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Mitochondria is the powerhouse of the cell

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RYRs located on SR

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Calcium storage in the ER

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RyRs are associated with severe skeletal muscle disorders or triggered cardiac arrhythmias

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Sarcoplasmic reticulum

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Ca can act as a ligand or second messenger

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Calcium!

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Ca2+ important! Need Ca2+

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Sarcoplasmic reticulum is the calcium credit union

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ATP depletion-> Calcium stores-> Arrythmias

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RyR arenegatively affected by low Ca++

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Cardiac receptors, sarcoplasmic reticulum, arrhythymia

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Mitochondria protects the cell from calcium

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RYR and arrhythmias

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Calcium is a ligand or 2nd messenger

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IP3R associated with GPCR (metabo)

RyR associated with LTCC (iono)

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Calmodulin

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Is low cortisol associated w/ high catecholamines?

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Is low cortisol associated w/ high catecholamines?

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RyR and IP3R located in the sarcoplasmic reticulum

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RyRs are linked to LTCC channels that cause influx of Calcium that will affect the activity of the cell by releasing more calcium. IP3Rs require IP3 for activation through GPCR activation

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depletion of ATP or calcium can cause dysfunction

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arrhythmia is related to calcium not enough

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IP3R require inosol 1, 4, 5 triphosphate

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IP3 is second messenger

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Cardiac arrhythmias are followed by low cortisol and abnormal catecholamines

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RyR in SR. Cardiac arrhythmia = fast Ca2+ release

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Located in SR; regulated by L type Ca channel; associated with severe skeletal muscle disorders or triggered cardiac arrhythmias; regulated by calcium, Mg, ATP, CaM, kinase/phosphatase

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RYRs and IP3R both use Ca2 and both are on SR

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Sr has RYR ip3r

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RyRs coupled to L-type Ca channels. IP3R coupled to GPCR

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RyRs coupled to L-type Ca channels. IP3R coupled to GPCR

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if ca or ryr messed up, cardiac issues

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RyR dependent on chaRge,

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Calcium is needed for muscle contraction. Calcium can be stored in the ER or SR. We need alot of calcium in our cells. If there is no ATP, calcium storage is modifided. Ca2+'s credit union is the endoplasmic reticulum.

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Present in the SR. L-type calcium channels and IP3 as a second messenger. Dysregulation of calcium levels can lead to cardiac arrhythmias. This can lead to low cortisol or abnormal catecholamines.

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Depolarization to release calcium from SR. Calcium binds to troponin to move it out of the way!

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when ACh binds to receptor, it triggers depolarization of muscle fiber. Ca2+ channels open and Ca2+ enters --> muscle contraction

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Depolarization in the SR causes release of Calcium which binds to troponin and allows for a contraction to occur. Pathologies can arise when there is low ATP in the cell or the body produces antibodies against calcium channels.

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Motor neuron and muscle fiber synapse at the NMJ >Ach binds receptors and causes action potential to move through the T tubule > Ca is released from the SR > Ca binds to troponin, which moves tropomyosin out of the way > myosin binds actin and causes contraction > ATP is used to clear Ca when contraction is over and reset

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Action potential in T-tubule --> depolarization --> Ca2+ channels open in SR --> Ca2+ moves to cell cytosol --> Ca2+ binds troponin --> contraction --> Ca2+ back to SR by ATP pump --> relaxation

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NMJ - synapse between motorneuron and muscle fiber

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from choline and acetyl CoA --> broke down by AChE

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Ca2+ pumped back into SR by ATP-dependent pumps

ACh is released from motor neuron is picked up by AChR on the muscle causing depolarization of the muscle cell

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Actin blocked by tropomyosin at rest Ca2+ released then binds troponin allowing muscle contraction, Ca2+ is then moved back to SR - ATP dependent - muscle relaxation

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muscle-type and neuronal type

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there are two types of nicotinic acetylcholine receptors: muscle-type and neuronal-type

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Quantal is the amount of Ach required to reach a muscle contraction

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Quantal is a measurement for the effective amount of ACh to get a muscle contraction

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Muscle Ach receptors 5 subunits

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ACh deficits lead to Alzheimer's disease

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Depolarization- Ca releases from sarcoplasmic reticulum- Ca binds to troponin- muscle contraction!!

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Ca+ enters the cell through the LTCC then binds to RyR to release Ca+2 from the SR to allow for MUSCLE CONTRACTION

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Mitochondria is the powerhouse of the cell

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Mitochondria is the powerhouse of the cell

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Acetylcholinesterase inhibitor for Alzheimer’s

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AchE is needed to clear Ach from the synapse. IP3 and RyR work together in response to nervous stimulation to cause muscle contraction via calcium release

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muscle type channels found at NMJ

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Open ca2+ channels in SR membranes so calcium can diffuse into cytosol

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Mitochondria is the powerhouse of the cell

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Mitochondria is the powerhouse of the cell

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Ach is released from the neurons. Ach binds to the Ach R triggers depolarizes the muscle fibers. Calcium is going to open, and cause m. contraction

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Don't smoke

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We can have many problems in the neurological pathway from the neuron until the contraction of the muscle.

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Ach from motor neuron thru synapse opens voltage gates channels enacting muscle contraction via RyR and IP3 alongside , reuptaken by ache

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NMJ is site for transmission of APs from nerve to muscle it is also site of action for pharmacological drugs

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Quantal is the amount of ACh needed to elicit an action potential

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RYR and IP3 receptors are important. Ach will bind, triggering depolarization, opening Ca2+ channels, allowing entry into the cytoplasm, binding to troponin and leading to contraction. Calcium will be pumped back into the SR using ATP to lead to muscle relaxation.

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Ach broken down by acetylcholinesterase

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Treat Alzheimer's with AChE inhibitors to keep the available Ach in the synaptic cleft

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Smoking is bad. Will interact with your nicotine receptor and MESS IT UP :)

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Choline and acetyl CoA make acetylcholine. Broken down by acetylcholinesterase, and choline will be transported back to the axon terminal to make more. QUANTAL

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Lambert-Eaton is a problem with ca2+ gated channels

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MG: autoimmune disorder. Abs -> reduction in function of RYR receptors

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low calcium quantal release contributes MG

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low calcium quantal release contributes MG

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MG: antibodies destroy N receptors, loss of motor function (mainly eye)

low calcium release... not necessarily low calcium (i think)

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In MG there are antibodies against ryanodine receptors and nicotinic receptors 

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In MG there are antibodies against ryanodine receptors and nicotinic receptors 

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main symptom of myasthenia gravis is ocular muscle weakness 

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main symptom of myasthenia gravis is ocular muscle weakness 

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antibodies against RyR and IP3R receptors --> no depolarization --> no muscle contraction --> ptosis and muscle weakness; specific to MG

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Ocular muscle weakness due to antibodies against the receptor is the main indicator of myasthenia gravis

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MG: Ocular muscle weakness the most common presenting symptom

Low quantal release and ineffective receptors leading to no depolarization and muscle contraction

Antibodies against the ryanodine receptors

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MG main sx is ptosis, caused by antibodies against Ach R and Ach

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MG: not enough Ach and receptors are not as effective (due to antibodies); leads to LACK of depolarization of muscle fibers; will see ocular muscle weakness; facial nerve is affected

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MG: not enough Ach and receptors are not as effective (due to antibodies); leads to LACK of depolarization of muscle fibers; will see ocular muscle weakness; facial nerve is affected

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LES has antibodies agains voltage gated calcium channels which will cause reduction in ACh release 

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LES has antibodies agains voltage gated calcium channels which will cause reduction in ACh release 

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LES: 50% have lung cancer,

due to voltage gated ca channel

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LES: low levels of Ach and Ca2+ that are not sufficient to cause normal muscle contraction causing muscle weakness

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antibodies against voltage-gated Ca2+ channels; low ACh and Ca2+; muscle weakness, small cell lung carcinoma in 50%; Proximal triad: weakness, depressed reflexes; autonomic dysfunction

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In botulism, BoNT blocks presynaptic ACh release and inhibits muscle which will cause flaccid paralysis

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In botulism, BoNT blocks presynaptic ACh release and inhibits muscle which will cause flaccid paralysis

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BoNT targets SNARE which is required for Ach release so without SNARE there is no depolarization or contraction of muscle cells.

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Myasthenia gravis - autoimmune; ocular muscle weakness/ptosis - one of first symptoms; antibodies against ACh R; bilaternal weakness/paralysis; CN VII; low quantal calcium release and decreased binding AChR and decreased depolarized of muscle; also antibodies against ryanodine receptor - specific for myasthenia gravis; Lambert Eaton Myasthenic syndrome - smoking and small cell lung cancer - antibodies against voltage gated calcium channel; reflexia; autonomic disruption; dry mouth; proximal muscle weakness; botulism - clostridium neurotoxin; common in infants; diffuse and flaccid paralysis; prevents fusion of NT vesicles; toxin crosses mucosal barriers to blood stream; end result - decreased release of ACh;

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BoNT targets SNARE --> no ACh --> blocks release and inhibits muscle contraction --> flaccid paralysis

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botulism: opposite symptoms than tetany.

due to bacteria

flaccid paralysis d/t inhibiting contraction

don't get botox?