptic cleft; numerous smaller fold in m membrane | parts of neuromuscular junction (4) |
| Acetylcholine- Ach | skeletal muscle synaptic vessels carry _____ an excitatory transmitter. |
| 1. made in cytoplasm of terminal using ATP from mitochondria
2. rapidly absorbed & stored in vesicles @ terminals of single end plate
3. released into synaptic space & excites m fiber membrane | basics of Ach (3) |
| 1. AP travels down axon to terminal
2. voltage-gated CA2+ channels open- Ca2+ comes into nerve terminal
3. Ca2+ induces fusion of synaptic vesicles with nerve cell membrane
4. fused vesicles release Ach into synaptic cleft | how does Ach get secreted? |
| 1. Ach receptors in m membrane are Ach-ligand-gated channels & remain closed until 2 Ach bind
2. once 2 binds, gate opens
3. large increase in Na+ ions come through the channel into m & increases positive charge of cell
4. creates local positive potential change which initiates AP that spreads along m membrane and causes m contraction | what is the effect of Ach on postsynaptic (muscle) membrane? |
| 1. RMP maintained w/o stimulus
2. Ach secreted & binds to receptors, opens Na+ channels, Na+ floods in (depolarization)
3. Na+ channels deactivate as voltage-gated K+ channels open delayed/slowly
4. K+ rushes out and allows repolarization of muscle membrane | review of AP in skeletal m (4 steps) |
| t-tubule system
-internal exterior of surface of cell membrane that penetrates all the way through m from one side to the other
-open to exterior of m fiber
-when AP spreads along m. fiber, spreads along t-tubule as well | how does AP spreading on surface of m fiber penetrate deeply into m fiber to cause max m contraction? |
| FALSE
-t-tubule is sandwiched b/w two SRs | T/F: t-tubule does not touch the sarcoplasmic reticulum. |
| DHP Receptors
-dihydropyridine receptor | an AP in the t-tubule alters conformation of what receptor to allow the release of Ca2+ from the SR into the m fiber? |
| 1. broken down by enzymes (acetylcholinesterase)
2. diffusion = small amount diffused out of synaptic cleft
3. reuptaken into presynaptic terminals | how is Ach removed after being released? (3) |
| chronic autoimmune disorder in neuromuscular junction
-has to do with issues related to Ach | what is myasthenia gravis? |
| 1. antibodies developed that are resistant to Ach receptors @ endplates
2. deficiency/abnormal behavior of Ach @ endplates | causes of myasthenia gravis (2) |
| abnormal fatigue of eye m that controls the eye, eyelid movement, facial expressions and swallowing | symptoms of myasthenia gravis |
| administration of antibodies against antibody-Ach-receptor complex which results in accumulation of increased amounts of Ach in synapse | treatments for myasthenia gravis |
| -not as organized at skeletal m
-large # of actin filaments attached to dense bodies
-contraction = prolonged
-neuron of ANS makes multiple contacts with cell
- innervated by more than one neuron
- mostly located in hollow organs (stomach, intestines, bladder) | basics of smooth m cells |
| 1. multi-unit
2. unitary (single unit) | organization types of smooth m (2) |
| -discrete separate fibers
-little electrical coupling with cells-> not many gap junctions
-each fiber can contract independently of each other
-capable of finer control
-innervated by single nerve fiber | multi-unit smooth muscle |
| -AKA syncytial m AKA visceral smooth m
-large group of fibers (100s-1000s)
-contract as one
-individual fibers adhere to each other through gap junctions
-ex. GI tract, uterus, blood vessels | unitary (single-use) smooth muscle |
| -nerve fibers don't make direct contract with m fiber-> form diffuse junctions
-terminal axons have variscosities along the axes-> NOT branching end | neuromuscular junctions of smooth muscle |
| 1. increased K+ gradient (lots K+ leaving cell)
2. increased Cl- gradient (lots of Cl- entering cell)
3. greater resting Cl- permeability | why does the muscle cell have a more negative RMP (-90mV)? (3) |
| look like mardi gras beads that run close to the smooth muscle cells but do not actually touch
-run all in b/w multi-unit cells since do not communicate
-run alongside unitary cells bc they communicate through gap junctions so will share everything quickly
-contain vesicles w/ neurotransmitters that diffuse into the cells | what are variscosities in smooth m? |
| 1. Acetylcholine (Ach)
2. Norepinephrine (NE) | what are the two types of smooth muscle neurotransmitters? |
| FALSE | T/F: Ach and Ne can be secreted by same nerve fiber. |
| action varies with organ type
- if one excites, other inhibits
-ultimate action of Ach & NE depends on type of receptor on cell (excitatory/inhibitory) | action of the two neurotransmitters |
| -nerve stimulation
-hormonal stimulation
-stretch of fiber
-change in environment of fiber | what can cause release of Ca2+ into cell in smooth m? |
| 1. initiating stimulus
2. Ca2+ enters cell from outside & SR releases more
3. Ca2+ binds to calmodulin
4. Ca2+-calmodulin activates myosin light chain kinase (MLCK) which increases myosin ATPase activity
5. active myosin crossbridges slide along actin- create crossbridges | regulation of contraction in smooth muscle (6 steps) |
| 1. removal of Ca2+ from ICF (1st step always)
2. MLCK activity decreases
3. myosin light chain dephosphorylated by myosin light chain phosphates
4. cross-bridge cycling stops
5. contraction ceases | termination of contraction in smooth muscle (5 steps) |
| 1. Ca2+ channels close when stimulus stops
2. Ca2+ ATPase pumps Ca2+ out of cell/into SR
3. ICF Ca2+ levels fall below "critical level" | steps to remove Ca2+ from ICF in smooth m contraction (3) |
| -RMP= (-50) - (-60) mV
-APs in unitary smooth m have slower upstroke & longer duration than skeletal m APs
-upstroke caused by opening of Ca2+ voltage-gated channels
-repolarized by K+ entering cell through channels | basics of membrane potentials & APs in smooth muscle |
| Ca2+ channels open more slowly than Na+ channels | why do APs in smooth muscle have slower uptake than those in skeletal muscle? |
| 1. spike potential
2. AP w/ plateau
3. slow waves | types of smooth muscle APs (3) |
| -typical-> same as skeletal m
-occurs in most types of unitary smooth m
-elicited by external stimuli
-influx in # of Ca2+ and smaller number of Na+ through Na-Ca channels | spike potential APs in smooth muscle |
| -onset similar to spike potential
-repolarization delayed due to slow nad prolonged opening of Ca2+ channels
-important with prolonged contractions (ex. cardiac m or uterus) | AP with plateau in smooth muscle |
| -some smooth muscle is self-excitatory (AP w/o external stimulus)
-associated with basic slow wave rhythm of membrane potential
-importance= when strong enough can initiate AP
-AKA pacemaker waves | slow wave APs in smooth muscle |
| a spontaneous AP can happen b/c of:
1. normal slow wave potentials: slow waves are oscillating depolarizing and repolarizing RMP
2. spikes (real APs): when RMP more +/greater than -40mV
- slow wave potential rises so increase in frequency of spike potentials | what can happen when the GI tract muscles are stretched? |
| -change in membrane potential allows Ca2+ entry
-generation of IP3 @ cell membrane can open intracellular SR Ca2+ stores
--either of these can cause SR to open Ca2+ channels
-when this depletes Ca2+ stores in SR it signals to allow Ca2+ in from ECF to refill | how can some smooth m contract without an AP? |
| IP3 allowing Ca2+ to be released from SR | what is most important way that smooth m can contract without an AP? |
| NO | are APs common in multi-unit smooth m? |
| 1. act directly on smooth m contractile machinery w/o APs: can cause contraction when m cell membrane contains excitatory receptors
2. can cause inhibition if membrane contains inhibitory receptors
3. contraction occurs by opening Na+/Ca2+ channels
4. inhibition= hormone closes Na/Ca2+ channels causing hyperpolarization of m (more - inside cell than normal)
--ex. Ach, NE, E | effects of circulatory hormones in blood (4) |
