The document discusses learning and synaptic plasticity, emphasizing how experiences lead to changes in neural circuits and synapses, allowing for long-term memory storage. It also examines types of amnesia, specifically anterograde and retrograde amnesia, their causes, and the role of brain regions in memory encoding and retrieval. Overall, it illustrates the dynamic nature of the brain in response to experiences, as well as the complexity of memory loss conditions.

1. 1) LEARNINGAND SYNAPTICPLASTICITY
Many everydayexperiencescauseschanges,thatcanmanifestthemselvesinalteringboththe
structure and functionof neural circuits,whichare builtbyneurons,whichform pointsof contacts
witheachother,THE SYNAPSES.A givenneuroncanformthousandsof synapsesonitsdendrites,cell
bodyand axonand throughsynaptictransmission,communicateinformation withotherneuronsin
the nervoussystem.Itisat the SYNAPSESthat changesinbrainfunctionoccur throughmodification
of synaptictransmissiontermedSYNAPTICPLASTICITY-the abilityof synapsestostrengthenor
weakenovertime,inresponsetoincrease ordecrease intheiractivity. The termplasticityhasits
origininscience more than100 yearsago bythe famousSpanishscientistSANTIAGORAMON Y CJAL
,whose ideaisthatthe braincan store informationbymodifyingsynaptictransmissionswas
expressedin1894 even3 yearsbefore CHARLESSHERRINGTON introducedthe termsynapse for
connectionsbetweenneurons.ItwasalsoCAJALwhoinsistedthatsmall spinyprotrusionsof
dendrites,dendriticspines,were notanartefactbutreal and that theyhave a keyrole inmediating
synapticconnectivity.The ideaandconceptof synapticplasticitygainedprominence inthe late
1940s withpioneeringworkbythe CanadianpsychologistDONALDHEBB.He suggested thatwhen
the axonof one neuronrepeatedlyorpersistentlytakespartinfiring,some growthprocessor
metabolicchange takesplace inone orboth the cellsthatincreasesthe subsequentabilityof AXON
A TO EXCITE CELL B .Inotherwords ,SYNAPTICPLASTICITYmeansthatthe connectionsbetweenthe
nerve cellsinthe brainare not staticbut can undergochanges,theyare plastic.Italso refersto
activity-dependentchangesinthe efficacyof synapticcommunicationandhasbeenproposedtobe
criticallyinvolvedinthe remarkable capacityof the braintotranslate transientexperiencesinto
apparentlyunlimitednumberof memoriesthatcanlastfor manyyears.Eventhoughthe notionof
synapticplasticitydatesbacktothe endof 19th
century,ittook almost80 yearsbefore experimental
evidence wasobtainedtodemonstrate thatsynapsesare capable of long-lastingchangesinsynaptic
strength. It also implies directregulationof pre-synapticandpost-synapticneuronsthroughthe
alterationsof the synapticmachinery.FOREXAMPLE-Changesof the numberof neurotransmitter
receptorsinthe post-synapticmembrane.Ithasbeen foundatsynapsesthatconveyGLUTAMATE-
MEDIATE- EXCITATION.Ittakesplace at differenttime-intervals,thatis whycan be short termas
well aslong-termorlife-long.The termsNEUROPLASTICITYORBRAIN PLASTICITYOR SYNAPTIC
PLASTICITY, are used ina broadercontexttoindicate changesthatoccur throughout a personlife
eitheratthe synapse orwhole neuronso0rentire brainregion.The basicpremise isthe same,
namelythatcertainaspectsof the brainor the brain functioncanbe changedthroughoutlife,which
was notalwaystrue ,as previousstudiesof the brainsuggestedthe existence of acritical period
earlyinlife duringwhichthe brainisamenable tochangesof structure andfunctionwouldremain
unchangeable thereafter. Likewise, synapses were consideredassimplerelaystationsfor
informationtransferfromone neurontoanother, whichwere thoughttobe establishedduring
developmentandtoremaininplace throughoutlife witharelatively fixedsynapticstrengthof the
connection.Plasticityisnowknowntobe an intrinsicpropertyof the brainsuchthat itis notlimited
by itsowngenome butcan adapt to external stressors,physiological alterationsandpersons
experiences.While SYNAPTICPLASTICITYisa keyconceptinitself forbrainfunctionanddysfunction,
it hasbecome central to our understandingof the mechanismsof learning.Synaptic plasticity is
intimatelyrelatedtolearningandmemoriesbecause memoriesare thoughttobe representedby
neural networksthatare connectedat synapses. As mentioned earlier,the HEBBIAN THEORY,
whichproposesanexplanationforneuronal adaptationduringthe learningprocessandis
consideredabasicmechanismforsynapticplasticity.He postulatedthatcoincidentactivityof
synaptically connectedneuronsleadstolastingchangesinthe efficacyof synaptictransmissions.
Experimentalevidence support this hypothesisbydemonstratingthatmodifiable synapsesexist

2. inthe brainand formthe basisof learningandmemory. Underconditionswhenapresynaptic
neuronrepeatedlyandpersistentlystimulatesapost-synapticneuron,thatiswhenboththe
neuronsare active,synapticconnectionsare modifiable intheirefficacy.One importanttheoryof
HEBBs THEORY relatestothe exacttimingof activityof activityof the presynapticneuroninrelation
to postsynapticactivity. The studyof SYNAPTICPLASTICITYincludes-
1)LONG TERM POTENTION(LTP)
2)LONG TERM DEPRESSION(LTD),asthese phenomenaare the basisof certaintypesof LEARNING
ANDMEMORY. LTP basicallyreferstothe strengtheningof synapses,lastingforhoursandperhaps
daysthat is inducedbythe synchronousandrepeatedactivationof manysynapses,whereasLTDis
the reverse of LTP and occurs whenindividualsynapses are activatedinisolation,responses get
smallerandstaythat way fora longtime. Ithas alsobeensaidthatthe effectivenessof particular
synapsescanthus be turnedupor down,throughsuccessive episodesof LTPAND LTD. These
phenomenaare knowntooccur inmany areasof the brain,but are most usuallystudiedina
particularregionknownasthe hippocampus,whichare frequentlyusedinthe investigationsof
LTP/LTD because the simple circuitryof the hippocampuspermitsactivationof uniformpopulation
of synapses.Until recentlythe analysisof MUTANTMICE lackingproteinsthatare clearlyimplicated
insynapticplasticityhassimilarlyshownagoodcorrelationbetweenthe extentof LTP/LTD
deficiencyandthe severityof behavioural impairmentinhippocampus-dependenttasks,including
SPATIALLEARNING.ELECTROPHYSIOLOGICAL RECORDINGSinhippocampal slicesobtainedfrom
PKA-mutantmice showspecificdefectsinLTP/LTDat a numberof synapticregions.WithLTP at
mossyfibre synapsesandLTD at the dentate regionsstronglyimpaired,andwithan additional
deficits inthe late phase of LTP forone of the mutants,the expectation,onthe basisof previous
knockoutmouse studiesisthatthese animalswouldperformpoorlyinspatial memorytasks,
howeverthe mutantmice exhibitnodefectintwodifferenttestsforspatial learning.Moreover,
CONDITIONING,anotherformof learningthatispartiallydependentonthe hippocampusisalso
unaffected.The mutantmice displaydeficiencyin at least one of the formsof synapticplasticity
at variouspointsinthe hippocampal circuitry , yettheyperformnormallyinhippocampus-
dependentlearningtasks.The PKA – mutantmice provides a conspicuousexceptiontothe no
LTP POOR LEARNINGPATTERN of the resultsseensofar. The studiesmentionedabovehave
weakenedthe correlationbetweenthe brainsabilitytoexhibitLTP/LTDandthe animalsspatial
learning.AlthoughLTP/LTDhave the rightpropertiesforlearningmechanisms,obviouslythisdoes
not meanthat these formsof synapticplasticityare indeedusedformemorystorage,evenif we
could showpreciselythatsome type of learningiseliminatedwhenNMDA receptorsare blocked.
For Example-modificationof hippocampal circuitsmightbe requiredforsome kindof learningto
occur-the circuitsmightnotbe tunedupto workwell fora particularsession-butthe memories
mightnot have to be actuallyrepresentedinthe spatial patternof synapticstrengths.
2)BRAIN ANDAMNESIA
Amnesiaisthe general termfora conditioninwhich memory (eitherstoredmemoriesorthe process
of committingsomethingtomemory) isdisturbedorlost,toa greaterextentthansimple everyday
forgettingorabsent-mindedness.Itmayresulteitherfromorganicor neurological causes(damage
to the brainthrough physical injury,orthe use of some drugs) or fromfunctional orpsychogenic
causes,suchas stressor anyof the disorder.There are 2 maintypesof amnesia:
1)ANTEROGADEAMNESIA,definedasthe lossof the abilityto CREATE NEW MEMORIES, leadingtoa
partial or complete inabilitytorecall the recent past , eventhoughlong-termmemoriesfrom
before the eventwhichcausedthe amnesiatoremainintact.Anterograde amnesiamaybe DRUG

3. INDUCED (several BENZODIAPHINESare knowntohave powerfulamnesiceffects) oritmayfollowa
traumaticbrain injuryorsurgeryinwhichthere isdamage to the HIPPOCAMPUSOR MEDIAL
TEMPORAL LOBE of the brainor an acute eventsuchas a concussion,a heartattack or an epileptic
attack, lesscommonlycausedbyanemotional disorder.Researchshowsthatthistype of amnesia
resultsfroma failure of MEMORY ENCODINGandstorage.More specificallyinnormal use,neurons
inthe mammillarybodiesof the HYPOTHALAMUSmake connectionswiththe THALAMUS,whichin
turn make connectionswiththe cortex of the brain,where longtermmemoriesare stored.It
therefore,canresultfromdamage tothe HYPOTHALAMUS and THALAMUS andTHE SURROUNDING
CORTICALSTRUCTURES, sothat encodedmemoriesare neverstoredsince connectionsbetween
HIPPOCAMPUSandCORTEX are developed.Sufferersfromanterograde amnesiausuallyonlylose
DECLARATIVFEMEMORY, buttheyretainnon-declarative orprocedural memory.
2)RETROGRADE AMNESIA
A formof amnesiawhere someone isunabletorecall eventsthatoccurredbefore the development
of amnesia,eventhoughtheymaybe able to encode andmemorize new thingsthatoccurafter the
onset.Itusuallyfollowsdamage toareasof the brainotherthan the HIPPOCAMPUS,because
alreadyexisting long-term memoriesare storedinthe neuronsandthe synapsesof various
differentbrainregions.FOREXAMPLE- Damage toBROCASAREA OF THE BRAIN,whichare
specificallylinkedtospeechproductionandlanguage formation,wouldprobablycause language-
relatedmemoryloss.Itusuallyresultsfromdamage tothe brainregionsmostcloselyassociated
withDECLARATIVEANDPARTICULARLYEPISODIC MEMORY, such as the TEMPORAL LOBE AND THE
PREFRONTALCORTEX. Thistype of amnesiaisoftentemporallygraded,meaningthatremote
memoriesare more easilyaccessiblethaneventsoccurringjustpriortothe trauma andthe events
nearestintime tothe eventthatcausedthe memory lossmayneverbe recovered.Thisisbecause
the neural pathwaysof newermemoriesare notas strongas olderonesthathave been
strengthenedbyyears of retrievalandre-consolidation.Sometimes boththese typesof amnesia
may occur together,sometimescalledGLOBALAMNESIA.Anothertype of amnesiaisPOST-
TRAUMATIC AMNESIA,a state of confusionandmemory lossthatoccurs aftera TRAUMATIC BRAIN
INJURY.Amnesiawhichoccursdue to psychological factorsisreferredtoasPSYCHOGENICAMNESIA,
alsoknownas FUNCTIONALAMNESIA ORDISSOCIATIVEAMNESIA,isadisordercharacterisedby
abnormal memoryfunctioninginthe absence of structural braindamage ora knownneurobiological
cause,whichresultsfromthe effectsof severe stressorpsychological traumaonthe brain,rather
than fromany physical orphysiological cause .Manykindsof amnesiaare associatedwithdamage to
the HIPPOCAMPUSANDRELATED AREASOF THE BRAIN whichare usedinencoding,storage and
retrieval of memories.
The usual CAUSESof amnesiaare BRAIN LESIONSto the brainfrom an accidentor neurological
disease, butintensestress,alcohol abuse,blood flow canall cause amnesia.Inmostcases,amnesia
isa TEMPORARY CONDITION,lastingfromafew secondstofew hours,butthe durationcan be
longerdependingonthe severityof the disease ortrauma,upto a few weeksorevenmonths.
REFRENCES
1)HebbDO. The Organisationof Behaviour:A Neuropsychological Theory.New York:Psychological
Press;2005
2)Carlson.N.R(2005) Foundations of Physiological Psychology,Boston.M.RPearson Education. Inc

4. 3)Kalat.J.W(2009) Biological Psychology,Belmont-C.AWadsworth.CengageLearning