Behavioural neuroscience Flashcards
what is phrenology
physical functions can be localized to different areas of cortex
so the brain is like a muscle - bits you use more get bigger and stronger
history of neuropsychology
gall 1800 first attempts to bring together biological and physiological concepts in the study of behaviour
alot of this is now very outdated
what is the aggregate field hypothesis
flourens 1850s
removed gall’s phrenological centres
concluded any part of the cerebral hemisphere could perform any higher function
why was the aggregate field hypothesis a popular theory
went against the reductionist idea that the human mind has biological basis
so was pro religion
how and who refined the aggregate field hypothesis
mass action
karl lashley 1900
size of brain lesion defines deficit not location
key concept behind distributed processing
individual areas of the brain perform specific functions but complex cognitive function involves interactions of many brian areas
ideas / evidence behind distributed processing - whats special about how they studied
Brocca - 8 patients with similar brain lesions who could not produce speech
wernicke - described patients with an inability to comprehend language
both studied patients deficits whilst alive then disected the brain once dead to find specific areas
the neuron doctrined
who and what
camillo golgi and santigo ramon y cajal
the neuron is the signalling unit of the brain
what is cellular connectivity
the idea neurons are organised into functional groups which are interconnected by specific neural pathways
what makes up a neuron
think of picture soma - cell body dendrities off the cell body axon inside the myelin sheath terminal buttons
in which direction does information travel around a neuron
from the dendrites on the soma to the terminal buttons
how are proteins moved around the neuron
vesicles walk proteins along microtubules
what are the threetypes of neurons
multipolar and biopolar and unipolar neurons
what are multipolar neurons
the most common type
soma, axon, terminal buttons
what are bipolar neurons
receptor on the dendrite - cilia are sensitive to physical stimuli
soma is then halfway along the axon
terminal buttons at the end carrying information towards the brain
where are bipolar neurons usually found
in sensory systems
what are unipolar neurons
many dendrites sensitive to physical stimuli
soma is separately attached halfway along the axon
terminal buttons carrying information towards the brain
where are unipolar neurons usually found
in the somatosensory system (warmth, pain etc)
how do neurons communicate with each other
action potentials
what is the resting potential of neurons and why (membrane potential)
-70mV
the force of diffusion vs
the force of electrostatic pressure (charges repelling)
the resting potential is due to a difference in the concentration of positively charged ions inside the neuron relative to the outside of the neuron
what are action potentials
a brief electrical impulse that provides the basis for conduction along an axon
what chemicals are usually intra and extra cellular
intra - A- (anions) and K+
extra - Cl- and Na+
where are axon potentials generated
in the cell body
what are the 6 steps to an action potential
1 Na+ channels open and Na+ begins to enter cell
2 K+ channels open, K+ begins to leave the cell
3 Na+ channels become refractory, no more Na+ enters the cell
4 K+ continues to leave the cell, causes membrane potential to return to resting level
5 K+ channel closes, Na+ channel resets
6 Extra K+ outside diffuses away
try put with diagram where 3 is the height of the action potential
what happens to action potentials as they are propogated down the cell
they don not change size
they are continually regenerated by ion channels along the axon
how is the resting potential restored after and action potential
by voltage dependent potassium channels
consequence of action potentials in terms of speed and energy
using ion channels to generate action potential is slow and uses energy
signal travels faster down insulated axons but it reduces in size and so needs to regenerate periodically
how are action potentials regenerated
saltatory action
action potentials are regenerated at nodes of ranvier - the gaps between the myelin sheaths
how much if the CNS do neurons make up
half the volume of the cns
what makes up the other half of the volums of the cns if not neurons
glia cells - supporting cells
3 main types of glia cells
oligodendrocytes
astrocytes
microgli
what do oligodendrocytes do
provide support from neurons and produce myelin
what do astrocytes do
housekeeping duties, support and insulation
provide energy in the form of lactate
small quantity of energy stored as glycogen
removal of dead tissue through phagocytosis
(these are the most well studied)
what do microglia do
inflammatroy response to infection and removal of dead tissue
what are the two ways we measure communication between neurons
electrically - neurophysiology
- branch of physiology that deals with the flow of ions in brain tissue and the measurement of that flow
chemically - microdialysis
- allows measurement of levels of chemicals (glucose, neurotransmitters) in the brain
how does microdialysis work
same way as standard dislyss
probe implanted into the brain (so only really possible to carry out on animals)
fluid pumped through inner cannula
neuro transmitters from extracellular fluid diffuse into dialysis tubing \we can measure this fluid and detect the changes
problem with microdialysis
takes a long time
if interested in cognition where we need measurements in millisecond intervals this is a problem
4 types of electrophysiology
electroencephalogram - EEG
single cell recording
multi-cell recording
intracellular
advantages of EEG
non invasive so can use in humans
high temporal resolution
disadvantages with EEG
low spatial resolution
only record from the cortex
example of the use of EEG
medically study sleep and pinpoint the focus of seizure activity in epilepsy
what is multi cell recording
used to record groups of neurons
record brain rhythms (local field potential LFP)
think of it like a crowd at a concert
if the crowd sings together then the song is recogniseable
so if neurons fire together this produces waves of activity that can be detected in other areas of the brain - co-ordinate different brain areas
advantages of multi-cell recording
ok spatial resolution (groups of neurons)
ok temporal resolution (brain rhythms)
disadvantages of multi-cell recording
only records groups of neurons
is invasive
example of how multi-cell recording can be used
in rats
memory and attention networks coordinate when rats use memory to make a decision
advantages of single-cell recording
very high spatial resilution (multiple single neurons)
high temporal resolution (action potentials!)
disadvantages to single-cell recording
extracellular recording (no knowledge of intracellular events) invasive
advantages of intracellular recording
very high spatial resolution (specific neuron)
examine sub-cellular processes
disadvantages of intracellular recorgind
only one cell at a time
only in anaesthesised animals
example of use of intracellular recording
allowed us to understand how action potentials worked
if action potentials are always the same size, how do neurons communicate with one another
- frequency is important and not size. stronger stimulus = more action potentials
where and how do neurons communicate
across synapses
neurotransmitters are released from the pre-synaptic membrane of the terminal button
entry of calcium opens fusion pores
pores widens, membrane of synaptic vesicle fuses with presynaptic membrane
molecules of neurotransmitter leave terminal button
where do neurotransmitters ac on post-synaptic receptors
on the dendrites
what are the two main types of receptor for neurotransmitters acting on post-synaptic receptors
ionotropic
metabotropic
how ionotropic receptors work
they transmit information quickly
relatively simple mechanism
how do metabotropic receptros work
slow acting and long lasting
complex mechanism
what are the two types of neurotransmitter
excitatory
inhibitory
how excitatory neurotransmitters work
causes depolarisation - produces actionpotentials
alos known as excitatory posy-synaptic potential
eg glutamate
how inhibitory neurotrasnmitters work
causes hyperpolarisation - stops action potentials being generated
also know as an inhibitory post-synaptic potential
eg GABA
what causes inhibition or excitation at the post-synaptic membrane
not the neurotransmitter!
the ion channel the neurotransmitter opens
which ion channels opening causes depolarization (excitation)
na+
which ion channel opening causes hyperpolirisation (inhibition)
K+ = efflux so goin out of the cell Cl- = influx so going into the cell
what is neural integration
all the time our neurons are procesing lots of information
enough excitation over threshold = action potential down axon
whilst still some residual excitation, next signal is inhibitory do no action potential
so neurons integrate excitation vs inhibition
IPSPs counteract EPSPs so action potential is not triggered in axon
what are the two theories of how neurons work tigetherq
referendum style - point neuron hypothesis
one synapse one vote
each synapse has equal weighting in a neuron. neurons will fire if ecitatroy input is greater than inhibiroty
OR
general election style
two compartment hypothesis
neurons split into 2 funcitnoal compartments
1 - soma, basal dendrites, axon
2 - apical dendrite tree
sum of inputs from apical dendrites passed onto soma
(More compartments?)
psychopharmacology - definition
the study of the effects of drugs on the nervous system and behaviour
uses of psychopharmacology
medicine
illegal drugs trade\cognitive enhancers
tool to study the mechanisms by which the brain controls psychological function
tool to study the mechanisms by which the brain controls psychological functions
agonist definition
a drug that facilitates the effects of a particular neurotransmitter on the postsynaptic cell
antagonist
a drug that inhibits the effects of a particular neurotransmitter on the postsynaptic cell
what is special about apomorphine
can be either an antagonist or an agonist depending on the dosage (relates to dopamine production)
glutamate and gamma-aminobutyric acid
most common neurotransmitter in the brain
nearly all neurons recieve inputs from GABA
what are the 4 types of glutamate receptor
NMDA
kainate
AMPA
metabotropic glutamate
what are the two types of GABA receptor
GABA little A (ionotropic)
GABA little B (metabotropic)
where are the signals usualy from in neural integration
glutamate and GABA inputs
what do other (not GABA and glutamate) neurotransmitter systems do
also produce action potentials in postsynaptic cells
neuromodulatorye effects
can increase or decrease the likelihood of glutamte or GABA release producing an action potential in the postsynaptic cell
Acetylcholine (ACh)
two types of ACh receptor: nicotinic (ionotropic) and muscarinic (metabotropic)
nicotinic receptors found in the brain responsible for nicotine addiction
also found in the muscles - these are blocked by botox injections
muscarinic cholinergic receptors found only in the brain
what are the three main systems of ACh (no explanation)
dorsolateral pons
basal forebrain
medial septum
dorsolateral pons system and ACh
traditionally associated with sleep
recently shown to play a role in higher cognitive functions like learning - rats with cholinergic lesions of the dorsolateral pons cannot learn the association between reward and location
basal forebrain system and ACh
provides large input to the cortex and has a role in learning and attention
historically studied as this area degrades in alzheimers. most treatments still try to fix the imbalance of ACh
medial septum system and ACh
involved in learning and memory
controls rhythsm in the LFP in the forebrain
lesions of the medial septum get rid of the LFP rhythm in the hippocampus
information about the dopamine system
catecholamine along with noradrenalin
at least 5 receptor sub types (D1-5) which are all metabotropic
3 major dopaminergic systems in the brain
nigrostriatal
mesolimbic mesocortical
path of nigrostriatal dopaminergic system in the brain
substanti nigra
caudate nucleus/ putamen
contorls action selection and coordinated movement
path of mesolimbic dopaminergic system in the brain
ventral tegmental area
nucleus accumbens
processing of reward
path of mesocortical dopaminergic system in the brain
ventral tegmentl area
prefrontal cortex
short term memory and planning
how have the role of mesolimbic dopamine system in behaviour signals been studied
using single-cell recording
dopaminergic neurons respond to the reward (primary reinforcer) during learning but this decreases as the animal learns the task
when the task is well learned the dopamine neurons respond to the cue (secondary reinforcer)
noradrenergic system
catecholamine (also called neuroepinephrine
4 types of receptors alpha 1 and 2, beta one and 2, all metabotropic
most important noradrenergic system originates in the locus coeruleus - involved in vigilance and attentiveness
serotinergic system
indolamine
at least 9 receptor subtypes - most are met\botropic
most important serotinergic system originates in the raphe nuclei of the midbrain and pons
functions are complex; regulation of mood, eating, sleeping and pain
what is neuromodulation
many of the systems all originate in relatively small nuclei in the brainstem and midbrain
they all send projection over the forebrain
activztion of these small areas of the brain can then have large impacts on the rest of the brain
are neurotransmitter systems independent and example
no
hippocampus
neurons predominantly use glutamate and GABA to transmit info
hippocampal neurons also modulate ACh and dopamine
to fully understand the function of the hippocampus the combined actions of these systems must be studied
rats learning food locations trial
rats can learn new food locations in the map in one trial
they spend more time digging in the correct locatin
these new memories are dependent on glutamate activity in the hippocampuse
we know this as when glutamate activity is blocked with pharmocology, they do not remeber the location of the food
block dopamine in the hippocampus you get similar effects
shows the interaction between neurotransmitter systems
sleep in the animal kingdom
sleep is seen throughout the animal kingdom
variation in sleep patterns
dolphin’s adaptation to sleep
bottlenose dolphins - sleep one hemisphere at a time
indus dolphins - never stop swimming but still sleep in brief 4-60s naps
sleep in humans
amount of sleep needed changes with age
no adapttion to sleep deprivation
very different to unconsciousness (coma / anaesthetic)
how the stages of sleep in humans work
awake = little alpha and beta
stage 1 = a little theta activity
stage 2 = k complex and sleep spindle
stage 3 = delta activity
stage 4 = loads of delta activity = slow wave sleep
REM sleep = theta activity and beta activity
REM vs slow wave sleep
REM is characterised by EEG desynchrony, lack of muscle tone (paralysis), and rapid eye movement
SWS is characterised by EEG synchrony, moderate muscle tone and absence of eye movement
sleep cycle
awake,1,2,3,4,3,2,1,REM,1,2,3,4… etc
disorders of sleep general information
affects 25% of the population (9% regularly)
self report is extremely unreliable
pharmalogical treatments
sleep apnea
stop breathing whilst asleep
treated surgically or by wearing pressurised breathing apparatus
can cause permanent damage
narcolepsy
primary symptom = sleep attack cataplexy = brief conscious paralysis sleep paralysis hypnagogic hallucinations genetic component causes loss of hypocretin / orexin neurons treated with modanfinil
REM sleep disorder
paralysis that normally appears during REM sleep is not present - people act out their dreams
genetic disorder involving accumulation of alpha synuclein in neurons
treated with benzodiazepine
name some disorders of slow wave sleep
sleep walking
bedwetting
night terrors
all associated with childhood and usually diminish with age
sleep eating disorder?? thought to be induced by sleeping medication so treatments involve refining this medication
how are levels or arousal controlleed
by a collection of modulatinf neurotransmitter systems usually in the brainstem eg ACh noradrenalin serotonin histamine orexin
where is histamine found
hypothalamus
when are noradrenalin neurons active
during waking
not active during sleep`
when are serotonin neurons active
active during waking hours and less active during sleep
when are orexinergic neurons active
active during waking and not during sleep
what is the flip-flop switch
switch of mutual inhibtion between ventrolateral preoptic area and the arousal systems (ACh, noradrenalin, serotonin, histamine)
control of REM sleep
second flip-flop switch to turn on REM
REM-on cells (ACh) found in sublaterdoesal nucleus in the dorsal pons
REM-off cells found in the ventrolateral periaqueductal gray matter
the REM off neurons get input from arousal system keep them active
REM-off neurons become gradually less active as the excitation from the arousal system deceases
when the off cells become less active the switch flips and the ACh REM-on neurons become active
what does sleep deprivation do
mainly affects cognitive abilities
we do not make up lost sleeo
following deprivation SWS and REM dominate
Rechtschaffen and Bergmann 1995 - sleep deprivation in rats what did they find
metabolic rate in sleep deprived rats increase to between 210-270% of normal levels
weigh loss despite increased food intake
inability to thermoregulate (excessive heat loss)
death after 2-3 weeks
function of SWS
reduced metabolic rate and blood flow rely on rest?
most active regions during waking show highest delta wave activity during SWS
cortex shuts down
protect free radicals and oxidative stress
what happens during sleep to protect the brain`
sleep drives metabolite clearance from the adult brain
what penetrates much further into the brain during sleep - why
CSF
toxic chemicals such as amalyoid beta are removed quicker during sleep
function of REM sleep
is seen the most in most active phases of brain development
more prevalent in new born animals with less well developed brains than animals born with well developed brains
if merely development related why do we see it in adults
learning and memory?
what is declarative memory
memory that can be consciously recalled
what is non-declaritive memory
automatic learning not under conscious control (eg riding a bike)
mednick et all 2003 - what was their sleep experiment
is sleep important for non-declarative memory
found REM sleep facilitates perceptual leraning
tucker et al 2006 - what was their sleep experiment
paired associate task - declaritive memory
SWS facilitates declarative learning
what are the mechanisms during sleep that improve memory
place cells
name the four types of biological rhythms
ultradian
circadian
infradian
circannual
ultradian rhythms
multiple cycles within a 24hr period eg appetite
circadian rhythms
24 hr cycles eg sleep-wake
infradian rhythsm
longer than 24hr eg menstruation
circannual rhythm
year long cycle eg hibernation
control of circadian rhythms
suprachiasmatic nucleus - lesions here disrupt the timing of sleep but quality is unchanged
recieves input from the retina
melanopsin containing ganglion cells are sensitive to light and connect the retina to the SCN
SCN projects indirectly to the VLPA and the orexin neurons of the lateral hypothalamus
what neurons have an internal mechanism that allows them to keep track of time
how do we know this
SCN
cells raised in culture have 24hr cycles of activity but they are offset from each other - ie are not in time
rhtyms are controlled by…
at least 7 proteins
pulses of light can reset the protein levels
how are infradian rhythms controlled in mammals
pineal galdn secrets melatonin
melatonin is secreted at night - longer nights mean higher melatonin levels = winter cycles
also some role in circadian (jet lag cure) and seasonal affective disorder
name 6 neurodegenerative disorders
parkinsons alzheumers huntingtons amyotrophic lateral sclerosis multiple sclerosis neurological disorders
parkinsons disease - why, how many effected
loss of dopamine neurons from the midbrain relatively common (2-3% of pop over 65, 3-4% over 85
parkinsons symptoms
muscle rigidity akinesia - inability to initiate movement bradykinesia - slowness of movment resting tremor cognitive deficits?
pathology of parkinsons
loss of the substantia nigra pars compacta
symptoms do not occur till 70% of DA neurons are loss
more loss from putamen than caudate nucleus
presence of lewy bodies in the cytoplasn of neurons = an index of neurodegeneration
what causes the symptoms of parkinsons
by excessive inhibitory activity in the basal ganglia
treatment for parkinsons and side effects
- also mention the experimental treatments
4 in total
L-DOPA = dopamine precursor
dopamine agonists to increase dopamine acticity
side effects
tardive dyskinesia (uncontrolled movements)
becomes less effective with time as it is not treating the cause and dopamine neurons are still being lost
OR
replace lost dopamine cells
-surgical implantation of fetal dopamine tissue
-stem cells
some positive results but also made some patients much worse so treatment no longer used
OR
lesion in global pallidus (internal segmentum)
OR
deep brain stimulation
OR potential for gene therapy as 5% of cases have a genetic cause
alzhiemer’s what is it characterised by and how many effected
characterised in its late stages by a general cognitive decline including deficits in memory, attention,language and spatial orientation
10% of pop over 65
50% of pop over 85
brain degeneration in alzheimers
starts with degeneration in the enthorhinal cortex but damage spreads through the hippocampus, neocortex into the modulatory system of the midbrain and pons
what are the biological makers of alzheimers
extracellular plaques made from the accumulation of the 40/42 amino acid beta-amyloid peptide
intracellular accumulation of neurofibrillary tangles mades from hyperphosphorrylated tau
treatment for alzheimers disease
drug therapy (ACh inhibitors, NMDA receptor antagonist memantine) these do nothing to treat the cause at least some cases are genetic (eg mutation in the presenilin gene results in AB production) most cases do not have an obvious genetic cause vaccination against AB protein
decrease in AB correlated with ….
how does this relate to vaccines
correlated with slowing dementia
further studies have shown AB can be reduced by immunisation
but this isnt correlated with slowing dementia so makes the role of AB unclear
huntingtons disease
background
who / how many
entirely hereditary
results from single genome on chromosome 4 which causes a protein called huntingtin (htt) to be produced
critical feature is a segment of repeated glutamine within the protein
affects the basal ganglia
symptoms include congitive deficits and uncontrollable movements
approx 5,000 people in the uk
key bio features of huntingtons
inclusion bodies (accumulation of htt)
role of these inclusion bodies is debated
could be neuroprotective
what is amyotrophic lateral sclerosis also known as
motor neuron disorder
motor neurons disorder
- what
- death
- treatment
progressive disorder attacking the spinal and cranial nerve motor neurons
no cognitive decline
death usually occurs after 5-10 years after onset as a result of respiratory muscle failure
no effective treatments
riluzole used to reduce glutamate neurotxicity but this only extends life by a few months
multilpe sclerosis
autoimmune demyelination
damage occurs in white matter located throughout the brain and spinal cord resulting in a variety of disorders
patients may suffer discrete attacks or a more progressive decline
life expectancy is reduce by 5-10 years
what causes tumors
uncontrolled and non-functional cell division
how do tumors cause damage
compression and infiltration
how are tumors treated
surgery and focused radiation
meningioma and glioma
which are malignant and which are benign
men - benign
glioma - malignant
two types of cerebrovascular accidents and what are they
hemorrhagic stroke - burst blood vessel
obstructive stroke - blood vessel blocked
how do cerebrovascular accidents cause damage
very quick depletion of oxygen and glucose
ion transporters disrupted and cells become depolarised
glutamate is produced producing a cycle of excitation and cells die through excessive sodium and calcium within the cell
damaged mitochondria then produce free radicals which are extremely toxic (attack proteins and DNA)
how are strokes treated
with drugs aimed at dissolving blockages
quick diagram to explain short vs long term memory
sensory info leads to short term memory leads to (this line is called consolidation), loop from here back to short term memory which is called rehersal long term memory
how could you define short term memory in terms of long term memory
short term memory (also called working memory) is the gateway for information to enter long term memory
explain the long term memory systems
long term memory declaritive vs non-declaritive inside declaritive episodic and semantic inside non-declaritive procedural (skill), priming and perceptual learning, non-associative learning, classical conditioning
what is priming
improvement in identifying or processing a stimulus as a result of its having been observed previously
priming increase the probability of choosing previously presented words for example
classical condition as part of memory
previously neutral stimuli (CS) is paired with a positive or negative stimulus (US) that produces a response (UR)
in subsequent trials the CS can illict a conditioned response which is very similar to the UR in the absence of the US
what is non-associative learning
learning that does not involve the association of two stimuli to illicit behavioural response
habituation - decrease in level of response through repeated exposure to a stimulu
sensitisation - increase in level of response through repeated exposure to a stimulus
two types of declaritive memory explained
sematic - memory for facts
episodic - memory for events
why is studying episodic memory important?
first symptom of mild cognitive impairment which often preceeds alzheimers
have a;sp recently been described in huntingtons following chemo and after ECT for depression
to understand the mechanisms underlying these disorders we need to understand the neural circuitry that supports episodic memory
hippocapus involved - we know because of HM
hippocampus is critical for….
episodic memory in humans
what is the big question surrounding episodic memory
-why does it matter
do animals have it
if they do then we can test new treatments for the early stages of AD
definition of episodic memory
receives and stores information about temporally dated episodes or events and the temporal-spatial relations among these events - tulving (what, where, when)
then autonoetic conscious later got added to this definition
example of episodic type memory in animals
scrub jays chose the worms when they are fresh but know they will be bad if return too long later so instead go for the other food
so the scrub jays can do what where and when
why are birds not a good model for neuroscience
brains are quite different from mammalian brains - hard to use homologous approach
very little known about their brains and behaviour (although this is changing)
good to study convergent evolution of psychological processes
do rats have episodic-like memory
they can do where but not when
how much do we use actual time
context?
what where and which might be more appropriate
lesions in rats show
hippocampus is vital for episodic type memory
what are the cellular mechanisms for memory consolidation
synaptic plasticity
learning must involve chmages in synaptic function
for long-term memory these changes must be long lasting
LTP
chemistry of short term LTP
dependent on NMDA receptors which allow Ca2+ ions into the cells once activated
these ions set in motion a cascade of reactions that result in more AMPA receptors being inserted into the postsynaptic membrane
more AMPA recpetors result in a stronger response to stimulation from the preseynaptic cell
synapse strenghten for a few hours - short term LTP
chemisty of long lasting LTP
requires proteins to stabilise short term chages already produced
these are captured by tags that are set at the releant synapse
for long lasting memory we need long lasting…
and explain
LTP
for this we need
short term LTP (insertion of AMPA receptors into postsynaptic membrane)
a chemical tag at the synapse to attract proteins
proteins to stabilise the changes induced in short term LTP
what is hebbs law
cells that fire together wire together
spatial memory is part of what type of memory
episodic
what did edward c tolman 1948 discover
first to suggest that rodent and humans have a cgonitive map of familiar enviornments
contemporary learning theory accounts held that navigation was completed by rule learning
during active navigation which brain area in rats showed inreased activation
right hippocampus
does the structure of the hippocampus change with navigational experience / expertise
maguire et al 2006
posterior hippocampus size in humans is larger in london taxi drivers than control subjects
posterior hippocampus volume correlates with years of taxi driving experience
increase not seen in bus drivers
how can spatial and navigational memory be tested in rats
the morris watermaze - big pool of water with a submerged platform the rats cant see
first rats swims till he finds the platform
pretty quickly rat learns to swim straight to the platform
hippocampal damage imparis what in rats
also how does this relate to experiment
spatial memory
the rats do learn where the platform is
just start slow and never get as good as control rats
they learn a rule eg go 20cm from wall and swim in a circke until they can find the platform
how does the brain make sure we don’t get lost
neurons in rat hippocampus fier when the rat is in a specific location = place cells
we know this from single cell recording
so map of your environment
are place cells responsible for spatial memory, navigation or both
each place cell recieves two different inputs
1 environment
2 navigtional system (grid cells?)
what are the inputs to hippocampus
medial entorhinal cortex (MEC) and lateral entrohinal cortex (LEC) feed into hippocampus (place cells)
is there spatial firing in medial entorhinal cortex (MEC)
not compared to place cells who fire in such a specific place
but in grid cells in MEC there are bursts of activity in lots of different places - if you look at these places they form a hexagonal grid
so one single cell can calculate perfect geometry + knows where rat is
arguments against spatial firing in medial entorhinal cortex
data is just correlational
lesions of dorsolateral band of the MEC were most grid cells does produce spatial maemory and navigational deficits but they didnt just remove grid cells, other cells were removed too
directional coding in medial entrohinal cortex
fired depending on direction rat head is facing
one cel fired when always facing the same direction
compass + sense of heading
what are the spatial memory and navigation systems
head direction cells tell us which way we are facing
grid cells tell us how far we have travelled and speed we have travelled - path integration
place cells keep the mao stable by providing landmarks
the hippocampal network keeps track of spatial location relative to landmarks - allocentric memory
schizophrenia
background
1% of pop will experience at least one major schizophrenic episode in their life
positive and negative cognitive symptoms
men and women equally affected but onset usually slightly later for women
early onset
twin studies show there is a genetic component
who first described schizophrenia and how did they describe it
Kraeplin 1887
dementia paradox
bleuler first used term schizophrenia and recognised positive and negative symptoms
history of treatment of schizophrenia
up to 1950s - insulin coma, frontal lobotomy or shock therapy
1952 - laborit discovers first drug therapy - dopamine antagonist
what is the dopamine hypothesis
D2 and D3 receptor antagonist greatly reduce the positive symptoms dopamine agonists (cocaine, amphetamine, L-DOPA etc) can produce psychotic symptoms of schizophrenia so is dopaminergic activity increased in schizophrenic patients
what did Laruelle et al 1996 discover in relation to the dopamine hypothesis
dopamine release in striatum in response to amphetamine greater in schizophrenics
brain abnormalitites in schizophrenia
ventricles are enlarged
reduced cerebral gray matter
dramatic loss of cortical gray matter in adolesence
hypofrontality (leads to decrease in NMDA and dopamine in prefrontal cortex, explains the dopamine hypothesis)
problem for drug therapy of schizophrenics
dopamine levels are decreased in the prefrontal cortex
dopamine levels are increase in the midbrain
how can we get dopamine in one area and decrease it in another
= partial agonists
what do atypical antischizophrenic drugs do
reduce dopamine in nucleus accumbens and increase dopamine in prefrontal cortex
are partial agonists
affective disorders
background
3% of males + 7% of females effected by depression
bipolar
unipolar
28.8 times more likely to commit suicide
some genetic basis although not a single gene is implicated
gene for the serotnin transporter is likely to be involved
what is the thought genetic basis of depression
short allels for the serotonin transporter gene increase risk of depression
but
only in individuals who have suffered stressful life event
interaction of genetics and environment
brain abnormalities in depression
reduced volume of amygdala and subgenual anterior cingulate cortex with one or two short alleles of the serotonin transporter gene
decreased activity in subgenual prefrontal cortex associated with depression
amygdala
-usually processes fear and anger then is reset after fearful stimuli
-this inhibition if less prominent in depressed patients
drugs (and theories those drugs are based on ) for affective disorders
monamine hypothesis
decreased monaminergic (particularly serotonin and noradrenalin) activity causes depression
many classes of drug that affect monoamine activity helps to alleviate depression
MOIs
tricyclic anti-depressants
specific serotonin reuptake inhiitors
serotonin and noradrenalin reuptake inhibitors
lithium
more extreme methods of treating depression
depp brain stimulation (subgenual anterior cingulate cortex, vagal nerve)
ECT
sleep and affective disorders
sleep is affected in depressed people (broken sleep, less REM)
sleep depriation can be used as a treatment
why do we study fear
adaptive mechanism
long lasting
underlies disorders like anxiety, PTSD, depression
easy to study
3 classifications of fear responses
behavioural - fight or flight
autonomic - heart rate, blood vessels change to enable behavioural response
hormonal - hormones produced to reinforce the autonomic response (eg adrenalin)
how do we study fear
fear conditioning in rats
fear and the role of the amygdala
experiment in rats
lesion of the central and lateral nuclei of the amygdala produced deficits in fear conditioning
(no freezing to tone)
single neurons in the lateral nucleus of the amygdala increase their firing rate to conditioned stimuli following training
evidence to show humans are social learners
fear response to the CS is seen in subjects with no experience of being shocked but who have observed someone else get shocked when the CS was present
it is also seen when subjects are instructed to expect a shock with the CS
brain results in whats activated in humans in response to fearful stimuli
left amygdala is activated in response to CS following instruction the CS will be paired with a shock (even when no shock given)
there is also laterality - but probably due to language being involved in the instruction
normal conditioned fear induces bilateral activation
3 ways to reduce fear
extinction
cognitive regulation
reconsolidation
extinction of fear in rats
in extinction the association between US and CS is not forgotten
we learn a new association between CS and lack of shock / fear
if new learning is blocked in the amygdala (block LTP using NMDA antagonist) then rats do not show extinction
what happens to the amygdala during extinction and how
amygdala is inhibited
this inhibiton comes from the ventromedial prefrontal cortex
neurons in this region become active during extinction
this inhibits the fear response produced by the amygdala
electrical stimulation of the vmPRC can speed up extinction
how can cognitive regulation reduce fear
decreases activation in the amygdala
again is mediated through vmPFC
so works by the same mechanism as extinction
basis for cognitive therapy for emotional disorders
how does memory reconsolidation reduce fear
can we block memory reconsolidation
LTP required
so we could block LTP by blocking protein synthesis
implications for PTSD
but remember this is permament - memories are removed 0 not inhibited as in extinciton which is useful but could potentially be dangerous
what is motor contorl and action selection
the brain is capabel of very compex sequences of actions
capable of performing multiple behaviours simultaneously
how does the brain control and coordinate movement
how is the primary motor cortex organised and who ofund this out and how did he find this out
topographically
penfield
during surgery for epilepsy he stimulated the primary motor cortex to examine which parts of the body are controlled by which parts of the primart motor cortex
what is the other system within the brain that controls motor function (if not primary motor cortex)
cerebellum
acts in conjunction with primary cortex
cerebellum computed the contributions of muscles to perform movements
cerebellum projects via the ventrolateral thalamus back to the motor cortex which allows current movements to be modified
damage to cerebellum causes movement effects. what problem is caused by
floccilonodular or vermis damage
postural and balance problems
damage to cerebellum causes movement effects. what problem is caused by
intermediate zone damage
limb rigidity
damage to cerebellum causes movement effects. what problem is caused by
lateral zone damage
weakness and decomposition of movemnt
damage to cerebellum causes movement effects. what problem is caused by
general cerebelum damage
cerebellar ataxia (lack of coordination)
how doe we plan and execute sequences of movement
premotor cortex and supplementary motor area involved in motor planning (SMA)
SMA is critical for….
learned sequences
lesions impair these
disrupts ability to make a sequence of 3 movements
how are actions encoded in the brain
mirror neurons
in the ventral premotor cortex and the inferior temporal lobe
respond to the sight of someone else performing a particular movement
research into mirror neurons in humans
hard to study as in humans not all neurons int he ventrolateral premotor cortes are mirror neurons
emerging evidence = increased activity in the ventral premotor cortex during execution and observation of actions
this area is often called the inferior frontal gyrus
when are mirror neurons most active
for well practiced beahviours eg playing the piano
what is the function of mirror neurons
imitation
mechanism for understadnign the actions of others
encode intention
mirror neurons in autistic children
autistic children have lower activity in the ventral premotor cortex when imitating facial expression compared to controls
the level of activity in the ventral premotor cortex during the task correlates with the symptom of severity
suggested mirror neurons enable us to process and understnad the actions and intentions of others
this anility underlies theory of mind
lack of mirror neuron activity could lead to autism
ways to have disorders of movement
cerebellar damage neurodegerative disorders damage to the cortical otor areas -apraxia -relates to deficits of skilled learned movements
what is limb apraxia
inappropriate limb movements especially to verbal commands
caused by damage to the left frontal / parietal cortex
often there are lesions to this area
lesions here also produce deficits in ability to comprehend gestures made by others
consistent with mirror neurons processing action / intention info
what is constructional apraxia
inability to percieve and imagine geometric relations
caused by damage to the right parietla cortex
key terms defining consciousness
internal knowledge
awareness of thought feeling and volition of the external world
sense of self
condition of waking life
sperling 1960 conscious experiment
letter grid for 500msec
letters disappeared and asked to recall
typically could recall 4
can also be paired with tones
tone comes as grid is disappearing but subjects will be able to recall all from that top line
so suggests subjects have conscious access to all the letters?
access overflow theory - ned block
perceptual consciousness has a higher capacity than cognitive access
the fact that when we are cued we can report all of the letters suggests that we are conscious of all of them
the mechanism that allows us to access this information have a limited caacity so we cannot recall all of the items even though we do consciously perceive them
what does access overflow theory suggest about consciouss
we have two forms of conscious
phenonmenal consciousness - creates a rich dertail perception of everythig]ng we see
access consciousness - information that we can access theough cognitive processez
what is inattentional blindness
we miss the gorilla in the ball throuwing counting video
not all information from visual experience is perceived
this argues against phenomenal consciousness
what is change blindness
details no in attentional focus are not consciously perceived
this is not consistent with phenomenal conscious
suggests that obviously different items are consciously processed but subtly different items are not consciously processed
the two problems of studying consciousness
easy problem
-understanding the mechanisms of supporting cognitive functinos such as language and attention and working memory
hard problem
-what is it like to be conscious
-how does phenonmenal experience arise from physical events in the brain
is it possible to study phenomenal consciouss in isolation of cognitive processes
daniel dennet - no
is beyond science
sonsciouss cannot be studied without using the set of cognitive capabilities that can access it
can neuroscience shed light on this?
is conscious something separate from the brain
what are the different ideas
yes -mind vs brain -dualism -religion no -reductionism (an extension of materialsim) = where most neuroscientists would sit maybe -emergent properties
what is the neurobiological basis of consciousness
blind sight
recurrent processing
blind sight
split brain patients (often split by severing the corpus callosum in patients with severe epilepsy)
split brain patients can often identify stimulus that they have previously encountered even though they have no conscious recollection of experiencing it
recurrent processing
what rather than where is conscious
are there neural mechanisms which support consciousness
visual information is processed very quickly by the visual cortex but this is sub-concsiocus
recurrent processing in the visual pathway conbined with recurrent processinf in the frontal-parietal regions results in conscious perception
so i recurrent processin consciouss?
are patients who cannot use language conscious
persisten vegetative state
patients who have come orund form a coma but show no awareness
eg 23 year old woman who had a traffic accident had preserved sleep cycles but was unresponsive to external stimuli = is she unconscious or locked in?
what do some patients in a persistent vegetative state do to communicate
imagine thing
imagining playing tennis = SMA activation
imagining spatial scenes (eg your house ) produces activation in spatial memory system - PPA
so set one as yes and other no
shows still has conscious even though she cant use language
however she still needs attention and working memory to produce this response
doesnt address whether conscious can be studied in isolation of cognition
