Karson Phippen

BIOL2420 VitalisAllorNothing:ACaseStudyinMuscleContraction
Due:Oct2011:59pm
Extracredit:upto6pts2ptsforeachpart.ReadthePDFforthestorylinesandthe
associatedwordbanksanddatatables.Sinceyouaregivenincrementalpiecesof
information,itismostinterestingtodoeachquestionsequentially.Youcancomplete
portionsoftheentirecasestudy(egwhatlooksmostinterestingtoyou)forpartialcredit
Iwanttoacknowledgethatthiscasestudywaswrittenbygraduatestudentsandtheir
advisoratTexasTechUniv,andIamgratefulthattheyhavemadeitpublicallyavailable.
Ifyouchoosetoworkthiscasestudy,itwillhelpyoulearnthestepsofnervoussystem
stimulationofskeletalmuscleandthemolecularprocessofmusclecontractionby
discoveringwhathappenswhenoneofthestepsgoeswrong.Notethatitis
considerableworkforthepoints,yetoughttobeavaluablelearningexperience.
PartITheTour
Questions
Usethewordbank(seePDFdocument)tomatchtheappropriatelettertothe
definitions/descriptions:
1.__(d)Actin_Thincontractileproteininvolvedincrossbridgeformation,comesin
filamentousorglobularforms.
2.__(i) Synaptic vesicles_Storeneurotransmitters,andfollowingaCa2+driven
signal,dumpneurotransmittersintothesynapse.
3._(n) Synaptic terminal__Thestructureattheendoftheaxonthatcontains
neurotransmittersandvesicles.
4.__(p) Sarcomere _ThefunctionalunitofthemusclefiberthatincludestheAband,
Iband,HzoneandtheMline.
5._(a) Sodium__Theionresponsiblefordepolarizingthemusclemembraneby
travelingthroughthenAChreceptor,downitselectrochemicalgradient.
6._(m) Ryanodine receptor__Locatedonthesarcoplasmicreticulumandonce
opened,allowsCa2+flowfromthesarcoplasmicreticulumintothesarcoplasm.
7._(c) Myosin__Thickfilamentouscontractileproteininvolvedincrossbridge
formation,hasaclublikeappearancewithahead.
8._(e) Acetylcholine (ACh)__Aneurotransmitterderivedfromcholine;responsible
forsendingtheexcitatorysignalintheneuromuscularjunction.

Karson Phippen
9._(j) T-tubule__Theseinvaginationsallowdepolarizationofthemusclemembraneto
quicklypenetratefromthesarcolemmatothemyofibril.
10._(g) Motor end plate__Largeandcomplexterminalformationbywhichanaxon
ofamotorneuronestablishessynapticcontactwithaskeletalmusclefiber,transmitting
neuralimpulsestoamuscle.
11._(o) Sarcolemma__Theplasmamembraneofamusclefiber.
12._(h) Acetylcholinesterase (AChE)__Theenzymeresponsibleforstoppingthe
AChsignal.FunctionsbymetabolizingAChintocholine,whichisrecycled,andacetate.
13._(b)Nicotinic acetylcholine receptor (nACh)__Responsibleforopeninga
ligandgatedNa+/K+channelinthemusclemembranewhentheproperligandbindstoit.
14._(l) Dihydropyridine receptor __ALtypecalciumchannelinthemusclecell
membrane,activatedupondepolarization,coupledepolarizationsignaltoreleaseof
calcium.
15.__(f) Depolarization_Anelectricalchangewhichbringstherelativechargeofthe
insideofthecellmorepositive;necessaryfortransmissionofelectricalimpulseswithina
cell,orfromonecelltoanother.
16._(k)Sarcoplasmicreticulum__Modifiedendoplasmicreticulum,storesandreleases
calcium.
Exercise
Usingtheslidingfilamenttheorydrawandexplaintheprocessofsarcomereshortening.
Startfromthepointwherecalciumwouldinteractwithtroponin.Makesuretoinclude
therolesofactin,myosin,andATP.

Karson Phippen

PartIIJeffSlater

Questions
1. WhatsymptomsisJeffexperiencing?
Dizzines,increaseHR,SOB,musclecramps,unconciousness.
2. WhatistheroleofAChEintheNMJ?
DegradesorclearsAchinthesynapticcleft
3. WhichofJeffslevelsareabnormal?
AChE Activity percentage is low
4.

Whatisthemechanismofactionofsarinorasarinlikechemical?
Sarininhibits/inactivatesacytlcholinesterase,bycovalentlybondtotheactivesiteand
disablesitsfunction.LeadingtoaincreaseinofAchintheNMJ

Karson Phippen
5.

HowwouldexposuretoasarinlikepoisonaffecttheamountsofNa+goingintothe
musclecell?Explainwhy.TheexcessAchwouldcontinuatlystimulateCholinergenic
receptorsandleavetheionchannelsopenfloodingmusclecellwithNa+,continually
depolarizingthemembraneandsendacontinualsignal.

6.

HowwouldexposuretoasarinorsarinlikechemicalaffectCa2+levelsinsidethe
sarcoplasmicreticulum?Why?
ThecontiunalelectricalsignalwouldcontinuallystimulateDHSRandtherforethe
Ryanodinereceptor,openingtheCalciumchannelsallowingthemtocontinuallybindto
thetroponin.

7.

HowdothesealteredCa2+levelsaffectthepositionoftheactinandmyosinfilaments?
Why/how?
Ca2+BindstoTroponin,whichmovestheTropomyosinandexposestheGsitesonthe
actin,thisallowstheheadsofthemyosintoformcrossbridgescausingpowerstrokes,
shorteningthesarcomereandleadingtocontractionorconstriction.

8.

WhatneedstohappentoJeffspostsynapticmembranetoremedyhisparalysis?
Physiologicallywhatdoweneedmoreof,andwhere?
MuscarrinicAchreceeptorsneedtobeantagonized,andCholinesterasesregenerated
inordertobeclearthesynapseoftheACh.
PartIIISandyThompson

Questions
1.
2.

Whatsymptomsissheexperiencing?
Droopingeyelids,WeaknessinarmsandLegs,diffucultyspeakingandswalloing,
Musclefatigueandweakness
Whatlevelsfromherbloodworkareabnormal?
AntibodiesforAchReceptorsarepresentallotherresultsareWNL(within
NormalLimits)

Karson Phippen
3.

HowwouldantibodiesagainstAChreceptorsaffecttheneuromuscularjunction?
AChRantibodieshinderAchactions,BindtoAchreceptorsanddestroysthem,prevent
bindingofACh,removeAChfromtheNMJ

4.

HowwouldantibodiesagainsttheAChreceptorsaffecttheinfluxofNa+intothecell?
Inhibitthedepolarizationandelectricalsignalingdownthettubluesandlimittheopening
oftheRyanodinereceptors

5.

HowwouldantibodiesagainsttheAChreceptorsaffectthelevelsofCa2+insidethe
sarcoplasmicreticulum?
LimitedfunctionofRyanodinereceptors,causedbylowAchandsignalconduction,
wouldnotreleasetheCa2+fromthevesicles,causingittoretainthehighstorage.

6.

Whateffectdoesthishaveontheactinandmyosinfilaments?
ThelackofCa2+wouldmeanthattheTropomyosinwouldremainblockingtheGsites
andinhibittheMyosinfrommakingbondswithActin,limitingmusclecontractions
7. WhatdisorderdoesSandyhave?Howdowetreat/managethisdiagnosis?
MyatheniaGravisMGtreatmentandmanagementinclude,bloodtranfusion,muscle
stregnhers,steroidstoreducedtheinflamiotyresponseThymectomyorremovalofthe
thymusgland
8. Usingthebelowtable,comparethemusclecontractionproblemsfacedbyJeffand
Sandytothatofanormalperson.Usenormal,increased,decreasedtocompletethetable.

SRCa2+
release

Cross
Frequencyof
bridge
muscle
formation contraction

ACh

AChE

AChReceptors Na+influx

Healthy
person

Normal

Normal

Normal

Normal

Normal

Normal

Normal

Jeff

Increased

Inactive

OverExcited

Increased

Increased

Increased

Increased

Sandy

Decreased

Normal
Malfunction/
butClears
Inhibited
lowACh

Decreased

Decreased

Decreased Decreased