Q1:

Def
ine‘
NernstPot
ent
ial
’
.Cal
cul
atet
heNer
nstpot
ent
ial
forsodi
um andpot
assi
um i
onsacr
osst
hecel
l
membr
ane.(1+4)

KEY:
NernstPot
enti
al:
Thepotent
ial
diff
erenceacr
ossamembr anethatexactl
yopposesthenetdi
ff
usi
onofapar
ti
cul
ari
ont
hrough
themembraneiscall heNer
edt nstpot
enti
alf
orthation. ( 1mark)

Cal
cul
ationofNernstpotent
ial
forsodi
um i
ons:
TheNernstequat
ion,canbeusedtocalcul
atet
heNer
nstpot
ent
ial
forsodi
um i
onatnor
mal
bodyt
emper
atur
e
of98.
6°F(37°C):

=-61xl
og14/
140
=-61xl
og0.
1
=-61x-
1
=+61mV (
2mar
ks)

Cal
cul
ati
onofNer
nstpot
ent
ial
forPot
assi
um i
ons:

=-61xl
og140/
04
=-61xl
og35
=-61x1.
54
=-94mV (
2mar
ks)
Q2.Enl
i
stt
hedi
ff
erentt
ypesofcel
l
sinNer
voussy
stem.Wr
it
edownt
hef
unct
ionsofeachcel
lty
pe.
(
1+4)

KEY:
Twomai nty pesofcel l
sinnervoussy stem are:
1.Nervecel l
sorNeur ons (0.
25mar ks)
2.Suppor t
ingcel lsorGl i
acell
s (0.
25marks)
a.Mi crogl iacells (0.
25mar ks)
b.Macr ogl iacell
s (0.
25mar ks)
I. Ast r
ocytes
II. Ol i
godendrocy t
es
III. Schwanncel ls
Funct
ionsofdi fferentcellsinnervoussy stem:
Funct
ionsofNeur on:
1.Recei veandi nt
egrat
einput s
2.Gener ateaner veimpulse(actionpotenti
al)
3.Conductt heact i
onpotent i
al
4.Tr ansmi tinf ormati
ontot argetcell
(neuron,muscl
e,gl
and) (
1mar
k)

Mi
crogl
ia:
1.Scav engercel
lst hatr
esembl et i
ssuemacrophages
2.Remov edebri
sr esult
ingfrom inj
ury,i
nfect
ion,
anddi seaseet
cmul
ti
plescl
erosi
s,AI
DS-
rel
ated
dementia,Par
kinsondi sease,andAlzheimerdisease (
1mar k)

Ast
rocy
tes:
1.mechani calsuppor t
2.met aboli
csuppor t
3.transportnutr
ientsandwast es
4.encapsulatesy napses
5.regulat
echemi cal andionicenvir
onment
6.form scarti
ssue
7.form Bloodbrainbar ri
er
(
0.25mar ks/eachpoi
nt,
ful
l01mar
kforwr
it
ingany4poi
nts)

Ol
i
godendr
ocytes:
Myel
inateaxonsofcent
ral
ner
voussy
stem (
0.5mar
ks)

Schwanncel
ls:
Myel
i
nateaxonsofper
ipher
alner
voussy
stem (
0.5mar
ks)
Q3:Descri
bethepropert
iesof‘
Ner
vefiber’
. (
5)
KEY:
1)Exci
tabi
li
ty,2)Conducti
vi
ty,
3)I
nfat
igabi
li
ty,
4)Al
lornonel
aw,
5)Ref
ract
oryper
iod

5.EXCITABILI
TY (0.
5mar ks)
 Abil
it
ytoreacttoastimulusisknownasExci tabi
l
ity
.
 Nervecell
shaveal owthresholdforexcit
ati
on.
 Fornerv
ef i
beritcanbeexplainedont hebasisof
Str
engthdurat
ioncurve

Rheobase: (0.
5mar ks)
 Iti
sthemini
mum vol
tageval
ueofast
imul
usneededt
ost
imul
ateaner
veormuscl
e.

Ut il
izati
onTime: (0.5mar ks)
 Themi nimum timet hatacur rentequaltotherheobasemustactt oi nduceanact
ionpotent
ial
.
 Expl anati
on:ast i
mul uswithacur r
entst
rengthlessthanr heobasewi llnotr
eacht
hreshol
dvalueeveni
f
appl i
edf orunli
mitedt i
me
Chr onaxie: ( 0.
5mar ks)
 Mi nimum t i
mer equiredforast imulusdoublethestrengthofther heobasetoexci
teamuscl eora
neur on.
 Tissueshav i
ngshor terchronaxiearemor eexcit
ablee.g.nervefibers.
 Damaget onervefiberisdetermi nedbymeasur i
ngchr onaxie.
 Iti
mpr oveswithrecov ery.

6.CONDUCTIVI
TY:
 Theimpulsei
snormallytr
ansmitt
ed(conducted)alongtheaxontoi
tst
erminat
ion
 Conducti
onisanact
ive,sel
f-
propagat
ingprocess,andtheimpulsemov
esalongt hener
veata
const
antampli
tudeandv el
oci
ty. (0.
5mar ks)

7.I
NFATIGABILI
TY:
 I
nthenerv
emuscleprepar
ati
on,ift
henervei
ssti
mulat
edrepeat
edl
y,t
henaft
eracert
ainper
iodt
he
muscl
efai
lstogi
veanyresponsebutner
veisnotf
ati
gued. (
0.5marks)

8.ALLORNONELAW:
 Whenat
hreshol
dst
imul
usi
sappli
ed,
ner
vef
iberi
sexci
ted(
depol
ari
zed)compl
etel
ythroughoutt
he
l
engt
hwit
hmaximum ampl
i
tude. (
0.5marks)
9.REFRACTORYPERI OD: (0.5marksf or
defini
tion)
 Per i
oddur ingwhi chsecondact i
onpot enti
al
cannotbei niti
atedinalr eadyexcitednerv
eor
muscl ef i
ber .
 Itcanbe:
Absol uterefractoryperiod ( 0.5mar ks)
 Istheper ioddur ingwhi chanotheract i
on
potent i
alcannotbeel i
cit ed,
nomat t
erhow
strongt hest i
mul us.
 Lastsf or1/ 2500sec.
Relativerefractoryperiod: ( 0.5mar ks)
 Beginsatt heendofabsol ut
erefractor
y
period&cont i
nuesunt i
l themembr ane
potent i
alreturnst other esti
nglevels.
Q4.A25y earol
dmangotst abinj
uryatthebackofl ef
tleg.Hissciat
icner
vewasdamagedandt
reat
edbya
sur
geonwhot oldthepati
entthatthenervewouldheal completel
yinoneyear
.
a)Whati stherol
eofschwanncel li
nr egenerat
ionofnervefiber
? (
1.5)
b)Whatar ethefunct
ionsofMy eli
nsheat h? (1.
5)
c) Whatarethechangesindistalst
em afterinj
urytonervefi
ber? (
2.0)
Key
:

Q3.
a)

Rol
eofschwanncel linregener ati
onofner v
ef i
ber (
1.5mar ks)
 From thecutdi st
al end, Schwanncel ldi
ffer
entiatesint
oelongatedcellswhichgrowi nall
dir
ect
ionsbut
usefulgrowthist owar dspr oximalend.
• Thegapbet weent het woendsi sfi
ll
edbyf i
broblastswhichhelpinunionofscartissue.Ther
eissome
growthofSchwanncel lsfrom proximalstem also
• Puedopodi alikepr ojecti
onsgr owt owardsdistalendwhi chisguidedbySchwanncel l.Someofthe
proj
ecti
onsgr owt owar dsdi stalend.Oneiselongat ed;
restdegenerates.
• Ult i
matel
yt hemy el i
nsheat hlaidbyschwancel l
soft wocutendsf uset oget
her
.
Q3.
b)
Funct
ionsofMy el
i
nsheat h
 I ncreaseveloci
tyofconduct
ionduet
onodet
onodet
ransmi
ssi
on. (
0.5mar
ks)
 I thasprotecti
vefuncti
on. (
0.5mar
ks)
 I tactsasani nsul
ator
. (
0.5mar
ks)

Q3.
c)
Changesindi stalstem (
2mar ks)
• Changesst artwi thi
n24hour safterinjur
y
• Axonswel lsup
• Br okeni ntopieces
• Swel l
ingofMSandr eplacedbyoilydroplets
• Macr ophagesf rom endonurium remov edebrisofaxonandMS
• Phy si
cal destructionofMSi n8-10day s
Chemi cal destruct i
onofMSi n8-32day s
• Thedi stalstem cont i
nuestoconductAPf or3days
• Wi thin3- 5day st heconductionisimpai r
ed.
• Af ter5thdayt heconduct i
onstops.
• Af terdegener ationonl yendoneuriuntubealongwithSchwanncel
li
slef
t(MSi
sdest
roy
ed)
Q5.Defi
neRest
ingMembranePot
ent
ial(
RMP).Di
scussthechannelsandioni
cmechani
smsresponsi
blef
or
t
heorigi
nofnormalRMP.WhyNa-KATPasepumpisknownasel ect
rogeni
cPump? (1+3+1)
Key
:
Defi
nit
ionofRestingMembr anePotenti
al(
:0.
75mar ksfordefi
nit
ion)
Thepotential
dif
ferenceacr
ossaner vemembr aneduri
ngresti
ngst at
eisknownasRest i
ngMembr ane
Potent
ial.
Or
Thepotential
dif
ferenceacr
ossaner vemembr aneduri
ngwheni tisnotconduct
inganerveimpulsei
sknown
asRestingMembr anePotenti
al. Or
Thepotential
inmi l
li
vol
tswhichispr
esentacrossthemembr aneofexcitabl
ecel
lsinunsti
mulat
edorrest
ing
phase.
 RMPofl argenervefi
bresis–90mV.( 0.25marksfornormalv al
ue)

Channel
sresponsi
blefort
heori
ginoft
henor RMP(
mal 1mark)
1.K+Na+Leakchannel s
2.ActiveNa+–K+pump
Al
lthevol
tagegatedchannel
sarecl
osedatRMPi.
e.v
oltagegat
edNa,
K,CaChannel
s.

I
onicMechani smsi nvolvedingener at
ionofRest i
ngMembr anePotent
ial
:
Contri
butionbyPot assium NernestPot enti (
al0.
75mar ks)
Concent r
ati
onofPot assium out si
de=4mEq/ L
Concent r
ati
onofPot assium inside=140mEq/ L
Forcalculat
ionofNer nstPotent i
alofPot assi
um, weassumecell
membr aneatr
esti
shi
ghl
yper
meabl
etoK+
Then
Potassium Ner nstPotential=- 61log140/ 4
Potassium Ner nstPotential=- 61log35
Potassium Ner nstPotential=- 61X1. 54
Potassium Ner nstPotential=- 94mV
Thi
s- 94mVi scalledNer nstpot ent
ial
f orPotassi
um whichisv
eryneartoRMP.

Contri
butionbySodium Ner nestPot enti
al( 0.
75mar ks)
Concentrati
onofSodium out side=140mEq/ L
Concentrati
onofSodium inside=14mEq/ L
Forcalculat
ionofNernstPot ent i
alofPotassium, weassumecel lmembr aneatr esti
shighl
ypermeabletoK+
Then
Sodium NernstPotent
ial=- 61l og14/ 140
Sodium NernstPotent
ial=- 61l og0. 1
Sodium NernstPotent
ial=- 61X- 1
Sodium NernstPotent
ial=+61
This+61mVi scall
edNer nstpot enti
alforSodi um.Howev er,astheK+Na+Leakchannel sar
ev er
yless
permeabl et
oSodium ascompar edtopot assium.Soi nwardSodi um di
ffusionactual
lygener
atesapotenti
alof
+8mVonl y.
Calcul
ationofNernstPotent i
al causedbysodi um andpot assium ascalculatedbyGoldman’sequati
onisequal
to-86mVwhi chi
smuchcl osert opotassi
um Ner nstpot
entialbecauseofK+Na+Leakchannel sbeing100
ti
mesmor eleakytopotassium ascompar edtosodi um.

Cont
ri
but
ionbyNa+-
K+ATPasePump:
Na+-
K+ATPasePumpwi
l
lgener
ateapot
ent
ial
of-
4mVi
nsi
de
becauseofpumpi ngofmorepositi
vechargeout side.(0.5marks)
Summar y
 Cont ri
buti
onbyPotassi
um Ner nestPot ential=−94mV
 Cont ri
buti
onbySodium NernstPotential=+8mV
 Cont ri
buti
onbyNa+- K+ATPasePump=- 4mV
 SoRest i
ngMembranePot ent
ial=(-94mV)+( +8mV)+( -4mV)=-90mV
Na+-K+ATPasePumpasEl ect
rogenicPump: Thi schannel act
iv ypumps3Na+i
el onsout
sideand2K+ions
i
nside.Soitispumpingmorepositi
vit
yout si
de.I tcontribut
estogenerat
ionofnegati
vi
tyi
nsideandhencei
tis
knownasel ect
r cpump.(
ogeni 1mar k)

Q6.Dr
awandl abel
nor
mal
act
ionpot
ent
ial
inaner
vef
iber
.Descr
ibev
ari
ousst
agesofAct
ionPot
ent
ial
ina
ner
vefi
ber
.(2+3)

KEY:
Label
edDi
agr
am ofAct
ionPot
ent
ial

(1 mar
ksf orpr
oper
lyl
abel
eddi
agr
am asanyoneoft
heabov
e)
St
agesofAct
ionPot
ent
i (
al3marks)

Depol
ari
zati
on:
 Whenst i
mul usisappli
ed,conformational changestartsi
nt heactiv
ationgateofthesodium channel
andt hisl eadstotheopeningofact i
vat i
ongat ecausingal i
ttl
einfl
uxofsodium andwhent he
membr anepot enti
alr
eachest oabout- 65mVt herei
scompl et
eopeningofact i
vati
ongate.This-65mV
iscalledt hresholdforexci
tat
ionorcr i
ticalvalueorFiri
nglevel.Whent hegatesareopenedthensodi um
channel saresaidtobeact i
vated.
 Wi t
hact ivat
ionofsodium channelsther eisrapidsodium i
nf l
uxfrom ECFleadingtotheposit
ivi
tyinside
andt hisi sknownasDEPOLARI ZATION.
 Sodium channel sremainacti
v at
edforf racti
onofasecondandt henthesechannelsbecome
inacti
v atedbyt heclosureofinacti
vationgat eleadi
ngt oendofDepol ari
zati
on.

Repol
ari
zati
on
 Afterdepol arizati
ontherei
sRepol ari
zationcausedbyact i
vati
onofVol t
agegat edPotassium channel
s.
 Whent hest imulusisappli
edthereissl owconformationalchangeinthegateofpot assium channel
s
causingi ttoopen.
 Thepot assium channelsareful
lyactivatedattheendofdepol ari
zat
ioncausingEffluxofpot assi
um
ionsleadi ngtor etur
nofnegativ
ityinsi
det hemembr aneknownasr epolar
izat
ion.
 Thei nactivati
ongat eofsodium channel swil
lnotreopentil
lthemembr anepot ent
ialbecomesneart o
 RMPandt hi
sisthecauseofr efractoryper
iod.
 Thelast30%ofr epolari
zati
onissl owandt hispar
ti edaf
scal
l terdepolar
izat
ion.Thecauseofaf
ter
depolari
zati
onisthatthepotassium ionsaccumulateontheoutersur
faceofthemembr anetosl
ow
downt herateoffurt
herrepolar
izati
on.

Hy
per
polarization
 Themembr anepot ent
ialaferaf
t t
erdepolarizati
onphasebecomesmor enegat
iveknownasaf t
er
hyper polar
izati
oncausedbysl owclosureofpot assium channelsleadingtoexcessiveeff
luxof
potassi um causingmor enegat i
vepotentiali.
e.hyperpol
arizat
ion.Alsosodium potassi
um pumpi s
acti
v atedallthetimewhi chalsocontributestot hehyperpolar
izat
ion.
 Thespi kepotential
ist
hepor tionofact i
onpot enti
albetweent hethreshol
dofexcitati
onandt hest
artof
aft
erdepol arizat
ion.

Q7.Ahypervent
ilat
ingyounggirlof16year sreport
stoherphysi
cianwi
that y
picalposi
ti
onofhandandwri
st
duetospasm ofmuscl es.AnI/
V( i
ntrav
enous)i nj
ecti
onofacalci
um sal
tresult
sinremarkabl
eimprov
ement
ofthegi
rl
’sconditi
on.
a)Whati sthetechnical
namegi vent othiscondi
ti
onofthegirl
? (
01)
b)Whywascal cium soeff
ectiv
e? (
02)
c) Whatistheroleofcalci
um inskeletalmusclecont
ract
ion? (
02)

Key

Q5.a)
Thegi
rli
ssuf
fer
ingf
rom “
Tet
any
”duet
oHy
pocal
cemi
a.(
1mar
k)

b)(
Q5. 2mar
ks)
 Extracellularfluidcalcium ionconcent r
ati
onnormallyremainsti
ghtl
ycontr
oll
edwi thi
nafewpercent
age
pointsofi tsnormal l
evel,2.4mEq/ L.
 Whencal cium ionconcent r
ationfall
stolowlevel
s(hypocalcemi
a),t
heexcit
abil
it
yofnerveandmuscl e
cel
lsi ncreasesmar kedlyandcani next
remecasesr esul
tinhypocal
cemictet
any.Thiscondit
ioni
s
charact eri
zedbyspast icskeletal
muscl econtr
acti
ons.
 WhenanI /Vinjecti
onofcal ci
um saltwasgiven,t
helowl ev
elsofcalci
um werebroughttonor
mal l
evel
s
asar esultofwhi chtheef fectsofexcessiv
eexcit
abili
tywereremovedandconditionofgir
lwas
i
mpr oved.

Q5.
c)
RoleofCal cium i nskeletalmuscl econtraction:
 Cal cium i onscombi newi thtr
oponi nCandeachmol eculeoft r
oponi nCcanbi ndst r
onglywi t
hupto
fourcal cium ions.
 Thet roponi ncompl exsupposedl yunder goesaconf ormational changet hati
nsomewayt ugsonthe
tropomy osinmol eculeandmov esitdeeperi nt
othegr oovebet weent het woacti
nst r
ands.
 Thi sact ion“ uncovers”theactivesitesoftheact i
n,thusallowingt heseact i
vesit
estoattractthe
my osincr oss-bri
dgeheadsandcausecont racti
ontopr oceed.
(1.
75mar ksf orabov eexplanati
on)
 Cal cium ent ersthener veterminalsthroughv ol
tagegat edcalcium channel swhendepolarizati
on
reachesneur omuscul arjunct
ion.
 Ther ei tcausest heagi t
at i
onofacet ylchol
inevesicl
esandt henexocy tosisofneurotr
ansmi t
ter.
(0.
25mar ksf orabov epoint)
Q8.Ay oungmanpresentswi t
hseveremuscleweakness&rapi
donsetofmuscl
efati
gueduringvolunt
ary
act
ions.Themanhasf ail
ureofneuromusculartr
ansmi
ssi
onduetolowvol
tageofendplatepotenti
al(
EPP).
a)Fr om whi
chdiseasethemani ssuf
fering? (01)
b)Gi vemechani
sm &f eatur
esofthedisease. (04)

Key
:

Q8.
a)
Themani
ssuf
fer
ingf
rom My
ast
heni
aGr
avs.(
i 1mar
k)

Q8.b)
Mechanism ofMy ast
heniaGr avis ( 2mar ks)
My ast
heniagr avisisanaut oi
mmunedi seaseinwhichant i
bodiesar eformedagainsttheprot
einchannelsi
.e.
acetyl
choli
negat edchannels.Sot henumberofr eceptor
sdecr eases.
My ast
heniagr av i
scausesmuscl epar al
ysisbecauseofi nabili
t yoftheneur omuscularj
unct
ionstot r
ansmit
enoughsignal sfrom thener v
efiber stothemuscl efibers.
Endplatepot entialst
hatoccuri nt hemuscl efibersaremost lytooweakt ost i
mulatethemusclefibers.
Featur
esofMy astheni
aGr avis (
2mar ks)
 Severemuscl eweakness
 Rapidonsetofmuscl ef at
igue.
 Muscl escommonl yaf fectedar eextr
aocularmuscl es,f
aci al
muscl es,musclesofmasti
cati
on,
swal l
owi ngandinsev erecasesr espir
ator
ymuscl es.
 Droopi ngofey el
ids
 Diplopia
 Inabil
itytoswal l
owf oodaf tersometime.
 Bedr i
ddeni nseverecasesanddeat hmayoccurduet or espi
rator
yf ai
l
ure
Q9.Wri
teshortnot
eson.
a)Rigormorti
s. (
02)

Key

Q10.
a)
Ri
gorMorti
s (
2mar ks)
 Severalhoursaft
erdeat h,allt
hemuscl esoft hebodygoi ntoast ateofcontract
urecall
ed“ri
gormorti
s”
 Themuscl escontractandbecomer igid,ev
enwi thoutactionpotential
s.
 Thisrigi
dit
yresult
sfrom l ossofal lt
heATP, whichisrequiredtocausesepar ati
onofthecross-
bri
dges
fr
om t heacti
nfil
ament sdur i
ngt herelaxati
onpr ocess.
 Themuscl esremaininr igoruntilthemuscl eprotei
nsdet erior
ateabout15t o25hourslater
,which
presumablyresult
sf r
om aut olysiscausedbyenzy mesr el
easedf rom l
ysosomes.
 Alltheseeventsoccurmor erapidlyathighertemper at
ures.
Q10.Whati
ssar
comer
e?Whatar
ethechangesi
nsar
comer
edur
ingskel
etal
muscl
econt
ract
ion?
(
5)

Key

Sar
comer e:
Partoft
heskelet
almusclemy of
ibr
ilbet
weentwosuccessi
veZl
i
nesi
scal
l
edsar
comer
e.I
tist
hest
ruct
ural
andfunct
ional
unitofskel
etal
muscle.(1mark)

(
1mar
kfordi
agr
am)

Changesi
nsar
comer
edur
ingskel
etal
muscl
econt
ract
i (
on:3mar
ks)

• Short
eni
ngofsar comere
• The2ZDi sksbecomecl oser
• Hzonedisappearsorreduces
• Endsofactinfi
lament
smayt ouchorov
erl
apeachot
her
• Ibanddecreases
 • Abandr
emainsunchanged
• Si
zeoft
heacti
nandmy osi
nfi
l
amentsremainunchanged
(0.
5mar ksforeachpoi
nt)

Q11.Descr
ibethemechani
sm ofskel
etal
muscl
econt
ract
ioni
ndet
ail
.Whati
sther
oleofATPandCa++i
ons
dur
ingskel
etal
musclecontr
acti
on?(5)

Key

Gener alMechani sm ofSkel etal Muscl eCont racton(

i 1mar kforexpl ai
ninggeneralmechani sm)
Thei nit
iati
onandexecut ionofmuscl econt r
act i
onoccuri nt hefollowingsequent i
al steps.
1.Anact i
onpot entialtravelsal ongamot ornerv etoitsendingsonmuscl efi
bers.
2.Ateachendi ng, t
hener vesecr et
esasmal l amountoft heneur otransmitt
ersubst anceacet ylcholine.
3.Theacet yl
cholineact sonal ocal areaoft hemuscl ef i
bermembr anetoopen“ acet ylcholinegat ed”cation
channel s.
4.Openi ngoft heacet y l
choline- gatedchannel sal l
owsl argequant iti
esofsodium ionst odi ffuset ot heint
erior
ofthemuscl efibermembr ane.Thi sact ioncausesal ocal depolarizati
onthatinturnl eadst oopeni ngof
voltage-gatedsodi um channel s, whichi niti
atesanact i
onpot entialatthemembr ane.
5.Theact i
onpot entialtravelsal ongt hemuscl efibermembr anei nthesamewayt hatact i
onpot ent i
alstr
avel
alongner vefibermembr anes.
6.Theact i
onpot entialdepol arizest hemuscl emembr ane,andmuchoft heact i
onpot ent i
alelectr
icityflows
throught hecent eroft hemuscl efi
ber .Her eitcausest hesar coplasmicreti
culum tor el easelargequant i
ti
esof
calcium ionsthathav ebeenst or edwi thinthisr eti
culum.
Oncet hecal ci
um i sreleasedt hemol ecul armechani sm ofcont r
act i
onstarts

Mol
ecul
arMechani
sm ofSkel
etal
Muscl
eCont
ract
ion(
3mar
ksf
orexpl
aini
ngal
l5st
epsgi
venbel
ow)
RoleofATP( 0.
5mar ks)
Beforethestartofmuscl econt r
acti
onamol eculeofATPi sattachedtomy osi
nhead.My osinheadhas
ATPaseact i
v i
ty.ThisATPasei scall
edMagnesi um ATPasebecausei trequi
resMagnesium foritsacti
vit
y.The
energyli
beratedduet obreakdownofATPi ntoADPi sstor
edint hemyosinhead.Thisenergyisstoredbefore
contract
ionandi susedf orpowerstroke.Whenonepowerst rokehasoccur r
ed,asecondmol eculeofATP
becomesat tachedwi t
hmy osinhead.Thisattachmentagaindetachesthemy osi
nheadf r
om act i
vesite.The
secondATPmol eculeishydroly
zedandener gyisli
berat
edwhi chisusedtomov ebackthemy osinheadto
ori
ginalposit
ionandt husmy osi
nheadf acesthenextactiv
esiteonactinfil
ament.

RoleofCal cium i nskeletalmuscl econtraction:

 Cal cium i onscombi newi thtr
oponi nCandeachmol eculeoft r
oponi nCcanbi ndst r
onglywi t
hupto
fourcal cium ions.
 Thet roponi ncompl exsupposedl yunder goesaconf ormational changet hati
nsomewayt ugsonthe
tropomy osinmol eculeandmov esitdeeperi nt
othegr oovebet weent het woacti
nst r
ands.
 Thi sact ion“ uncovers”theactivesitesoftheact i
n,thusallowingt heseact i
vesit
estoattractthe
my osincr oss-bri
dgeheadsandcausecont racti
ontopr oceed.
(1.
25mar ksf orabov eexplanati
on)
 Cal cium ent ersthener veterminalsthroughv ol
tagegat edcalcium channel swhendepolarizati
on
reachesneur omuscul arjunct
ion.
 Ther ei tcausest heagi t
at i
onofacet ylchol
inevesicl
esandt henexocy tosisofneurotr
ansmi t
ter.
(0.
25mar ksf orabov epoint)
Q12.
a)Whati sexcit
ati
oncontr
acti
oncoupl ingmechani sm?
(2.5)
b)Descr ibetherol
eofsarcoplasmicreticulum. (2.
5)
Key:
Q13.a)
Exci
tati
oncont r
acti
oncouplng(
i 2.
5mar ks)
Theprocessofconv ert
inganelect
rical
stimul usi.
e.Acti
onpotent
ial
toamechanical
responsei.
e.muscular
contr
actioniscall
edasExcit
ati
oncont r
actioncoupl i
ng.Cal
cium i
onspl
ayt
hepivotalr
oleinthi
sprocess.

• Aft
ertheNMJt ransmissi
on,acti
onpot enti
altr
avel
salongtheSarcol
emma.
• Thenitentersdeepintothemuscl efi
berthroughTTubules.
• Depolar
izati
onfrom herespreadstot hemembr aneofterminal
cist
ernae.
• Thiscausestheopeningofv olt
agegat edcalci
um channel
scausingreleaseofcal
cium f
ormt
he
ter
minalcist
ernaeintothesarcoplasm.
• Thiscal
cium thenbindswithtroponinCt ostar
tcontr
acti
on.
Q13.
b)
Rol
eofSar
copl
asmi
cRet
icul
um (
2.5mar
ks)
• TheSar coplasmi cr eticulum i nskelet almuscl ef iberhasgot
speci fi
ct ypeofar r
angementcal l
edsar cot ubul arsy stem.
•I tconsi stsofl ongi tudi nal t
ubul esandt ransv erset ubules
• Thel ongi tudi nal tubul eshav egotdi latedt er minal ends
calledt ermi nal ci st
er naeandt hesesur roundt heTTubul es
• TTubul esst artf rom onesi deoft hemuscl ef i
bert ot he
othersi de.
• TTubul esopeni ntot heECFandal socont ainst heECF.
•I fwet akel ongi tudi nal sectionweseet wot ermi nal cist
ernae
andi nt hecent eraTTubul e.
• Thisi scal ledTr iad.
• Triadi nskel et al muscl eispr esentatj unct i
onofAandI
Bands.
• Sar cotubul arsy stem i simpor t
antforst or age, rel easeand
reupt akeofcal cium i ons.
• Calcium i onsr eleasedf rom t heTer mi nal Cister naeofSar co
tubularsy stem i ni t
iatest hemechani sm ofCont raction.
• Acont inual l
yact ivecal cium pumpl ocat edi nt hewal lsoft he
sarcopl asmi cr eticulum pumpscal cium i onsawayf rom the
my ofibr i
lsbacki ntot hesar coplasmi ct ubul es.
• Thispumpcanconcent ratet hecalcium i onsabout10, 000-
foldinsi det het ubul es.
•I naddi tion, i
nsi det her eticulum isapr oteincal led
Q13.Gi
vedi
ff
erent
iat
ingpoi
ntsbet
weencar
diacmuscl
e,smoot
hmuscl
e&skel
etal
muscl
eindet
ail
.
(05)
Key:

Car diacmuscl e Skeletalmuscle Smoot hmuscl e

1.stri
at ed 1.str
iated 1.Non- stri
ated
2.Involuntarily 2.controll
edbyt he 2.Involuntaril
y
cont rol
led. somat icnervous cont r
olled.
3.cardi acmuscl eis system 3. muscl eisfoundinthe
foundi nt hehear t. 3.att
achedt othebone, viscera
4. Branchingchai nsof 4.cyl
indricali
nshape 4.Spindl eshaped
cellsconnect edby 5.l
ongert hancar di
ac 5.Shor ter
porousi nt er
calated muscl e 6.gapj unctions
discs, withsingle 6.nogapj uncti
ons 7.single
nucl eusandst riati
ons 7.multi-
nucleated. 8.Tt ubulesar enotwell
5.shor terthanskel et
al 8.l
essdense dev el
oped
 muscl e endomy sium and 9.Nof at
ique
6.gapj unctions fewermi t
ochondria. 10.Rhy
thmiccont
ract
ions
7.oneort wonucl ei 9.Fat i
guesEasi l
y
8.hav eadense 10.Norhythmi c
endomy sium,many contr
actions
mitochondr ia,
andT-
tubulest hatarewider
andf ewer .
9.Nof atique
10.Rhythmi ccontracti
ons

(
Studentget
sful
l5mar
ksi
fhe/
shewr
it
es10di
ff
erencesi
.e.0.
5mar
ksf
oreachdi
ff
erence)

Q14.Howi stheActi
onPotenti
alpr
opagat
edalongamy el
i
natednervef
iber
?Whatareadvantagesoft
his
pr
opagation?(3,
2)
Propagat
ionofacti
onpotenti
alal
ongamy el
i
natedner
vefiberoccur
sbySalt
ator
yconduct
ion(1mark)

(
2mar
ksfordescripti
onanddi agram)
• Thereisjumpingofact ionpotenti
alfrom nodetonode
• Myeli
nsheat hispresentwhi chisinsulator
.
• Atnodesofr anvi
ermy eli
nsheathisabsentandi onchannelsar
epresent.
• Solocalcir
cuitofcurrentcanbeest ablishedbet
weent wonodesofr anv
ier
.
• Localci
rcuitofcurr
enti sestabl
ishedbet weendepol
arizednodeofranvi
erandt
headj
acentpol
ari
zed
nodeofranv i
er.
 AdvanatagesofSalt
ator
yConduction:1.LessEnergyRequi
red,2.Fastconduct
ionVeloci
ty,
3.
Repolar
izat
ionoccurswit
hveryli
tt
letr
ansferofions
(2mar ksforwri
ti
ng3advantages,1.
5mar ksfor2and0.5mar ksforwrit
ing1advantage)

Q15.
a)Drawandl
abel
str
ength-
durat
ioncur
ve. (
2)
b)Defi
neChr
onaxi
e,Rheoabseanduti
l
izat
ionTi
me. (
3)

Q7.
a)
St
rengt
hDur
ati
onCur
ve
 (
2 mar
ks)

Q7.
b)

Chronaxi
e:Mi
nimum t
imer
equi
redf
orast
imul
usdoubl
ethest
rengt
hoft
her
heobaset
oexci
teamuscl
eora
neuron.(
1mark)

Rheobase:Iti
sthelowesti
ntensi
tyst
imul
uswhichwhenappl
i
edf
orinf
ini
tet
ime(
inapr
act
ical
sense,
about
300mill
iseconds)l
eadstostimul
ati
onofaneur
onormuscle. (1mark)

Ut
il
izat
ionTi
me:
Timet
akenbyr
heobaset
opr
oduceexci
tat
ion. (
1mar
k)

Q16.Whati
sLATCHphenomenoni
nsmoot
hmuscl
efi
ber
?Whati
sit
simpor
tanceandhowi
sitr
egul
ated?
(2,
1,2)
Key
LatchPhenomenon: (2marks)
LatchPhenomenonall
owslongter
m mai
ntenanceoft
onei
nmanysmoot
hmuscl
eor
ganswi
thoutmuch
expendi
tur
eofenergy

Impor
tanceofLatchPhenomenon:(1mark)
LessATParerequir
edtomaint
ainthepr
olongedcont
ract
ioni
nsmoot
hmuscl
e

Regulati
onofLat chPhenomenon: (2mar ks)
Whent hemy osi
nkinaseandmy osinphosphat aseenzy mesar ebot hstronglyact i
v at
ed,thecy cl
ingfr
equency
ofthemy osi
nheadsandt hevelocit
yofcont r
actionar egreat.Then, ast
heact iv at
ionoft heenzymes
decreases, t
hecycli
ngfrequencydecr eases,butatt hesamet i
me, thedeact i
vat i
onoft heseenzy mesallows
themy osinheadstor emai natt
achedt otheact i
nflamentf oral ongerandl ongerpr oportionofthecycli
ng
peri
od.Ther efor
e,t
henumberofheadsat tachedt ot heacti
nf l
amentatanygi v ent i
mer emai nsl
arge.Because
thenumberofheadsat tachedtot heactindeterminest hestaticforceofcont raction,t
ensi onismaintai
ned,or
“l
atched,”yetli
tt
leenergyisusedbyt hemusclebecauseATPi snotdegr adedt oADPexceptont herare
occasionwhenaheaddet aches.
Q17.
Wri
teshortnoteson:
a)Changesi nsarcomereduringskel
etal
musclecontr
act
ion
(
1.5)
b)CompoundAct ionPotent
ial (
1.5)
c) Whatissalt
atoryconduct
ion?Givei
tssigni
fi
cance. (
2)
Key

Q5.a)
Changesinsarcomer eduringskel et
almusclecontract
ion(1.
5mar
ksf
orwr
it
inganysexbel
ow changesi
.e.
0.
25mar ksf
oreachchange)
• Thereisshor t
eningofsar comere
• The2ZDi sksbecomecl oser
• Hzonedi sappear sorreduces
• Endsofact infi
lamentsmayt ouchorover
lapeachother
• Ibanddecr eases
• Abandr emai nsunchanged
• Sizeoftheact i
nandmy osinfil
amentsremainunchanged

Q5.
b)
CompoundActionPot
enti
al
Compoundactionpot
enti
alisameasur
eoft
hecombi
nedel
ect
ri
calpot
ent
ialofagr
oupofcel
l
sorf
iber
sina
si
ngl
enerve.(
1markfordefi
nit
ion)
• I
tisthemul t
ipeakedacti
onpot entialrecordedf r
om aner vetr
unk.
• I
fwest imulateaner vet
runklikesci ati
cner vether ecor
dobt ai
nedconsi sts
ofmulti
plepeaks.
• Aner v
et r
unkiscomposedofl ar genumberofner v
ef i
bers.
• Somear emy el
inatedandsomear eunmy eli
natedsot her
ei svar
iableveloci
ty
ofconducti
on.
• Therecordi
ngel ectr
odewil
lrecor dtheact ionpotentialf
irstf
rom thef ast
est
fi
berandthenf r
om slowfi
bersl eadingtomul ti
peakedr ecordfor
mat ion.

(
1mar
kforabov
eexpl
anat
ion)
(
0.5marksf
or
di
agr
am)
Q5.
c)
Sal
tat
oryconduct i
on:(1.
5mar ksfordescriptionanddiagram)
• Ther eisjumpingofact ionpotenti
al fr
om nodet onode
• My eli
nsheat hispresentwhichi sinsulator
.
• Atnodesofr anvi
ermy eli
nsheathisabsentandi onchannelsar
epresent.
• Sol ocalcir
cuitofcurrentcanbeest abli
shedbetweentwonodesofr anv
ier
.
• Local ci
rcuitofcurr
enti sestabl
ishedbet weendepolar
izednodeofranvi
erandt
headj
acentpol
ari
zed
nodeofranv i
er.

Si
gnif
icanceofSaltat
oryConduct
ion:
1.LessEner
gyRequi
red,2.Fastconduct
ionVel
oci
ty,
3.
Repol
arizat
ionoccurswit
hveryli
tt
let
ransf ons(
erofi 0.5mar ks)
Q18. a)Bri
efl
ydescri
bethegener
almechani
sm ofskel
etal
muscl
econt
ract
ion.
(
04)
b)Enl
istdi
ff
erentt
ypesofnerv
efi
bers.
(
01)

Gener alMechani sm ofSkel etal Muscl eCont racton(

i 4mar ksf orwr it
ingbelowmechani sm)
Thei nit
iati
onandexecut ionofmuscl econt r
act i
onoccuri nt hefollowi ngsequent i
al steps.
1.Anact i
onpot entialtravelsal ongamot ornerv etoitsendingsonmuscl ef i
bers.
2.Ateachendi ng, t
hener vesecr et
esasmal l amountoft heneur otransmi t
tersubst anceacet ylcholine.
3.Theacet yl
cholineact sonal ocal areaoft hemuscl ef i
bermembr anet oopen“ acet ylcholinegat ed”cation
channel s.
4.Openi ngoft heacet y l
choline- gatedchannel sal l
owsl argequant iti
esofsodi um ionst odi ffuset ot heint
erior
ofthemuscl efibermembr ane.Thi sact ioncausesal ocal depolarizati
ont hati
nt urnl eadst oopeni ngof
voltage-gatedsodi um channel s, whichi niti
atesanact i
onpot entialatt hemembr ane.
5.Theact i
onpot entialtravelsal ongt hemuscl efibermembr anei nthesamewayt hatact i
onpot ent i
alstr
avel
alongner vefibermembr anes.
6.Theact i
onpot entialdepol arizest hemuscl emembr ane,andmuchoft heact i
onpot ent i
alelectr
icityflows
throught hecent eroft hemuscl efi
ber .Her eitcausest hesar coplasmi creti
culum tor el easelargequant i
ti
esof
calcium ionsthathav ebeenst or edwi thinthisr eti
culum.
Oncet hecal ci
um i sreleasedt hemol ecul armechani sm ofcont r
act i
onst art
s

(Belowdiagr
am i
snotneededandi
sjustf
orr
efer
ence) b)1mar
Q2. kforwr
it
ingonl
ynamesofany
classi
fi
cati
on
Q19. a)Def
ineRheobaseandChronaxi
e. (
02)
b)Whatissal
tat
oryconduct
ion?Gi
vei
tssi
gni
fi
cance.
(
03)

Q2.a)
Rheobase:
Rheobaseisthelowesti
ntensi
tyst
imul
uswhichwhenappli
edf
ori
nfi
nit
eti
me(
inapr
act
ical
sense,
about300
mil
li
seconds)leadstost
imulat
ionofaneur
onormuscle.(
1mark)

Chronaxi
e:
Minimum ti
mer
equi
redf
orast
imul
usdoubl
ethest
rengt
hoft
her
heobaset
oexci
teamuscl
eoraneur
on..(
1
mark)

Q2.
b)

Sal
tat
oryconduct i
on
(2marksfordescripti
onanddi agram)
• Ther eisjumpingofact ionpotenti
alfrom nodetonode
• My eli
nsheat hispresentwhi chisinsulator
.
• Atnodesofr anvi
ermy eli
nsheathisabsentandi onchannelsar
epresent.
• Sol ocalcir
cuitofcurrentcanbeest ablishedbet
weent wonodesofr anv
ier
.
• Local ci
rcuitofcurr
enti sestabl
ishedbet weendepol
arizednodeofranvi
erandt
headj
acentpol
ari
zed
nodeofranv i
er.

Signi
fi
canceofSal t
atoryConducti
on: 1.LessEner
gyRequi
red,2.Fastconduct
ionVel
oci
ty,3.Repol
arizat
ion
occurswit
hv eryli
tt
letr
ansferofions
(1mar kforwr i
ti
ng3adv antages,0.75marksf
orwri
ting2adv ant
agesand0.5marksforwri
ting1
advantage)
Q20.Ay oungmanpresentswithseveremuscl eweakness&r
apidonsetofmuscl
efati
gueduringvoluntar
y
act
ions.Themanhasf ail
ureofneur
omuscul artr
ansmissi
onduetolowvolt
ageofendplatepotenti
al(EPP).
c) From whi
chdiseasethemani ssuff
ering? (01)
d)Gi vemechani
sm &f eat
uresofthedisease. (02)
e) Drawandlabelneuromuscul
arjunct
ion. (02)

Key
:

Q2.
a)
Themani
ssuf
fer
ingf
rom My
ast
heni
aGr
avs.(
i 1mar
k)

Q2.b)
Mechanism ofMy ast
heniaGr avis ( 1mar k)
My ast
heniagr avisisanaut oi
mmunedi seaseinwhichant i
bodiesar eformedagai nstt
heprot
einchannelsi
.e.
acetyl
choli
negat edchannels.Sot henumberofr eceptor
sdecr eases.
My ast
heniagr av i
scausesmuscl epar al
ysisbecauseofi nabilityoft heneur omuscularj
uncti
onstot r
ansmit
enoughsignal sfrom thener v
efiber stothemuscl efibers.
Endplatepot entialst
hatoccuri nt hemuscl efibersaremost lytooweakt ost i
mulatethemusclefibers.
Featur
esofMy astheni
aGr avis (
1mar kforwri
ti
nganyf ourf eatur
esi.e.0.25mar ksf
oreachpoint
)
 Severemuscl eweakness
 Rapidonsetofmuscl ef at
igue.
 Muscl escommonl yaf fectedar eextr
aocularmuscl es,facialmuscl es,musclesofmasti
cati
on,
swal l
owi ngandinsev erecasesr espir
ator
ymuscl es.
 Droopi ngofey el
ids
 Diplopia
 Inabil
itytoswal l
owf oodaf tersometime.
 Bedr i
ddeni nseverecasesanddeat hmayoccurduet or espirator
yf ai
l
ure

Neur
omuscul
arJunct
ion (2mar
ksf
orpr
operl
abel
l
ing)
Q21.
a)Def i
neresti
ngmembr anepotenti
al(RMP).
(01)
b)Enumer atethethr
eefactor
sthatexplai
nRMP.
(1.
5)
c) Expl
ainthefact
orthatcont
ri
butesthemost. (
2.5)

Key
Q3.a)
Defini
ti
onofRestingMembr anePotenti
al(
:0.
75mar ksfordefi
nit
ion)
Thepot ent
ial
dif
ferenceacr
ossaner vemembr aneduri
ngresti
ngst at
eisknownasRest i
ngMembr ane
Potenti
al.
Or
Thepot ent
ial
dif
ferenceacr
ossaner vemembr aneduri
ngwheni tisnotconduct
inganerveimpulsei
sknown
asRestingMembr anePotenti
al. Or
Thepot ent
ial
inmi l
li
vol
tswhichispr
esentacrossthemembr aneofexcitabl
ecel
lsinunsti
mulat
edorrest
ing
phase.
 RMPofl argenervefi
bresis–90mV.( 0.25marksfornormalv al
ue)

Q3.
b)
Namesoffactor
sthatexplainRMP
1.Contr
ibut
ionbyPot assi
um NernestPotent
ial (
0.5mark)
2.Contr
ibut
ionbySodi um Ner
nestPotental (
i 0.5mark)
3.Contr
ibut
ionbyNa+- K+ATPasePump (
0.5mark)
Q3.
c)
Thefact
ort
hatcontr
ibutesthemostinRMPi sContr
ibut
ionbyPotassi
um Ner
nestPot
ent
ial (
0.5mar
ks)

Expl
anati
onofContri
butionbyPotassium NernestPot
ental(
i 2marksf
orexplanati
on)
Concent
rati
onofPotassium out
side=4mEq/ L
Concent
rati
onofPotassium i
nsi
de=140mEq/ L
Forcal
culat
ionofNernstPotent
ialofPotassi
um, weassumecel
lmembraneatresti
shighl
yper
meabl
etoK+
Then
Potassi
um Ner
nstPot
ent
ial=-61log140/ 4
Potassi
um Ner
nstPot
ent
ial=-61log35
Potassi
um Ner
nstPot
ent
ial=-61X1. 54
Potassi
um Ner
nstPot
ent
ial=-94mV
Thi
s- 94mViscal
ledNer
nstpotent
ial
f orPot
assi
um whi
chi
sver
yneart
oRMP.

Q22.Amar athonr unnerst artedhi srace,her anataf astspeedf orfewmi nutesbutaftert

hathekepton
runningatasl owspeedf oronehour .
a)Whatar esour cesofener gyformuscl ef r
om st arttoendofr ace? (04)
b)Whatar ethet y pesofmuscl ef i
berspr edomi nantlyparti
cipatinginslowpr ol
ongedmuscle
cont ractions? (01)
Key
Q4.a)
Sourcesofener gyf ormuscl ef rom starttoendofr ace
Therearet hreesour cesofener gyf orSkeletal Muscl e
1)PhosphagenSy stem
2)Gl y
cogenLact icaci dsy stem
3)Aer obicSy stem
(1mar kforment ioni ngabov enamesonl y)
PhosphagenSy stem ( 1mar k)
• I tisthei mmedi atesour ceofener gyandi tincl udesATPandCr eati
nPhophat e.
• ATP+H2O ADP+H3PO4+7. 3Kcal EnzymeATPase
• ADP AMP+7. 3Kcal
• TheATPav ailabl eintheskel etalmuscl ecanmai ntai
ncont r
actiononlyforfewseconds
• Af t
ert hatCr eat inPhosphat ehelptor econst i
tuteATP
• ADP+CP ATP+C Enzy mei scr eati
nphosphoki nase
• Cr eat i
nPhospaht ecan’ tsuppl yenergydir ect l
y.
• I tmustf irstbeconv ertedt oATP.
• Socur rencyf orener gyi nbodyi sATP.
• Ener gyf rom Phosphagensy stem canmai nt aincont r
actiononl yfor8to10seconds.
• Soi tsuppl i
esener gyf orf ir
st100m whent her unnerranf ast
Gly
cogenLact icaci dsy stem ( 1mar k)
• I tisanaer obi c.
 • Glycogeni sbr okendownt oglucose6phosphat ebygl
y coly
sisint
oPy ruvate
• Ifoxy geni
sav ail
ablet
henpy ruvatewil
lbecomeacet ylCoAandent erscit
ricaci
dcycle.
• Duringexer cisethereisanaer obiccondit
ionsandpy r
uvat ei
sconv ert
edintoLacti
cAci d.
• Whenoxy genbecomesav ai l
abl
e, i
tisconvert
edbackint opyruv
ate.
• Lacticacidcannotbemet aboli
zedinmuscl e.
• Soi tenter
st hebloodandr eachesl i
verandent er
sCORRI ’scycl
ewher eitisusedforgluconeogenesi
s.
• Hear tcanal soutili
zeLacticacid.
• Thissecondsy st
em providesener gytomai nt
aincontr
act i
onfor1.3to1.6mi nut
es.
• Soi tprovi
desener gyrequiredfortherunnerforupto400met er
s.

Aer
obi
cSy st
em (
1mar k)
• I ti
ncludest hecompl et
eoxidati
onofnutr
ients.
• Acet yl CoAent ersthemitochondr
iawhereitenter
scitr
icacidcycl
e.
• Aer obicsy stem canprovi
deenergyformusclecontract
ionforunli
mit
edper
iodasl
ongast
henut
ri
ent
s
areav ail
able.

Q4.b)
Typesofmusclef i
berspredomi nantl
ypar t
icipat i
nginslowpr ol
ongedmusclecont
ractions
TypeIorslow,redoxidati
vefibers ( 0.75mar skforname)
• Cont ai
nmanymi tochondria
• Abundantmy oglobi
n, aprotei
nwi thirongr oupst hatbindO2andproduceadar kredcolor
.
• Redf i
bersderiv
eener gyprimarilyfrom aer obicoxidativ
ephosphor
ylat
ionoffattyaci
ds.
• Adapt edforslow,continuouscont ractionsov erprolongedperi
ods
• Exampl e:Posturalmusclesoft heback.
(
0.25mar ksforabov eexplanati
onpoi nts)

Q23.Comparet
heconduct
ionofact
ionpot
ent
ial
alongt
hemy
eli
nat
edner
vef
iberwi
tht
hatal
ongt
he
unmyel
inat
ednerv
efi
ber.(
05)
Key

Conducti
onofact i
onpotential
alongt hemyeli
nated conductionofact ionpot entialal
ongthe
ner
vefiber unmyel
inatedner vef i
ber
1)Saltat
oryconduction 1)Cont i
nuousconduct ion
2)Depolari
zationonlyatnodesofr anvier 2)St epbyst epdepol ar
izati
onofeachporti
on
3)Voltagegatedionchannel sareconcentrat
ed alongent irelengthofaxol emma
onl
yatnodesofr anvier 3)Vol tagegat edionchannel saredisper
sed
acr osstheent ir
el engthofaxolemma
4)ConductionVelocityisveryfast 4)Slowconduct i
onVel ocity
5)Lessener gyisr
equi r
edforconduction 5)Mor eenergyi srequiredforcondcti
on
(3mar
ksforwr i
tingabov epoi nts)
 (
2mar
ksf
ormaki
ngabov
edi
agr
amsandexpl
aini
ngt
heconduct
ionpr
ocess)

Q24.Aresearchstudentofneurophysi
ologydidner v
econductionstudi
esonasubject
.Hef
oundt
hatt
he
conduct
ionveloci
tiesar
ediff
erentinnerves.
a)Whichtypeofnervefi
bershav efastestandslowestconducti
onveloci
ti
es? (
01)
b)Howisr est
ingmembr anepotentialgenerat
ed?
(
04)

KEY:
Q1a)
FastestConduct
ionv
elocit
y:GroupAFibersi
. pha (
e.Aal 0.5mar
ks)
SlowestConducti
onVeloci
ty:GroupCFiber
s (0.
5mar
ks)

Q1b)
I
onicMechanismsi
nvol
vedingenerat
ionofResti
ngMembranePot
ent
ial
:
Contr
ibut
ionbyPot
assi
um NernestPotent
i (
al1.
5marks)
Concent r
ati
onofPot assium outsi
de=4mEq/ L
Concent r
ati
onofPot assium i
nside=140mEq/ L
Forcalculat
ionofNer nstPotenti
alofPot assi
um, weassumecel
lmembraneatr
esti
shi
ghl
yper
meabl
etoK+
Then
Potassium NernstPotential=-61log140/ 4
Potassium NernstPotential=-61log35
Potassium NernstPotential=-61X1. 54
Potassium NernstPotential=-94mV
Thi
s- 94mVi scal
ledNer nstpotent
ial
f orPotassi
um whichi
sver
yneart
oRMP.

Contri
butionbySodium Ner nestPot enti
al( 1.
5mar ks)
Concentrati
onofSodium out side=140mEq/ L
Concentrati
onofSodium inside=14mEq/ L
Forcalculat
ionofNernstPot ent i
alofPotassium, weassumecel lmembr aneatr esti
shighl
ypermeabletoK+
Then
Sodium NernstPotent
ial=- 61l og14/ 140
Sodium NernstPotent
ial=- 61l og0. 1
Sodium NernstPotent
ial=- 61X- 1
Sodium NernstPotent
ial=+61
This+61mVi scall
edNer nstpot enti
alforSodi um.Howev er,astheK+Na+Leakchannel sar
ev er
yless
permeabl et
oSodium ascompar edtopot assium.Soi nwardSodi um di
ffusionactual
lygener
atesapotenti
alof
+8mVonl y.
Calcul
ationofNernstPotent i
al causedbysodi um andpot assium ascalculatedbyGoldman’sequati
onisequal
to-86mVwhi chi
smuchcl osert opotassi
um Ner nstpot
entialbecauseofK+Na+Leakchannel sbeing100
ti
mesmor eleakytopotassium ascompar edtosodi um.

Contri
but
ionbyNa+- K+ATPasePump: Na+-K+ATPasePumpwi l
lgener
ateapot
ent
ial
of-
4mVi
nsi
de
becauseofpumpi ngofmoreposit
ivechargeout de.(
si 1mar
k)
Summar y
 Cont r
ibuti
onbyPotassi
um Ner nestPotenti
al=−94mV
 Cont r
ibuti
onbySodium NernstPotenti
al=+8mV
 Cont r
ibuti
onbyNa+- K+ATPasePump=- 4mV
 SoRest ingMembranePotential=(-94mV)+( +8mV)+(-
4mV)=- 90mV

Q25.
a)Whati send-pl
atepot
ential?Howiti
spr
oduced?I
nwhichdi
seaseend-
plat
epot
ent
ial
isofl
owv
olt
age.
(1+1+1)
b)Diff
erenti
atebetweenIsotoni
c&Isomet
ri
cmusclecont
ract
ions. (02)

Key:
Q2.a)
EndPlatePotent
ial
:
Endpl at
epotenti
als(EPPs)arethedepolar
izat
ionsofskel
etalmuscl
efi
berscausedbyneur
otr
ansmi
tt
ers
bi
ndingtothepostsynapt
icmembr anei
ntheneuromuscul
arj
uncton.(
i 1mark)
Producti
onofEndPlatePotent
ial
:(1mark)
 • Acet yl
cholinebi ndswiththerecept orsatt hemuscl emembr aneandt heser ecept
orsar ethepartoft he
acetylcholi
negat edchannelswhi char eligandgat edchannel s.
• Eachr ecept orhasgot5subuni t
s:2al pha, 1bet a,1gamma, 1del t
a
• Ther eisbindingwi ththealphauni tleadingt ochangei notheruintscausingopeni ng
• Ther earemi ll
i
onsoft heser eceptorsatt heNM j unct
ion.Thesechannel sar ecat ionschannel s.So
positiveionsi .e.sodium infl
uxoccur sandt hi
sr esultintolocali
zedhy popolari
zationduet osodi um
i
nflux.Thev olt
ageofendpl at
epot ent i
alis50t o75mV.
• RMPi nskel et
al muscleis-90mV.At- 65mVt hereisopeningofVol t
agegat edsodi um channel s.
• Sot hepur poseofEPPi stobr i
ngt hemembr anepot enti
altothresholdpot enti
alwhichshoul dbe-25mV.
Sot heEPP pr oducedi smuchmor et hanr equired.Thisi scalledsaf et
yf act
or ,whi chensuret he
product i
onofdepol ar
izati
on.
Diseaseinwhi chendpl atepotent
iali
sofl owv oltage: (
1mar k)
My ast
heni agr avi
si sbel i
evedtobeanaut oimmunedi seasei nwhicht hepatientshav edevel opedant i
bodies
thatblockordest roytheirownace¬t ylcholi
ner ecept orsatt hepostsynapticneur omuscularj unction.Theend
platepotent i
alsthatoccuri nthemuscl efi
ber sar emost lytooweakt oinit
iateopeni ngofthev olt
age-gat
ed
sodium channel s,andt husmusclef i
berdepol arizati
ondoesnotoccur .

Q2.
a)

I
sot
oni
cMuscl
eContr
act
ion I
somet
ri
cMuscl
eContract
ion
• Reduct
ioni
nmusclel
engt
h • Muscl
elengt
hremai nsunchanged

• Tensi
onr
emai
nssame • Ther
eisi
ncr
easedt
ensi
oni
nthemuscl
e

• Oneendoft
hemuscl
eishel
dfi
xedot
heri
s • Bot
hendsoft
hemuscl
ear
ehel
dfi
xed
fr
ee.
• Muchshorteningofmuscl
efiberi
snot
• Short
eningofmuscleismorethanrequi
red al
lowed.Thereissomeshort
eningofmuscl
e
toneutr
ali
zethest
retchi
ngofelast
ic fi
bersneut
rali
zedbythest
ret
chingofel
asti
c
component. componentsonochangeinmuscl el
engt
h
occurs.

• Wor
kisnotdonei
nthi
scont
ract
ion.
• Wor
kisdone.
• LessATPi
sused.
• Muchmor
eATPi
sut
il
ized.
• I
ni sometri
ccont r
actiononlysomegr oupof
• I
nisotonicexerci
ses,mostofthemusclesof muscl esareacti
ve.Intheseact i
v emuscles
t
hebodyar eactiv
eandpr edominant
lyt
here thereisvasodil
atat
ionwhi l
eint herestofthe
i
svasodil
ati
onandt hustherewill
notbe bodyt her
ewi l
lbev asoconstr
iction.So,t
here
muchriseinbloodpressure. willbegreatert
endencyt oincreaseblood
pressure.

• Examples:
• Examples: • Bodybuildershowingthemuscles.
Swi
mming,
Running,
Cycl
i
ngpr
edomi
nant
lyi
nvol
ve • I
nstandingmuscl esoflegcont
ract
i
sot
oni
ccontr
acti
ons i
sometricall
ytomai nt
ainer
ectpostur
e.

(
Studentgetsf
ull2marksifhe/shewrit
esany4di
ff
erencesi.
e.0.5marksf
oreachdi
ff
erence)
Q26.Descri
beexcit
ati
oncontract
ioncoupl
i
ngmechanism i
nskeletal
muscl
e. (05)

Key

Exci
tat
ioncontr
acti ng(
oncoupl
i 4marksforexpl
anati
on)
Theprocessofconver
ti
nganel
ect
ri
calst
imulusi
.e.Acti
onpot
ent
ial
toamechani
cal
responsei
.e.muscul
ar
cont
ract
ioni
scal
l
edasExci
tat
ioncont
ract
ioncoupl
i
ng.Cal
cium i
onspl
ayt
hepi
vot
alr
olei
nthi
spr
ocess.

1.Act i
onpot ent ialsi nasomat icmot orneur oncauset her eleaseofacet ylcholi
neneur ot
ransmitt
eratt he
my oneur al junct ion( onemy oneur al j
unct i
onpermy ofi
ber ).
2.Acet yl
chol i
ne,t hroughi tsi nteract i
onwi t
hr eceptorsi nt hemuscl ecellmembr ane( sarcolemma) ,produces
actionpot ent ialst hatar er egener atedacr osst hesar colemma.
3.Themembr anesoft het ransv erset ubul es(Tt ubul es)ar econt i
nuouswi t
ht hesar colemmaandconduct
actionpot ent ialsdeepi ntot hemuscl efiber.
4.Act ionpot ent i
al sint heTt ubul es,act i
ngt hroughamechani sm thatisi ncompl etelyunder stood,sti
mulate
ther eleaseofCa2+f rom t het ermi nal ci
sternaeoft hesar copl asmi cret
icul
um.
5.Ca2+r el easedi nt ot hesar coplasm at tachest ot roponi n,causingachangei nitsst r
uct ure.
6.Theshapechangei nt roponi ncausesi tsat t
achedt ropomy osintoshi f
tposi ti
oni nt heact infi
lament,thus
exposi ngbi ndi ngsi tesf ort hemy osincr ossbr i
dges.
7.My osincr ossbr idges, previousl yact i
vatedbyt hehy drolysisofATP, att
acht oact in.
8.Oncet hepr eviousl yact i
vat edcr ossbr i
dgesat t
acht oact in,theyunder goapowerst r
okeandpul lthet hi
n
fi
lament sov ert het hickf i
lament s.
9.At tachmentoff reshATPal l
owst hecr ossbr idgest odet achf rom acti
nandr epeatt hecont r
acti
oncy cl
eas
l
ongasCa2+r emai nsat tachedt ot roponin.
10.Whenact ionpot entialsst opbei ngpr oduced,t hesar coplasmi creti
culum act ivel
yaccumul atesCa2+and
tropomy osi nr etur nst oi tsinhibitoryposi t
ion

(
1mar
kfordi
agr
am)

Q27.
a)Gi
vest
epsofneur
omusculart
ransmissi
on. (
03)
b)Dr
awandlabel
adiagr
am ofneuromuscularj
unct
ion. (
02)

Key
:
Q2.
a)
Neur
omuscul
art
ransmi
ssi
on:

(
1 mar
ksf
orwr
it
ingabov
e6st
eps.Di
agr
am i
snotnecessar
yforexpl
aini
ngst
eps)

Q2.
b)

Si
milardi
agr
am asabov
ewi
thoutst
epsandment
ioni
ngal
lthei
mpor
tantsi
tesofNeur
omuscul
arj
unct
ion.(
2
marks)

Q28.Amanof35y ear
swi t
hcomplai
nt sofsever
emuscl eweaknessandrapi
donsetoffat
igueduri
ngt
he
vol
untar
yact i
onsconsultedaphysi
cian.Heishavingdroppi
ngofeyel
ids.Whenashortact
ing
anti
chol
inester
aseisgivenint
rav
enously,markedimprovementoccur
s.
a)From whichdiseasethemanissufferi
ng? (
01)
b)Whati
sthepat
hophysi
ologyoft
hisdi
sease? (
03)
c)Whi
chdrugi
sgiveni
nthiscondi
ti
on? (
01)

a)(
Q2.( 1mar
k)

My
ast
heni
aGr
avi
s

b)(
Q2.( 3mar
ks)

Pat
hophy
siol
ogy
:

Myastheni
agravi
scausesmuscl
eparal
ysi
sbecauseofinabi
l
ityoft
heneur
omuscul
arj
unct
ionst
otr
ansmi
t
enoughsignal
sfr
om t
hener
vefiberst
othemuscl
efibers.

My ast
heni
agr
avi
si sanaut
oimmunediseasei
nwhi
cht
hepat
ient
shav
edev
elopedi
mmuni
tyagai
nstt
hei
rown
acetyl
chol
i
ne-
act
ivatedi
onchannel
s.

Endpl
atepot
ent
ial
sthatoccuri
nthemuscl
efiber
sar
emost
lyt
ooweakt
ost
imul
atet
hemuscl
efiber
s.

I
fthedi
seasei
sint
enseenough,
thepat
ientdi
esofpar
aly
sis—i
npar
ti
cul
ar,
par
aly
sisoft
her
espi
rat
orymuscl
es.

Q2.(
c)

Ant
ichol
i
nest
eraseDr
ugsi
.e.Neost
igmi
ne/Phy
sost
igmi
ne

(
Studentget
sful
l1mar
kifhe/
shewr
it
esanyoft
heabov
e-ment
ionedname)
.

Q29.Whati
sther
oleoft
ropomy
osi
nandt
roponi
ninskel
etal
muscl
e? (
05)
Key

Rol
eoft
ropomy
osi
ninskel
etal
muscl
e (
2mar
ks)
 • Atresttr
opomy oi
nstrandsareinsuchaposi
ti
onthatthesecovert
heactiv
esit
esonactinf
il
ament
s
physical
ly
• Thisprevent
stheint
eracti
onbetweenacti
nandmy osi
nandt huspr
eventcont
racti
on
• Duringcontr
act
ionthesestrandsmovetodeeperposi
ti
onstounmaskt heact
ivesi
test
ostart
contract
ion.

Rol
eoftr
oponininskel
etalmuscle( 2mar ks)
• Iti
sacompl exofsmal lpr
oteinsattachedt otropomy osi
natadistanceof40nm.
• Therearethreet
ypesoft roponinsi
.e.Tr oponi
nT, TroponinIandTr oponi
nC.
• TroponinThasaffini
tyfortropomyosi n.Sothroughthisthecompl exisboundtot
ropomyosin.
• TroponinIhasAffi
nit
yforAct inandt heboundt roponinIandActinkeepstropomy
osininsucha
posit
ionthatatr
est,t
ropomy osi
nphy sical
lycoverstheactiv
esites.
• TroponinChasgotaf fi
nit
yf orcal
cium Ions.

Whenther
eisbindi
ngofcal
cium wit
hTroponi
nC,thebondbet
weent r
oponi
nIandacti
nisbrokensothat
tr
opomyosi
ntropnoi
ncomplexbecomesfreetopassi
ntoadeeperposi
ti
on.Thi
scausestheacti
vesi
teson
acti
nfi
l
amentstobecomeuncovered.

Tr
opomyosinandt
roponi
nar
ecol
l
ect
ivel
ycal
l
edasr
elaxi
ngpr
otei
nsbecauseatr
estt
heycov
ert
heact
ive
si
tesonact
in.

Assoonastheacti
vesit
esonact
inareuncov
ered,
myosinheadi
sat
tract
edt
owar
dst
heact
ivesi
teandt
her
e
i
sanint
eract
ionbetweenthet
woresul
ti
ngint
oPowerst
roke.

(
1mar
kforabov
eexpl
anat
ion)
Q30.
a) WhatisLatchmechani
sm? (02)
b)Wherearethecalci
um i
onsst
oredi
nskel
etalmuscl
esandhowar
ethesecal
cium i
onsr
eleasedt
oinit
iat
e
contr
action? (
03)
KEY

Q2.a)
LatchMechani
sm:
LatchPhenomenonall
owsl
ongter
m mai
ntenanceoft
onei
nmanysmoot
hmuscl
eor
ganswi
thoutmuch
expendi
tur
eofener .(
gy 1mark)

Explanati
on: (
1mar k)
Whent hemy osi
nkinaseandmy osinphosphat aseenzymesar ebothstronglyact i
vated,thecycl
i
ngf r
equency
ofthemy osi
nheadsandt hevelocit
yofcont r
actionaregreat.Then,astheactivati
onoft heenzymes
decreases, t
hecycli
ngfrequencydecr eases,butatthesamet i
me, t
hedeact i
vationoftheseenzy mesallows
themy osinheadstor emai natt
achedt otheact i
nfil
amentforal ongerandlongerpr oportionoft
hecy cl
ing
peri
od.Ther efor
e,t
henumberofheadsat tachedt otheacti
nf i
lamentatanygi ventimer emainslar
ge.Because
thenumberofheadsat tachedtot heactindeterminesthestaticfor
ceofcont racti
on, t
ensionismaintai
ned,or
“l
atched,”yetli
tt
leenergyisusedbyt hemusclebecauseATPi snotdegr adedt oADPexceptont herare
occasionwhenaheaddet aches.

Q2.b)
Storageofcal
cium i
onsi
nskelet
almuscl
es:
Calcium i
onsar
estoredi
nsarcopl
asmicr
eti
cul
um (
sar
cot
ubul
arsy
stem)i
nskel
etal
muscl
es.(
1mar
k)

Rel
easeofcalcium ionstoi nit
iatecont racti
on:
 Af tertheNMJt ransmi ssion, acti
onpot entialtravelsal ongt heSarcolemma.
 Theni tenter
sdeepi ntot hemuscl efi
bert hroughTTubul es
 Theact ionpotentialoft heTt ubulecausescur rentflowi ntothesarcopl asmicret
icularcist
ernaewher e
theyabutt heTt ubule.
 Ast heactionpot entialreachest heTt ubule,thev oltagechangei ssensedbydi hydropy r
idi
nereceptors
thatar eli
nkedt ocal cium r eleasechannel s,alsocal edr
l yanodiner eceptorchannel s,i
nt headjacent
sarcoplasmicr eti
cularcisternae.
 Act ivati
onofdi hydropy r
idiner eceptorst ri
gger st heopeni ngoft hecal ci
um rel
easechannel sint he
cister
nae,aswel l
asi ntheirat tachedlongi t
udinal tubul es.
 Thesechannel sr emai nopenf oraf ew mi ll
isec¬onds,r eleasi
ngcal cium i
onsi ntot hesarcoplasm
sur¬roundingthemy ofibril
sandcausi ngcont r
action.
(
2mar ksf orabov eexpl anat i
on)
Q31.
a)Defi
neFennef fect
. (01)
b)WhatisEndPl atePot
ent
ial
?Howi si
tproduced?I
nwhi
chdi
seaseendpl
atepot
enti
ali
soflowv olt
age?
(1,
1,2)
KEY
Q9.a)
FennEffect:
Thegreatertheamountofworkper
formedbythemuscl
e,t
hegr
eatert
heamountofATPthatiscleaved/
uti
lzed.(
i 1mark)

Q9.b)
EndPlat ePot ential:
Endpl atepot enti
al s( EPPs)ar ethedepol arizationsofskel etalmuscl ef i
berscausedbyneur ot
ransmi t
ters
bi
ndingt ot hepost synapt i
cmembr aneint heneur omuscularj unction.(1mar k)
ProductionofEndPl atePot ential
:(2mar ks)
• Acet yl
cholinebi ndswi thther eceptorsatt hemuscl emembr aneandt heser ecept
orsar ethepartoft he
acetylcholinegat edchannel swhi char eligandgat edchannel s.
• Eachr ecept orhasgot5subuni t
s:2al pha, 1beta,1gamma, 1del t
a
• Ther eisbindi ngwi ththeal phauni tleadingt ochangei not heruintscausingopening
• Ther ear emi ll
i
onsoft heser ecept or
satt heNM j unction.Thesechannel sar ecat ionschannels.So
positiveionsi .e.sodium i nfl
uxoccur sandt hi
sr esulti ntolocali
zedhy popolari
zationduet osodi um
i
nflux.Thev olt
ageofendpl atepotent i
al is50t o75mV.
• RMPi nskel etal muscl eis-90mV.At- 65mVt hereisopeni ngofVol tagegatedsodi um channels.
• Sot hepur poseofEPPi stobr ingthemembr anepot enti
al tothreshol
dpot enti
alwhichshouldbe- 25mV.
Sot heEPP pr oducedi smuchmor et hanr equired.Thi si scalledsaf et
yf act
or ,whichensuret he
product i
onofdepol ari
zat i
on.

Diseaseinwhichendplatepotenti
ali
soflowv ol
tage:(1mar k)
My ast
heniagravi
sisbeli
ev edtobeanautoimmunedi seaseinwhichthepati
ent
shavedevelopedanti
bodies
thatblockordestr
oytheirownace¬tyl
choli
nereceptorsatthepostsy
napti
cneuromuscul
arjunct
ion.Theend
platepotent
ial
sthatoccurinthemusclefi
bersaremost l
ytooweakt oini
ti
ateopeni
ngofthevolt
age-gat
ed
sodium channel
s,andthusmuscl efi
berdepol
ari
zati
ondoesnotoccur .