Nerve Muscle Physiology injury and regeneration

Physiology of nerve injury

1. Prasanta Deb
Assistant Professor
Dept. of Human Physiology
M.B.B. College, Agartala

2. P.Deb 2

3. Degeneration:
Aftercompletetransactionofthenerve,theperipheralpartsoftheaxons
undergocertaindegenerativechangeswhichareoftencalledWallerian
degeneration.
Degenerationtakesplaceatthreelevels:
•Inthenervecell
•Intheproximalpartofthecutfibreand
•Inthedistalpartofthecutfibre
Degeneration:Changeoccurringintheproximalpartoftheaxonsandalsothe
cellbodiesfollowingsectionofanaxonisknownasretrogradedegeneration.The
changesinthecellbodiesare:
1.Chromatolysis:Nisslgranulesdisappear.Itstartswithin48hoursand
becomesmaximumby15-20days.
2.Golgiapparatus,mitochondriaandneurofibrilsbreakupanddisappear.
3.Thecelldrawsinmorefluid,swellsupandbecomesrounded.
3P.Deb

4. 4.Thenucleusispushedtotheperiphery.Inseverecasesitmaybetotally
extruded,inwhichcase,thenervecellcompletelydiesanddisappears.
Thedegreeofdamageandchromatolysisdependon:
a)Thedistanceoflesionsfromthenervecell-Lesserthedistancegreaterwill
bethedamage.
b)NatureofSection:Ifitisasharpcut,theeffectswillbeless.Butifforcibly
torn,thedamageissevereandoftenthecelldies.
Degeneration in the Proximal part of the cut fibre
Sincethispartremainsconnectedwiththemothercell,degenerationcannotbe
completeunlessthenervecelldies.Ordinarily,degenerationproceeds
centrallyasfarasuptothefirstnodeofRanvierandinmostcases
degenerativechangesmayextenduptoafewinternodeswhenregenerative
changesareinitiatedfromtheendofthecentralstump.Inmoreseverecases,
itmayproceedtoalittlehigher.Thenatureofthisdegenerationandthe
subsequentregenerationissameasinthedistalstumporpart.Regeneration
takesplaceiftheneuronesurvives.
4P.Deb

5. Degenerationinthedistalpartofthecutfibre
Sincethispartistotallyseparatedfromthemothercell,itdegenerates
completely.Degenerationstartssimultaneouslyinthewholelengthofthefibre
uptoitsterminalarborizationswithin24hoursandiscompletedby3weeks.
Followingdegenerativechangesareseen:
HistologicalChanges:
1.Theneurofibrilsswell,becometortuousandultimatelydisappearandthe
axiscylinderbreaksupintoshortlengths.
2.Themyelinsheathdisintegratesintodropletsoffat.Lecithinsplitsupinto
glycerol,phosphoricacid,fattyacidandcholine.Theyarepartlyremoved
bymacrophagesandpartlywashedoutinthebloodstream.Ifthedamage
beinsidethecentralnervoussystem,nofurtherchangetakesplace.
But if it be in the peripheral nervous system the neurolemmashows the
following changes :
5P.Deb

6. ThenucleiofSchwanncellmultiplymitoticallyandtheSchwanncell
cytoplasmincreasesinamount.Itstarts4-9daysaftersection.The
macrophagespenetratetheneurolemmaltubesandremovethedebris.The
Schwanntissuegraduallyfillupthewholetubeandtheprocessiscompletedby
threemonths.Fromthecutofthedistalend,theproliferatingSchwanntissue
spreadsupwardstowardthecentralcutendandinthiswaymaybridgeupa
considerablegap(evenupto3cm)betweenthetwocutends.Therateof
progressofthisgrowthis1-2mmperday.Theperipheralneurolemmaltube
shrinkstohalfitsoriginaldiameterin7weeksandmayremainsoforabout18
months.Theabovedegenerativechangesinthedistalcutendofthefibreswere
firstobservedbyWallerandaccordingtohimitisknownasWallerian
degeneration.
DegenerationofNerveendings:
Theframeworkofbothsensoryandmotorendingscanresistdegenerationfor
months.Ifthenervefibrefailtoregenerate,theendingsalsoatrophy.
Transneuronaldegeneration:
Whenneuroneoritsmotorfibredegenerates,theneuronenextinthechainis
oftenfoundtodegeneratealso.Thistakesplaceinspiteofthefactthatthereis
noanatomicalcontinuitythroughthesynapses.
6P.Deb

7. Itisprobablyanexampleofdisuseatrophy.Inmanyconditions,thistype
ofdegenerationoccurse.g.,
1.Aftersectionoftheopticnerve,thecellsinthelateralgeniculatebody
degenerate.
2.Aftersectionoftheposteriorspinalroot,theposteriorhorncells
degenerate.
3.Inlesionsofthemotorcortexorpyramidaltracts,theanteriorhorncells
maydegenerate.
Thistypeofdegenerationmaybetheunderlyingcauseoftheso-called
Systemdiseasesviz.,Amyotorphiclateralsclerosis,etc.,where
degenerationofanteriorhorncellsfollowsthatofthepyramidaltracts.
7P.Deb

8. Regeneration:
Regenerationtakesplaceonlyoutsidethecentralnervoussystemwhere
neurolemmaispresent.Presenceofneurolemmais,therefore,essentialforthe
process.Hence,inthecentralnervoussystem,neurolemmabeingabsent,nerve
fibredonotregenerateatall.Thefollowingstepsareseenduringregeneration:
Theaxiscylindergrowsfromthecentralcutendasaroundedsproutand
proceedstowardsthesolidneurolemmalcord.TheproliferatedSchwanntissue
intheperipheralcutendanditsprolongationtowardsthecentralcutend
provideaninfluencewhichguidestheapproachingaxiscylinder.Eachgrowing
fibresplitsupintonumerousneurofibrils(evenupto100),theSchwanncells
disappearandthefibrilsenterthenewlymadeneurolemmaltube(2-3weeks
afterthesection,theinnerwallofthetubemaycontainanumberoffibrils).All
thefibrilsdegenerate,exceptingasingleone,whichgraduallyenlargesand
occupiesthecentralpartofthewholelengthofthetubeproceeding
peripherally.Thedailyrateofgrowthisabout0.25mminthescartissue
betweenthetwocutendsand3-4mmintheperipheralneurolemmaltubes.
8P.Deb

9. Myelinsheathbeginstoappearinabout15daysandproceedsperipherally
alongthefibreataslowerratethanthegrowingaxiscylinder.
Increaseinthediameterofthefibretakesplaceslowly.Thediameterofthe
fibreislimitedbythesizeoftheneurolemmaltubeandthatoftheparent
nervecell.
Withacleansharpwoundandthecutendsbeinginapposition,somedegree
ofrecoveryusuallytakesplacein6-24months.Foramotornerve,recovery
maybecomplete.Butforamixednerve,itisrarelyso.
Intheregeneratedfibrestheaxiscylinderandmyelinsheatharereducedin
thickness,theintermodaldistanceisalsodiminished.Buttherateof
conductionofnerveimpulsesintheregeneratedfibresremainsthesame.
Completefunctionalregenerationoccursafterhistologicalregeneration-3
weeksincaseofmotornervefibresand5weeksincaseofsensorynerve
fibres.
9P.Deb

10. P.Deb 10

11. P.Deb 11
Modern concept of Generation of
Resting Potential

12. P.Deb 12
Restingmembranepotential(RMP)isthedifferencebetweenelectrical
potentialexistingontheoutsideandinsideofacellatrest.Thisvariesin
differenttypesofcells.
Inanerve,usuallyitis-70mV.Inaskeletalmuscle,itisabout-90mV.In
intestinalsmoothmuscle,itisabout-50mV.
CauseofRestingMembranePotential:
TheintracellularandextracellularconcentrationofionssuchasNa
+
,
K
+
,Cl
-
aredifferent.Also,thepermeabilityofcellmembranetothe
individualionsisalsodifferent.Thesetwofactorsaremainlyresponsible
forthemagnitudeofRMP.
[K
+
]insidethecellis155meq/Land[K
+
]outsidethecellis4meq/L.
AsthecellmembraneisfreelypermeabletoK
+
ions,K
+
tendstomoveout
ofthecellalongtheconcentrationgradient.ButasK
+
movesoutofthe
cell,theinteriorofthecellbecomesnegativelychargedduetolossof
cations.Thiscouldhavebeenprevented-
a.IfNa
+
ionsenteredintothecellbutthecellmembraneisimpermeable
toNa
+
ions.

13. P.Deb 13
b.Proteinsanionsinsidethecellscouldhavemovedouttoneutralise
intracellularnegativitybuttheyaretoolargetopassthroughthecell
membrane.
c.Cl
-
ionsalsocannotmoveoutofthecellagainstthesteep
concentrationgradient.
So,intracellularnegativitypersists.
ThiswillattracttheoutgoingpositivelychargedK
+
ionsinwardsdue
toelectricalgradient.
Ataparticularelectricalpotential,thesetwoforcesdueto
concentrationandelectricalgradientbalanceeachotherandan
equilibriumisestablished.Thisisknownasthediffusionor
equilibriumpotentialofK
+
.
ThiscanbemathematicallyderivedfromNernstequation,according
towhich
RT [K
+
]
0
E
K= ------------ln_______
FZ [K
+
]
I

14. P.Deb 14
Where, E
K= Equilibrium potential of K
+
ions
R= Gas Constant
T= Absolute temperature
F= Faraday (96500 Coulombs)
Z= Valencyof K
+
ln= Natural log
[K
+
]
0= K
+
concentration outside the cell
[K
+
]
I= K
+
concentration inside the cell
In contrast to K
+
ions, Na+ ions have electrical gradient and
concentration gradient both directed to the inside of the cell.
From the Nearstequation, we get
E
Na=+65 mV
Similarly, E
Cl= -70mV

15. P.Deb 15
So, K
+
ions tend to move the RMP to its equilibrium potential (E
K) i.e.,
-90mV, whereas Na
+
ions tend to pull the RMP in the opposite direction
to E
Na
+
, which is +65mV. Similarly Cl
-
ions try to maintain the RMP at
its own equilibrium potential which is -70mV.
Cl
-
ionshaveatendencytomoveoutofthecellbeingrepelledbythe
electronegativecellinteriorwhereasithasatendencytomoveintothe
cellduetoconcentrationgradientdirectedtowardsinsideofthecell.
Normally,thesetwooppositetendenciesalmostexactlybalanceeach
otherandCl
-
ionhasverylittleeffectonRMP.
TheresultantRMPnowdependsonthepermeabilityorconductanceof
theindividualions.
AstheK
+
ionsis10-25timesmorepermeablethanNa
+
ion,theresting
membranepotentialismuchclosertoE
K.ActualRMPstandsat-70
mV.
ItcanbemathematicallyderivedfromtheGoldmanconstant-field
equation.

16. P.Deb 16
RT P
K[K
+
]
o+P
Na[Na
+
]
o+P
Cl[Cl
-
]
i
RMP = ln
F P
K[K
+
]
i+P
Na[Na
+
]
i+P
Cl[Cl
-
]
o
Where, P stands for permeability, ‘o’ and ‘I’ stand for outside and inside
respectively and third brackets indicate concentration.

17. P.Deb 17
ItistobenotedthatatRMP,neitherK
+
ionsnorNa
+
ionsareattheir
equilibriumpotential.So,thereismovementofNa
+
ionsintothecelland
K
+
ionsoutofthecell.However,thisdoesnotaltertheintracellularor
extracellularNa
+
andK
+
ionconcentrationsasNa
+
-K
+
-ATPasepumps
constantlypumpoutNa
+
outofthecellandbringK
+
intothecell,thus
restoringionicbalance.
AsmallpartoftheRMPiscontributeddirectlybytheelectrogenicNa
+
-K
+
-
ATPasepump,asitdrivesout3Na
+
ionsfromthecellandbrings2K
+
ions
intothecell,thuscausingslightintracellularnegativity.
Although,thedirectcontributionofNa
+
-K
+
-ATPasepumptoRMPissmall,
ithasafarmoreimportantindirectroleinthegenesisofRMPasitplaysa
pivotalroleinmaintainingconcentrationgradientsofNa
+
andK
+
ions
acrossthecellmembrane.
Donnanmembraneequilibriumresultsinunequaldistributionsofanions
andcationsacrossthecellmembraneduetothepresenceofnon-diffusible
anions(Proteins)asaresultanelectricalpotentialdifferenceissetupin
accordancewithNernstequation.

18. P.Deb 18
GENERATION OF ACTION POTENTIAL

19. P.Deb 19
Inrestingstatethenervefibreremainsinpolarizedstateandthe
membranepotentiallieswithin-70mV.Theinsideofthenerveisnegative
andtheoutsideofthenerveispositive.Na
+
concentrationoutsidethe
membraneishigherthanthatofinsidethemembrane.K
+
concentration
insidethemembraneisalsohigherthanthatoftheoutside.K
+
can
permeatethroughthemembraneatrestingstatebutNa
+
cannot
permeate.PermeabilityofNa
+
tomembraneisincreasedonlyafter
excitationandisthefirsteventoftheactionpotential.Theaction
potentialoccursinsuccessivestagesofdepolarization,repolarization,
negativeafterpotentialandpositiveafterpotential.Ithasbeenpostulated
thatinrestingstatecalciumions(Ca
++
)remainboundtotheprotein
throughtheserestingpores.DuringexcitationCa
++
isdislodgedfromits
bindingsiteandthepermeabilitytoNa
+
isincreased.Sothe
depolarizationstartswiththeonsetofNa
+
entryandthusanincreasein
Na
+
conductanceistakenplace.

20. P.Deb 20

21. P.Deb 21

22. P.Deb 22
ThetremendousincreaseinNa
+
conductanceduringthisperiodisknown
asactivationofmembrane.Duetothis,thereversalofpotentialiscaused
withthedevelopmentofpositivityinsidethemembraneandnegativity
outside.Butwiththeincreaseofpositivityinside,furtherentryofNa
+
is
preventedandcalciumbeginstobindwiththeproteinsofthemembrane
pores.Butassoonastheactionpotentialattainsthevoltage
approximately+35mV,K
+
beginstocomeoutfrominsidethemembrane.
Theinsidebecomesnegativeandoutsidebecomespositiveagain.This
stageistherepolarizationphase,K
+
conductanceisincreasedtothe
maximum.ThemechanismunderlyingtheprocessofK
+
conductanceis
mostlyhypotheticalandincreasedpositivityinsidethemembranedueto
Na
+
entryduringdepolarizationphase,allowstheK
+
tocomeoutandthe
restingpotentialisslowlyachieved.Butatthelaterperiodofthisphase
(attheterminationofspikepotential)K
+
conductanceisalloweddown
andthusafewmillisecondsaredelayedinrestoringthemembrane
potential.Thisstateisknownasnegativeafterpotentialwhichhasbeen
describedtobethecauseofincreasedK
+
concentrationoutsidethe
membrane.

23. P.Deb 23
Withthedisappearanceofthenegative-afterpotential,thoughthe
restingmembranepotentialisachievedyettherestingionicstatusis
notestablished.ItisachievedbytheactiveNa
+
pumpmechanismand
Na
+
beginstocomeoutfrominsidethemembranecreatingnegativity
again.ThepositiveafterpotentialisduetothisprocessofNa
+
diffusion
frominsidetooutsidethemembrane.Thenegativityproduceddueto
activeNa
+
pumpmechanism,causestheK
+
todiffusebacktothe
interiorofthenervefibre.FortheactiveNa
+
andK
+
pumpmechanism
highenergyphosphate(ATP)isrequired.Inthiswayrestingnormal
ionicstatusisestablishedduringtheperiodofpositive-afterpotential.

24. P.Deb 24

25. P.Deb 25
PROPERTIES OF SYNAPSE
1.ONE WAY CONDUCTION (BELL-MAGENDIE LAW)
AccordingtoBell-Magendielaw,theimpulsesaretransmittedonlyinone
directioninsynapse,i.e.frompresynapticneurontopostsynaptic
neuron.
2.THESYNAPTICDELAY
Duringthetransmissionofimpulsesviathesynapse,thereisashort
delayintransmission.Itiscalledthesynapticdelay.Itisduetothetime
takenfor:
i.Releaseofneurotransmitter
ii.Movementofneurotransmitterfromaxonterminaltopostsynaptic
membrane.
iii.Actionoftheneurotransmittertoopentheionicchannelsinpost
synapticmembrane.
Thesynapticdelayisoneofthecausesforthelatentperiodofthereflex
activity.

26. P.Deb 26
3. FATIGUE
Duringcontinuousmuscularactivity,thesynapseformstheseatoffatigue
alongwiththeBetzcellspresentinthemotorareaofthefrontallobeofthe
cerebralcortex.Thefatigueatthesynapseisduetothedepletionof
neurotransmittersubstance,acetylcholine.
Depletionofacetylcholineoccursbytwofactors:
i.Soonaftertheaction,acetylcholineisdestroyedby
acetylcholinesterase.
ii.Duetocontinuousaction,newacetylcholineisnotsynthesized.
Thesetwofactorsleadstolackofacetylcholineresultinginfatigue.
4. SUMMATION
Whenmanypresynapticexcitatoryterminalsarestimulatedsimultaneously
orwhensinglepresynapticterminalisstimulatedrepeatedly,thereis
summationorfusionofeffectsinpostsynapticneuron,i.e.thereisprogressive
increaseintheexcitatorypostsynapticpotential.Itiscalledsummation.
Summationisoftwotypes:

27. P.Deb 27
i.SpatialSummation:
Itoccurswhenmanypresynapticterminalsarestimulated
simultaneously.
ii.TemporalSummation:
Itoccurswhenonepresynapticterminalisstimulatedrepeatedly.
Thus,bothspatialsummationandtemporalsummationplayan
importantroleinthefacilitationofresponse.
5. ELECTRICAL PROPERTY
TheelectricalpropertiesofsynapsearetheEPSPandIPSP.
Whenactionpotentialcausesincreasedpermeabilityofthe
postsynapticmembranetoallionsviz.,Na
+
,K
+
andCl
-
,thenitresultsin
EPSP(Excitatorypostsynapticpotential)
Whenactionpotentialcausesselectivepermeabilityofthepostsynaptic
membranetoK
+
ions,thenitresultsinIPSP(Inhibitorypostsynaptic
potential)

28. P.Deb 28
NEURO-MUSCULAR JUNCTION

29. P.Deb 29
Theskeletalmusclefibresareinnervatedbylarge,myelinnatednervefibres
thatoriginatefromlargemotorneuronsintheanteriorhornsofthespinal
cord.
Eachnerveendingmakeajunction,calledtheneuromuscularjunction,with
themusclefibrenearitsmidpoint.Theactionpotentialinitiatedinthe
musclefibrebythenervesignalstravelsinbothdirectionstowardthe
musclefibreends.
Physiologicanatomyoftheneuromuscularjunction-Themotor
endplate
Theneuromuscularjunctionformalarge,myelinatednervefibretoa
skeletalmusclefibre.Thenervefibreformsacomplexofbranchingnerve
terminalsthatinvaginateintothesurfaceofthemusclefibrebutlieoutside
themusclefibreplasmamembrane.Theentirestructureiscalledthemotor
endplate.ItiscoveredbyoneormoreSchwanncellsthatinsulateitfrom
thesurroundingsfluids.
Theinvaginatedmembraneofthemusclefibremembraneiscalledthe
synapticgutterorsynaptictrough.

30. P.Deb 30
Thespacebetweentheterminalandthefibremembraneiscalledthe
synapticspaceorsynapticcleft.Thisspaceis20-30nmwide.
Atthebottomofthegutterarenumeroussmallerfoldsofthemuscle
membranecalledsubneuralclefts,whichgreatlyincreasethesurfaceareaat
whichthesynaptictransmittercanact.
IntheaxonterminalnumerousmitochondriasupplyATPforthesynthesis
ofneurotransmitteracetylcholine.
Theacetylcholineinturnexcitesthemusclefibremembrane.Acetylcholine
issynthesizedinthecytoplasmofaxonterminalsbutareabsorbedrapidlyin
tomanysmallsynapticvesiclesabout300,000intheterminalofasingleend
plate.
Inthesynapticspacearelargequantitiesoftheenzymeacetylcholine
esterase,whichdestroysacetylcholineinafewmillisecondsafterithasbeen
releasedfromthesynapticvesicles.

31. P.Deb 31
Mechanismoftransmissionofnerveimpulseacrossthe
neuromuscularjunction
Whenanerveimpulsereachestheneuromuscularjunction,about125
vesiclesofacetylcholineisreleasedfromtheterminalsintothesynapticspace.
Ontheinsidesurfaceoftheneuralmembranearelineardensebars.Toeach
sideofeachdensebarareproteinparticlesthatpenetratetheneural
membrane,thesearevoltagegatedcalciumchannels.
Whenactionpotentialspreadsovertheterminals,thesechannelsopenand
allowcalciumionstodiffusefromthesynapticspacetotheinteriorofthe
nerveterminal.Thecalciumions,inturn,arebelievedtoexertanattractive
influenceontheacetylcholinevesicles,drawingthemtotheneuralmembrane
adjacenttothedensebars.Thevesiclesthenfusewiththeneuralmembrane
andemptytheiracetylcholineintothesynapticspacebytheprocessof
exocytosis.
Attheneckofthesubneuralcleftsthereexiststheacetylcholinereceptorsin
themusclefibremembrane.

32. P.Deb 32

33. P.Deb 33
Theseareacetylcholine-gatedionchannels,andtheyarelocatedalmost
entirelynearthemouthsofthesubneuralcleftslyingimmediatelybelow
thedensebarareas,whereacetylcholineisemptiedintothesynapticspace.
Thereceptorisaproteincomplex(MW-275,000),thecomplexis
composedoffivesubunitsproteins,twoalphaproteinsandoneeachof
beta,delta,andgammaproteins.Theseproteinmoleculespenetrateallthe
waythroughthemembrane,lyingsidebysideinacircletoformatubular
channel.
Thechannelremainsconstricteduntiltwoacetylcholinemoleculesattach
respectivelytothetwoalphasubunitproteins.Thiscausesa
conformationalchangethatopensthechannel.
Theopenedacetylcholinechannelhasadiameterof0.65nm,whichis
largeenoughtoallowtheimportantpositiveions–Na
+
,K
+
andCa
++
to
moveeasilythroughtheopening.

34. P.Deb 34

35. P.Deb 35
WhereasthenegativeionssuchasCl
-
ionscannotpassthroughbecauseof
strongnegativechargesinthemouthofthechannelthatrepelthesenegative
ions.
InpracticefarmoreNa
+
ionsmovethroughtheacetylcholinechannelsthan
anyotherionsduetotworeasons:
1.TheextracellularconcentrationofNa
+
ionsismore,and
2.Theinsideiselectronegative(-70to-90mV)whicheasilyallowstheNa
+
ionstoenterandatthesametimepreventstheeffluxoftheK
+
ionsto
outside.
Thiscreatesalocalpositivepotentialchangeinsidethemusclefiber
membrane,calledtheend-platepotential.
Inturn,thisendplatepotentialinitiatesanactionpotentialthatspreads
alongthemusclemembraneandthuscausesmusclecontraction.
Theacetylcholine,oncereleasedintothesynapticspace,continuesto
activatetheacetylcholinereceptorsaslongastheacetylcholinepersistsin
thespace.

36. P.Deb 36
Acetylcholine Receptor

37. P.Deb 37
Acetylcholineisremovedbytwomeans-
1.Mostoftheacetylcholineisdestroyedbytheacetylcholinesterase
enzymepresentinthesynapticspaceremainsattachedtothefine
connectivetissues.
2.Asmallamountofacetylcholinediffusesoutofthesynapticspaceandis
thennolongeravailabletoactonthemusclefibremembrane.

38. P.Deb 38
What is Reflex ?
Itistheinvoluntaryorautonomicresponseelicitedbyspecificstimulusof
thresholdintensitywiththeinvolvementofCNS.
ReflexArc:
Itisthepathwaythroughwhichanyreflexactionismediated.
TheComponentsofreflexarcareasfollows:
i.Receptor:Thisdetectsthechangeofinternalorexternalenvironmentand
transmitstheimpulsetocenter.
ii.Afferent(sensory)nerve-Itcarriestheimpulsefromreceptortocenter.
iii.Highercenters-ItisthepartofCNSwhereafferentlimbendsandeither
synapsesdirectlywithefferentmotorneuronorestablishconnectionwith
theefferentneuronviainterneurones.
iv.Efferent(Motor)nerve-Itcarriestheefferentimpulsesfromthecentreto
theefferentorgan.
v.Efferentorgan–Thesearebasicallymusclesorglandswhichshowsthe
reflexaction.

39. P.Deb 39
Classification of reflexes :
a.Depending on inborn or acquired : It is of two types-
i. Unconditioned reflex : These reflexes are present since birth i.e. inborn.
Example : Salivation after taking food, knee jerk etc.
ii. Conditioned reflex : These are not present from birth but acquired in later life
on the basis of past experiences through conditioning and learning.
Example : Salivation by seeing tasty food the taste of which is known.
b. Depending on the number of synapses present in the reflex arc :
It is of two types :
i.Monosynaptic reflex :
When there is only one synapse present in the reflex arc it is known as
monosynaptic
reflex. Example : Knee jerk, Ankle jerk etc.

40. P.Deb 40
ii.Polysynaptic reflex :
When more than one synapse is present in the reflex arc it is known as
polysynaptic reflex.
Example : Withdrawlreflex i.e., protective reflex e.g. automatic
withdrawlof limb if it comes in contact with hot object.
C. Physiological Classification : It is of two types :
i.Extensor reflex :
These reflexes are responsible for extensor movement of limbs at joints.
Stretch reflexes are extensor reflexes. These are responsible for muscle
tone and posture.
ii. Flexor reflexes : These are reflexes which cause flexion of the joints in
response to nociceptive(pain) stimuli. Withdrawlreflexes are the example
of flexor reflex.
D. Functional classification : are of two types-
i.Somatic reflex : It involves the somatic nervous system. Example-Knee
jerk
ii.Autonomic reflex : It involves the autonomic nervous system. Example-
Sino-aortic reflex.

41. P.Deb 41
E.ClinicalClassification:Itisoffourtypes:
i.Superficialreflexes:Theseareinitiatedbystimulatingappropriate
receptorsofskinandmucousmembrane.Theseareusuallypolysynaptic.
Example:Planterreflex,cornealreflexetc.
ii.Deepreflexes:Theseareelicitedonstrokingthetendon.Theseare
basicallystretchreflexes.Example:Kneejerk,anklejerketc.
iii.Visceralreflexes:Thesearereflexesinwhichpartofthereflexarcisformed
byautonomicnervoussystem.Example-Papillaryreflex,Carotidsinus
reflexetc.
iv.Pathologicalreflexes:Thesearenotfoundnormally.Elicitedincaseof
diseasedstate.

42. P.Deb 42

43. P.Deb 43

44. P.Deb 44

45. P.Deb 45

46. P.Deb 46

47. P.Deb 47

48. P.Deb 48
ReflexAction:
Reflexactionisaninvoluntaryeffectorresponseduetoasensorystimulus.
Itisthebasicphysiologicalunitofintegrationintheneuralactivity.
UnconditionedReflex:Unconditionedreflexesareinborn.Thenervepaths
arefixedfromtheverybirth.Anymaterialalterationisconsideredas
disease.Hence,examinationofreflexesisagreathelpinthediagnosisof
variousdiseases.
ConditionedReflex:Theconditionedreflexesareacquiredafterbirth.Such
reflexesneedpreviouslearning,training,orconditioning.Theexampleisthe
secretionofsalivabythesight,smell,thoughtorhearingofaknownedible
substance.
Cerebralcortexisresponsiblefortheestablishmentofconditionedreflexes
throughthedevelopmentofnewconnectionwithdifferentsubcortical
centres.Forestablishmentofconditionedresponseorreflexthroughspecific

49. P.Deb 49
conditionedstimuli,specificcorticalandsubcorticalcentresare
responsibleforitsdevelopment.Asforexample,fortheproductionof
conditionedsalivationreflexes,thecorticaltastecentresaswellasthe
visualandauditoryareasalongwithitssubcorticalcentresareresponsible
iftheconditionedstimulusaretheringingofbellandgivingoffood.

50. P.Deb 50
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