2 Flashcards
Lines of the brain
1- frontal, processing info, relaying sensory info
2 Temporal
3- parietal
4- occipital
Prefrontal cortex- frontal lobe anterior to motor cortex- universally decided have subregions-dorsolateral pfc, ventrolateral pfc, ventromedial pfc, dorsomedial pfc
Makes up a lot of the brain- linked to executive functions- process that function on short sided behaviour to acheieve a goal- self control, goal monitoring, problem solving- probably many areas of brain as it is very complex- distributed networks
When PFC damaged- executive function impaired- cannot assign specific roles to pfc subregions- probably due to interaction of these regions and the communication via the rest of the body
It’s receives the sensory info and sends it to the areas of brain to carry out a function- moving,
Cortical areas named by parts of skull
Cortical areas named by parts of skull
Organization of brain- linked to function based on the lobes of the brain
Lobes- assigned before anyone knew the brain- relied on parts of skull as landmarks
Main bones= match up to the lobes
Areas of the brain
Areas of brain named based on the bone plates that lie around it- arbitrary way of divided complicated organ into manageable lobes- much more complex than one function
Central sulcus and Sylvia’s fissure- gyri- grooves in brain- seperated brain
Cerrebelum- thinner, has thinner gyri
Lobe that has singular function- occipital- vision- relay on it to make sense of surroundings- big part of our brain functioning= needs large area- not only area= sends it to other areas to make sense of what we are seeing- object identity, recognizing faces, making sense of shapes
Temporal- processes hearing, dedicated to language, has memory storage, many functions, hippocampus located here
Parietal- interpret touch and somatic sensory info, touch sensations create movement and identify movement
Frontal- posterior- has production of movement, plans movement, brocade area- controls speech, has executive functioning area
Frontal- important for behaviour functioning
Functional division of the cortex
Executive
Action
Sensory Functionally distinguish it
Executive- most associated with abnormal psych- linked to many disorders- addiction, depression, schizophrenia- linked to frontal cortex functioning
Phineas gage
Wilder Penfield reported the “silent cortex” - areas of frontal cortex appeared to have no function.
Ex. Phineas Gage’s personality changed so radically that he was “no longer Gage.”
.what are executive functions- what traits- planning, self control, causing movement= *GUESS
Many people don’t know the meaning- took science years to find out what rental cortex does and how it regulates the rest of the body
Penfield- probed brain with electromagnetic for epilepsy- done during consciousness- want to make sure you don’t damage important areas- some regions when stimulated- led to vivid scenes, emotions, smells- burnt toast
Even though he did this couldn’t figure out functions for prefrontal cortex- called t silent cortex
Caused them to look at other cases- Gage- iron rod blew through skull- he survived another 12 years- left side of PFC was destroyed- he had changes in personality and mood- no longer himself- was balanced, smart after was reactive, aggressive couldn’t hold a job- everyone noticed
Frontal lobe- regulating the balance between animal and human behaviour
From Silent Lobes to CEOs
Does the prefrontal cortex separate human from animal?
Brodmann (1912)
The relative size of prefrontal cortex is nearly twice as large as any other animal.
Gage- brought attention to brain what seperated human brain from other animals
Brodmann- used cellular markers for animal brains- compared size of human and animals frontal lobe- we have a much greater portion of frontal lobe- occupies 30% in humans, 4%- in cats, 17% in monkeys
The prefrontal cortex is twice as large than predicted based on evolution- frontal lobe has evolved to be bigger
size of human frontal lobes
The absolute size of human frontal lobes is 3x larger than great apes. If size matters what about the absolute size o the brain. The absolute size of human frontal lobes is 3x larger than great apes.- humans have a bigger frontal lobe- relativ sense- twice as big
Parietal cortex size
Other intelligent animals have bigger brains than humans, but the parietal cortex is proportionately larger.
What about in intelligent animas- they have a larger parietal not a frontal cortex
Parietal- sensation, sense of enviroment, knowing where you are
Deficits Following Frontal Lobe Damage
Case study:
3 patients with prefrontal lobe damage.
personality changes.
Normal movement and perception.
No impairment of intelligence.
Case study evidence supports that PFC is important in behaviour and personality
3 patients had damage to prefrontal lobe- had change in behaviour or personality- and normal movement, defects in behaviour
Multiple Errands Task
How are those with frontal lobe damage impacted in real life- asked to go to market- given to do list- have to visit multiple places seek out info without aids
Frontal lobe damage- struggled- strayed from where they wanted to go, less organized- brain may be disorganized
Deficits in Strategy Application Following Frontal Lobe Damage
Patients made more errors vs controls
Executive Functions
Flexible, goal-directed behaviour in response to internal and external cues.
Executive function- broad term-focused on goal directed behaviour
Higher level cognitive processes- people better than animals
Action selection VLPFC
Self regulation DLPFC
Weighing alternatives OFC
Goal setting PFC
Plannng DLPFC
Structures and functions of the cortex
Lobes not limited to a single function.
General organization of sensory (posterior) and motor/action behaviours (anterior).
Executive behaviour localized to prefrontal cortex.
Executive functions focus on controlling goal-directed behaviours.
Executive functioning not limited to PFC
Executive behaviour- only in PFC- if damages not good at it
Linking behaviour to function of prefrontal cortex
Major Subdivisions of the Prefrontal Cortex (PFC)
Dorsolateral (DLPFC)
Ventral (VPFC)
Orbital (OFC)
PFC- frontal lobe
Takes sensory info and relies it to other areas of brain
PFC- most of frontal lobe- except for motor cortex
DL-PFC and working memory
DLPFC- towards the top and to the side- most recently evolved, goes under long period of maturation
PFC last to develop- still not fully mature
Time management, working memory, cognitive flexibility-change actions, planning, holding info in mind- problem solving, directing and maintaining attention
Connecting to hippocampus, emotions important here
If have PTSD- have deficits in DLPFC- cognitive and memory problems, can cause lack of emotion, attention deficit problems
Some say sig difference in hemispheres- left side- approach behaviour nd happy emotions left= avoidant
DLPFC interacts with others area of brain- parietal lobe
DLPPFC- linked to object permanence- subject has to find object after certain delay- able to do this with more developed DLPFC- 2 years old
DLPFC defects- have deficits In working memory- less activation there when have no object permanence- when develop it have more activity in DLPFC
Role of DL-PFC in
Cognitive Flexibility
Lots of evidence links executive function to PFc
Cognitive flexibility- think of multiple things at once, strop task- hard for most people
Cog flexibility- crucial aspect of frontal lobe processing those with frontal lobe damage- mentally rigid
Wisconsin task- solution is constantly changing- have to not stick to what you think is role- have to be able to change thinking
Those with frontal lobe injury- cant change mental state or approach to problem
Associated to DLPFC
Ventrolateral prefrontal Cortex (VL-PFC)
Motor Inhibition
Updating Action Plans-Right posterior
Decision uncertainty-Right middle
Control attention-Left
Well connected
Functionally different from DLPFC
Hemispheres have different functions
Right- motor inhibition, updating actions, control attention
No go task
Measure reaction time to stimulus- add decision- inhibit behaviour- only click when no patter
Increased VL-PFC Activity During No-Go.
Shows ‘contrast’ of activity between Go and No-Go tasks. More activity on ‘No-Go’ will appear as brighter red.
Inc of activity in the no go- have to inhibit behaviour
Compare left and right hemisphere activity.
The Cognitive Reflection Test
(updating action plans / override response)
Right VLPFC- updates actions plans, controls attention
Left VLPFC- more important for attentional control, resisting temptations
Makes decisions based on connections from other areas, amygdala, hippocampus, temporal lobe, thalamus
VLPFC- connected to rest of brain
VMPFC- helps VLPFC in social decisions, social nctioningm suppressing negative emotions
CRT- measure tendenc to override problem solving processes that are incorrect- predicts how they can overcome cog biases
Increased VL-PFC Activity while adjusting decisions
On the fly activity adjustment induced greater activity in right ventrolateral prefrontal cortex
CRT- measure ability to reflect on question and inhibit first response that comes To mind- inc activity in right side
Ventromedial prefrontal Cortex (vm-PFC)
Connected with amygdala,hypothalamus, PAG
Emotional regulation
Orbitofrontal (Orbital-Frontal) Cortex
(OFC)
signalling rewards/punishments
decision making
L vs R
Regulating decisions in socia situations
Introspective decision making
Learn from mistakes
Value-based decision-making
(OFC)
Monkeys choose between two types of juice (A and B; where A is preferred) offered in different amounts. Behaviourally, there is a trade-off between juice type and juice quantity.
In experiments- monkeys have preferred juice- monkeys choose juice a when juice b is offered- if you offer 4 times more of b- will pick b
They are swayed by quantity of juice and flavour
the cell’s activity varies with the offer ‘type’.
When the choice (above) is roughly equal (no difference in value), OFC neurons respond the least.
Only when there is a value preference do we see elevated activity.
OFC- plays a role in this- when its equal- doesn’t respond
Value difference= activity difference- causes them to weigh options
Linking experience to reward
A(fMRI) study using show that the more we like what we eat, the more active our OFC.
FMRI during these task- show selective activation on anterior parts- link to pleasantness rating
Pleasant- higher- more activity in OFC
Executive functioning= very vast term- depends on the area but is goal directed behaviour- higher level cog processes
Cells of the Nervous System
Embryonic stem cells that form the nervous system become two primary cell types:
Neurons
Glial cells
We start at stem cells in specialized Neurons transmit information in the form of electrical signaling.
Sensory, motor, interneurons
Glial cells provide metabolic support, protection, and insulation for neurons.
Filial- support- insulate neurons, part of blood brain barrier
Features of neurons
Common features of neurons:
Cell body
Dendrites
Axon
Cell body • Cell body; contains nucleus and other organelles.
Ex. Mitochondria for ATP
Dendrites - branches upon which incoming fibers make connections (at synapses) with other neurons
receiving stations for excitation or inhibition
Dendrites- receiving area- information transfer happens between neurons at the synapses
Branches of dendrites lined with receptors- get excited or inhabited
Axon- releases the signal out to the synapses
Many receptors throughout the brain
Axon- conducts electrical signals away from cell body to synapses
Principal parts of neuron
Transmission occurs from the presynaptic cell to the postsynaptic cell
Flow of information:
Synapse dendrite soma axon synapse
Transmission between neurons- happens at axon- axon makes neurons different- transmit info in form of AP
Happens from the presynaptic cell synapsing with the dendrites of another cell AP- generated at axon hillock
Neurons that need the info to transfer fast- myelin sheaths made by glial cells
Terminal buttons- neurotransmitter release
receptor at synapse to the dendrites info goes to cell body, AP is generated at axon hillock travels to terminal button and synapse wth another dendrite
Dendritic spine
Dendrites are covered with short dendritic spines
Dendrites and their spines are constantly modified and canchange rapidly in response to changes in synaptictransmission: #, size, shape, etc.
Dendritic spine- inc surface area, constantly modified- change rapidly based on info in brain and neurotransmitters, the dendrites themselves change in #- inc or Dec, Chang in size and shape
Disorders- have different amount of dendritic spines
Drugs of abuse- change dendritic spines- may be key to drug addicted state
Components of axons
Axons transmit electrical signals from the axon hillock (at the soma) to the terminals.
A neuron usually has one axon, but it may branch to form axon collaterals.
Terminal buttons have synaptic vesicles containing neurotransmitter chemicals.
Axon hillock- goes down to terminals- usually have one axon- can form collaterals the terminal buttons release- dopamine, gaba
Rrelease from synaptic vesicles
Most axons are wrapped with myelin sheath, a fatty insulating coating created by layers of glial cells:
Schwann cells
Oligodendroglia
Fatty insulated cells made by Schwann cells in the periphery,
Oliginderia- myelinated nerves in the spinal cords and brain
Both are glial cells- protect neurons
Multiple sclerosis caused by determined myelin sheaths= less communication
Myelin sheath
Node of Ranvier = break in myelin sheath increases speed of
AP conduction Breaks in the sheath= nodes of fancier- AP jump along= spreads up
Myelin breaks down- nerotransmission doesn’t happen as well
Schwann cells: form myelin sheaths in peripheral nervous system (PNS); wrap only one axon; release growth factors and promote regeneration of damaged axons
Oligodendroglia: form myelin sheaths in central nervous system (CNS); wrap many axons
Astrotes: provide structural support for neurons and help maintain ionic balance in the extracellular environment; take up excess NTs- maintain homeostasis- take up excess transmitters
Microglia: remove dying cells by phagocytosis at sites of nerve damage; responsible for immune response- waste removal, immune response
All glial cells important
May contribute to disorders
Transcription of genes
Soma (cell body) performs most metabolic functions.
The nucleus contains pairs of chromosomes.
Chromosomes = strands of DNA; gene = section of chromosome coding specific proteinComplementary RNA made by transcription factors: nuclear proteins that bind to DNA, transcribing it to make RNA-Experiences can affect gene transcription
Protein translation in cytoplasmic ribosomes.
More interested in neurons but glial do cause abnormalities
Cell body- metabolic functions, energy production
Nucleus- has chromosomes- genes- read by mRNA to make proteins0 very important
Transcription can be modified- dna doesn change much- expression of genes changes- transcription factors- gets read by enzymes after mRNA to make proteins- experiences and stressors- effect gene transcription= epigenetics
Epigenetics
Epigenetics: control of gene expression by chromosome modifications that do not affect the DNA code.
Ex. DNA Methylation: attachment of methyl groups to a gene reduces its expression (blocks translation).
Epigenetics- change gene expression not gene itself
DNA methylation- methyl attached to gain= blocks transcription- doesn’t turn into protein
Acetylation of chromatin(dna wrapped around his tones)- can be changed when added acetylate - makes it unwind DNA= more likely to be transcribed
Chang expression of dna
Trauma, drug use, causes acetylation- changing expression of genes
When chromatin tails acetylated, charges open up chromatin (part B) allows transcription factors to bind increases transcription
Methylation of histone tails (part C) pulls chromatin tighter prevents transcription factor binding reduces transcription
Opens chromatin- allows transcription to bing
Methylation- maes it harder to read
May explain the differences not caused ny genes- differences in twin- how experiences change behaviour
Axoplasmic transport
Axoplasmic transportUses cytoskeleton: network of microtubules and neurofilaments that provide shape and structure to the cell. Microtubules form a track that proteins travel along by the action of motor proteins. Proteins that are made in the soma neeed to be transported
Uses or cytoskeleton
Help form a path for proteins- Alzheimer’s- microtubules get tangled causing tangled neurons
Proteins in the Cell Membrane
Proteins in the Cell Membrane
Receptors: cell membrane proteins -initial sites of action of neurotransmitters (NTs), hormones, and drugs.
Enzymes: catalyze biochemical reactions
Transporters: for charged molecules (Ex. amino acids, glucose, metabolic products)
Many proteins - many are receptors= where chemicals bind to
Enzyme- help w biochemical reaction
Transporters- help them get across cell membrane
Resting membrane potential (RMP)
more negative ions (and amino acids) inside the cell, and more positive ions outside.
Distribution f ions in neuron when at rest
Difference in charged ions and proteins= more negative inside then outside
Neurons can get only so positive before reach AP(0-50)
Voltage-Clamp Technique
Allowed H & H to set the membrane potential (clamp it) at any level, and simultaneously measure underlying permeability changes (current flowing across membrane) Used voltage lamp on squid’s
Set membrane potential to level amd stimulate axon and observe ion channel
Electrostatic pressure and concentration gradient
Most ion channels are gated, but some K+ channels are not (=leaky); K+ moves freely
K+ moves into the cell because it is attracted to the negatively charged particles (electrostatic pressure)
K+ moves back out of cell when its concentrationrises (down its concentration gradient)
In open channel- potassium called it of neuron- slowly
Equilibrium potential for potassium (
Equilibrium potential for potassium (EK): when the two forces are balanced. The membrane potential is still more negative inside (~-58 mV).
When two forces are balanced- potassium wont move(-58)- these. Forces generate action potential
Equilibrium reached when ions are balanced
Interior- high concentration of negative charge
Ions cant diffuse across membrane except for with channels
Neuron at rest- most are closed
But potassium can be open- they d not allow other ions- only few are open- the intercellular concentration is higher then outside- potassium is moving in and out of the cell- diffusion and electrical forces- when come in balance= potassium equilibrium= no movement
Maintain resting potential and returning it- because of sodium potassium pump takes 3 Na out for every k moved in- ions pumped against their concentration gradients – r=needs energy
All cell membranes are polarized
Action potential (AP): a rapid change in membrane potential that is propagated down the length of the axon
Threshold potential for AP firing = ~-50 mV -Voltage-gated Na+ channels open, Na+ flows in; generates rapid change in membrane potential to more +ve = depolarization
Polarized- more negative inside
AP- happen at myelin sheath- every once and a whole
Rest, receptors bound, channels open- change into positive= AP
Voltage gated channel is open- when cell gets more pos- sodium rushes in causing It to become pos- potasssium- leaves
How are AP caused
Various stimuli can cause an AP and open ion channels:
electrical change
chemical (taste, drugs, smell, neurotransmitters)
mechanical (touch, pressure, sound)
light (vision, photodetection)
temperature (hot and cold receptors)
Small amounts of ion channels opening causes small, local changes in ion distribution and potential differences called local potentials-Depolarizations and hyperpolarizations
Many stimuli can cause AP
Small changes in the ions- graded potential-
If Na+ channels open, Na+ enters cell and causes local depolarization excitatory post-synaptic potential (EPSP)
If Cl– channels are stimulated to open, Cl– enters cell and results in hyperpolarization, which is inhibitory. inhibitory post-synaptic potential (IPSP)
If gated K+ channels open, K+ leaves the cell which also results in hyperpolarization.
Depolorazied- sodium channel open sodium flows in- EPSP- ion come in make it more pos
CL- channels open- make it more negative- harder to generate AP-
Local potentials and action potentials
Graded: larger stimulus greater magnitude of hyperpolarization or depolarization
Summation: several small depolarizations big changes
Bigger stimuli- lead to bigger responses= leads to AP
Summation- adding the stimulations t reach potential
Action potentials- only depolarize
If summation of local potentials reaches the threshold, large numbers of Na+ channels open and Na+ rushes into the cell very quickly.
-Causes rapid change in membrane potential from –50 mV to +40 mV = rising phase of AP
Getting stimulation and inhibiting- reach temporal summation- fire an AP
Stages of the action potential
Resting potentials
Threshold
Happening very quick
430 km/hr
Have thought- say it= instant
Different channels going on all the time
Potassium= leaky channel- always open
AP Refractory Periods
Absolute refractory period - the time following an AP where a stimulus can’t elicit a second AP due to closure of Na+ channels
Relative refractory period - the time following an absolute refractory period when the threshold for initiation of a second action potential is increased: Na+ channels recover from inactivation and K+ channels close
absolute- sodium channel closed- can relate to disorderds- constantly firing
nodes of Ranvier
In myelinated axons, regeneration of the action potential occurs only at nodes of Ranvier
The conduction seems to jump along the axon = saltatory conduction.
Less energy is needed because Na+-K+ pumps are only at the nodes. - AP moves along axon because Na+ ions spread passively to nearby regions, which changes the membrane potential to threshold, which opens more Na+ channels.
AP- only generated at nodes of fancier- sodium ions spread across the myelin
tetrodotoxin (TTX)
Some drugs alter AP conduction by blocking the voltage-gated Na+ channels (e.g., Novocaine): These drugs are used for local anesthesia.
Bacteria within the pufferfish generate a toxin called tetrodotoxin (TTX) TTX blocks Na+ channels, paralyzing its victim
Cocaine- block sodium channel- touch info doesn get to brain
TTX- block sodium channel get paralyzed but conciuos- sodium cant get I n
2 major classes: Local graded potentials & Action potentials
Graded- differ in size- more stimuli bigger response= signal lessens as it goes o rest of body
AP- happens or doesn’t, not graded, same intensity through out spatially- how many across pace, temporal- time
AP fires based on how many AP you see
Development of the brain
Brain development depends upon:
Maturation
Learning
We can refine this understanding by learning how:
Neurons develop
Their axons connect
Experience modifies development (Plasticity!)
Neural development- depends on maturation and learning-brain changes from learning
Is it due to brain just maturing- growing in size- no learning plays a part- new synaptic connections
Brain development needs both learning and maturation
Start in fertilization- sperm fertilizes egg- cell division starts
Day 15- considerend embryo
At day 20- neural plate starts to form- a couple weeks after conception- brain starts to form- neural plate is first neural tissue- becomes a groove- forms a neural tube
The neural tube closes
Maturation of the embryo Brain
Human CNS begins to form when embryo is ~3 weeks old:
Dorsal surface thickens, forming neural tube surrounding fluid filled cavity
Anterior end enlarges, sinks under skin surface
Hindbrain, midbrain, forebrain, spinal cord
Our CNS- brain and spinal score form at 3 weeks- neural tube forms- completed at 4 weeks
Cerebral hemispheres- side of brain formed
Brain gets bigger and grows- gets bumps that become parts of brain
Forebrain- covers midbrain and hindbrain- rest is spinal cord in CNS
Fluid (CSF)-filled cavity becomes central canal & 4 ventricles (walls = neuron production)
The rest of the neural tube becomes the spinal cord
Has cerebral spinal fluid- neural cavity filled with CSF- becomes spinal cord and ventricles in brain(fluid filled space) where neurons are produced
During brain development- the neurons start in walls of ventricle
Neural tube folds on to itself
Forebrain- gets bumpy- form gyro- covers midbrain and Hindbrain
Changes happen during development- brain gets bigger but looks the sa,e
Brain weight
At birth, brain weighs ~350 g
By the first year, brain weighs ~1000 g
By 18 years old, (adult) brain weighs ~1400 g
18 years is adult- no finished (especially prefrontal cortex) until 30 brain develops front to back
Brain develops in proportion with body- but connections change brain through life
The Development of Neurons
The development of neurons in the brain involves the following processes:
Neurogenesis
Migration
Differentiation
Maturation
Synaptogenesis
Pruning & Cell Death
Myelination
Neurogenesis happens first- around 2 months- rest is out of order – once neurons formed- migrate
Later processes- continue after birth
Littleneurogenesis occurs through life
Neurogenesis
The production of new cells/neurons in the brain
Early in devt, cells lining the ventricles (in the subventricular zone) divide
Stem cells continue to divide
Neurons (E42) or glia migrate to other locations
>250,000/min!
Almost all form within ~28 weeks of gestation
Proliferation of new neurons
Primarily in early life- but some areas do form neurons
Cell lining ventricles(subventricular zone) dividing a lot and specializing- continue to divide and form cells- some become neurons or glial cells(migrate)
Cell division at this time produces one stem cell and one neuron- have stem cell and neuron each division of ste, cell
Sem cell stays there neuron leave and
migrate Around 100 billion neurons
Developing of neurons is happening very fast- if anything happens during this development that causes abnormal development
Born before 28 weeks- brain not fully developed- more vulnerable to abnormalities
Environment changes and neuron production is inhibited
Stem cells in pancreas, hippocampus, can develop new stem cells- turn into neurons
Nerve cells in hippocampus in adult brain- need these them cells of new neurons to learn new info
In general new neurons do not form in other areas
Migration
The movement of the newly formed primitive neurons and glia to their eventual locations
Some don’t reach their destinations until adulthood
Occurs in a variety of directions throughout the brain
Chemicals known as immunoglobulins and chemokines guide neuron migration
After become neuron or glial cell- migrate to new location
Some don’t reach destination to adulthood
Damage to brain- can damage migration
Moves in different directions- some slide along glial cells(help neuron migrate)- radial glia
Tips of migrating neurons form growth cone- has feelerssensing environment- guiding neuron
Chemicals- help neuron find way- act as guide-
Migration requires precise chemical environment
Differentiation
Local environmental signals (ie. chemicals produced by other cells) influence the way cells develop & form layers in the cortex
Intercellular signals progressively restrict the choice of traits a cell can express
G X E
Local environmental signals(neuron reached destination) has signals and chemicals that influence development of cell and layers it forms in cortex
Differentiation forms these layers
Cells release different neurotransmitters,otters- because of neuron itself- restricts development of certain genes
All have same gene- environment activates certain genes
Maturation
Formation of axon & dendrites
The axon grows first: either during migration or once it has reached its target-followed by the development of the dendrites
Maturation and ifferation go hand in hand
Forms axon and dendrites- give neuron shape
As neuron mature- form structures- axon grows first
After migrating- dendrites start to form- happens before birth continues forever- as experiencing- dendrites change
Axon grow 1000 time faster
Newborn- broccas area- don’t have many dendritic formation
Have same cell body across time- by 2 years old have many more dendrites- as forms synaptic connections
Dendritic branches & spines
In lab animals- the formation of dendritic spine and branches- influenced by environment and environment simulation (friends vs no friends)
Autisms- partly due to abnormal neural maturation- have different dendrites
Have less dendritic spines,, size is different
Environment- chemical and social- lead to growth and maturation o neuron
Pathfinding by Axons
Axons must travel great distances,form correct connections
Sperry’s (1954) research on newts shows axons follow a chemical trail to reach appropriate targets
Growing tips of axons also respond to cues from:
Cell adhesion molecules (CAMs)
Tropic molecules
Netrins
Axon and dendrites need to find way- what to synapse with
Axon travels great distanced to connect
Not easy for axons to find way
In 1920- graphed extra leg on salamander axons grew into it causing them to move together
1954- cut the optic neurve and rotated it- found the axons grew back to original target- had to travel different difference but went to were they should \
The chemical environment is important to signal correct axonal growt
CAMS- growth cone and growing axon, stick to it or repealed high causes guidance and tropic molecules- attracts or repels neurons
Netrins
EMX2 PAX6
Protein got rid of certain axon
Emx2- in normal- more posterior- causes normal development
Mutate emx2- pax6 tries to shift it- causing change in development
Mutaepax6- causes change in development
Proteins and correct level- important for normal development
Axon guidance
A growing axon follows a oath of molecules attracted by chemicals and repelled by others. Eventually axons sort themselves over the surface of their target by following this molecular trail
Axon follow molecular trail- certain proteins guiding axon along causing proper development
Synaptogenesis
Formation of synapses
Begins before birth, occurs throughout life: neurons are constantly forming new connections (& discarding old ones!)
Slows significantly later in life
Each neuron may synapse with >1000 others adult brain estimated to have > a quadrillionsynapses!
Formation of synapse- connect neurons
Synapses change all the time- slows down in later life
Synapses dependent on genetic info and experiences
- Pruning & Cell Death
When axons initially reach their targets, they form synapses with several cells (in approximately the correct location).
Postsynaptic cells strengthen connection with the most appropriate cells and eliminate connections with others.
Elimination = synaptic pruning -depends on the pattern of input from incoming axons
Chemical gradient is not perfect don’t use it you lose it
Cells may die as we;;- depends on environment and input from axon- selection process- neural darwinism- only most stimulated survive
Huge synaptic pruning in puberty bug decrease in amount of synapses
As solidifying personality- selective pruning
Influenced by a lot of factors
The Life Span of Neurons
Different cells have different life spans:
-Skin cells are the newest; most under a year old
-Heart cells tend to be as old as the person
Mammalian cerebral cortices form few new neurons after birth
Some cells survive longer than other- neurons not often replaced
Determinants of Neuronal Survival
Neuronal targets determine who survives
Nerve growth factor (NGF): protein released by neuronal targets, promotes survival & axonal growth
The brain’s system of overproducing neurons, then applying apoptosis (cell death) if they don’t get NGF, enables the exact matching of the number of incoming axons to the number of receiving cells
Sympathetic ganglian- muscles that synapse with axon that come from ganglia- ganglia- don’t determine how many neurons- target of the synapse- decides what synapse stays
Muscles creates NGF- any neurons without enough ngf- experience apoptosis
Brain is overproducing neurons- expecting some to die
Only neurons that make sig connections survive
U to 50% of neurons produced may die off
