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level: neuromusc transmission & excitation-contraction smooth muscle

Questions and Answers List

level questions: neuromusc transmission & excitation-contraction smooth muscle

Question	Answer
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)