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PSYCH 261 Week 6: Module 4.2
MATURATION OF THE VERTEBRATE BRAIN
series of genes called homoebox genes are found in a shit ton of things
vertebrates, insects, plants, fungi, and yeast
what they do is they regulate the expression of other genes and control the start of anatomically development
all homeobox genes share a large sequence of dna bases. mutations can result in abnormalities. in insects, they can form legs where anthennas hsould be, or an extra set of wings.
in humans, mutations in homeobox genes have been linked to serious mental and physical disorders
HUMAN CNS
begins forming at 2 weeks
dorsal surface thickens, long thin lips rise, curl and merge
neural tube forms (in the center is the central canal where theres cerebrospinal fluid)
as tube sinks under surface of skin, forward end enlarges and differentiates into hindbrain, midbrain and forebrain, other end becomes spinal cord
neural tube becomes central canal + four ventricles of the brain (all containing four ventricles of brain and csf)
first muscle movemnents at 7.5 weeks DUE TO SPONTANEOUS ACTIVITY IN SPINAL CORD!!!! but sensory organs arent functional yet, so movements actually start first before sensations
in early infancy, primary sensory areas of cortex that are responsible for vision, hearing and other senses are actually more mature than the prefrontal cortex!!!!!!! and areas responsible for attention, memory and deciison making!!!!
these develop super slowly through teenage years as well, which makes a lot of sense lol like your sensory stuff develop first, and theyre so good in infancy, but everything else takes FOREVERRR to develop
GROWTH AND DEVELOPMETN OF NEURONS
proliferation
production of new cells
the cells lining the ventricles divide (in the ventricular zone, the neuroepithelial cells)
stem cells
the ones that remain as they are, and keep dividing
but some others migrate to other parts of the nervous system
in humans most of this migration happens before birth, but some migrate for the first few months after birth
major difference between human and chimpanzee brains is HUMAN NEURONS CONTINUE PROLIFERATING (new fucking cells) FOR LONGER
early in development, primitive cells begin to migrate
chemicals known as immunoglobulins and chemokines guide neuron migration
not enough of these chemicals? well YOUR MIGRATION IS FUCKED, YOUR BRAIN IS SMALLER, YOUR INTELLECTUAL ABILITIES ARE IMPAIRED
cells differentiate into neurons, and when this hapens you can see the dendrites, axons and synapses
birth to age 2.5, dendritic trees EXPAND CRAZY FAST, and literally by age 2.5 theyre close to the adult pattern
based on when and where neurons are developed and what genes they express THEY LITERALLY LOOK DIFFERENT, and also have diff functions (sensoyr, motor, dopaminergic…)
synaptogensis
the formation of synapses!!!
begins in the uterus, continues through lfie as we learn, we form new synapses, and we lose old ones
this process slows down in older ppl, as does hte process of forming new dendritic branches
which results in slower processing speed im assuming.
myelination
a slower stage of neuronal development!!
by which glia produce the insulating fatty sheaths that make neuron communicaiton faster in the axons!!!
myelin first forms in the spinal cord, then in the hindbrain, midbrain, forebrain
it continues slowly thorugh life and is changed by certain types of learning
wait HOLD THE FUCK UP. MYELINATION IS MODIFIED BY CERTAIN TYPES OF LEARNING???????
STOP AND CHECK
what causes the first muscle movements in a developing embryo?
spontaneous activity in the spinal cord!! sensory organs arent developed yet tho, so you cant feel it!
which comes first: migration, synaptogenesis, or myelination
migration!!
neuroepithelial cells migrate from the ventricular zone
synaptigensis
once theyve differntiated into neurons, they will form synapses
myelination
glial cells will myelinate neurons
NEW NEURONS LATER IN LIFE
cajal’s work said that vetebrate brains formed ALL neurons early on in life or in uterus
he said the neurons can change shap since, but NO MORE NEW NEURONS
mostly, this is right!! but in some areas, we absolutely have neurogenesis later in life
first exception is olfactory receptors
nose has stem cells that stay immature throughout life!! periodically they divide
when they divide into two, one of them stays immature, and the other one DIFFERENTIATES to replace a dying olfactory receptor due to toxic chemicals in the environment
this happens like all through life
in songbirds
in the fall, brain area responsible for singing losing neurons, in the spring, it regains them (bcz mating season)
how to see if there are new neurons in adult human brain or not??
CARBON DATING!!
they use radioactive isotope of carbon (the carbon element with 14 neutrons), and they look a the concentration of this isotope in the atmosphere
why? cause dude, the concentration of C14 in the atmosphere was nearly CONSTNAT OVER TIME until NCULEAR BOMB TESTING, WHICH RELEASED A SHIT TON OF RADIOACTIVITY
this was banned in 1963, and the C14 peaked and has been declining since
if you acc look at tree rings, youll find each ring has the C14 content typical of that year
so they do the same thing in human cells, looking at the carbon in the DNA of various human cells
when seeing skin cels, they found a concentration of C14 corresponding to hte year they did the test in. skin cells turn over every year, so its only ever the same as a year ago, skeletal muscles replaced slowly so that makes an average cell there 15 yeras old
they basically measure the level of this radioactive isotope of carbon in your cells to figure out how old that cell is (when i learned about this in grade 9, we used it to carbon date biological material like centuries ago. as far as i can remember)
so basically, with all this, they find that the CEREBRAL CORTEX, forms NO NEW NERUONS after the year of birth
but other parts, we find that new small interneurons acc do form thruogh life in HIPPOCAMPUS, which is MEMORY
so new neurons, keeps hippocampus “young” to learn new tasks
new neurons can be found in the human hippocampus up to about age 7, but beyond that, evidence of neruogenesis is a bit shaky (fwith other findings that mice have greatest number of new neurons, and almost non in humans)
STOP AND CHECK
new receptor neurons form in which sensory system?
olfactory system
what evidence demonstrates that new neurons dont form in the human cerebral cortex?
carbon dating
PATHFINDING BY AXONS
so paul weiss conducted an expeirment where he grafted an extra leg to a salamander and waited for axons to grow into it
salamanders acc do except transplants of extra limbs and do generate new axon branches to these extra limbs!! thats fucking crazy
anyways, so the axons just reach the muscles, the extra leg moved IN SYNCHONY, and weiss was like ‘what no way that each axon found its way the right muscle in the extra limb. its so much more probably that the nerves just attached to muscles at random and then sent messages, and these messages were linked to a different muscle)
like muscles were like radios tuned to diff statios, and each muscles recieved many signals but only responded to one
LATER EVIDENCE SAYS NO!!
that the salamders extra leg moved in synchrony with neighbour BECAUSE EACH AXON ACTUALLY DID FIND THE RIGHT MUSCLE
robert sperry did the crazy ass experiment with the newt’s optic nerves
he did this to see how sensory axons find their way to their correct targets
he said sensory axons find their way in the same way axons to muscles find their way
so basically what did he do?
he cut the optic nerves of newts (they grow back in amphibians which was instrumental bcz he wanted to see if he switched the eyeball around, would the optic nerves regenerate in the same areas as it used to (which was opp), or to the same one?)
what happened was the damaged optic nerve grew back and connected wtih the tectum, where amphibians take in visual info
so first, he acc ust cut them and had them regenerate, and it was all good they could see again!!
and that was great, but he wanted to kjnow, did they grow at random or tdid they grow to a specific target?
so for the next set, he cut the optic nerve then rotated the eye by 180 degrees
when axons grew back to tectum, the axons from what was in dorsal first, grew back in area resposnible fro vision in dorsal retina!!
and axons from other parts ALSO GREW BACK TO ORIGINAL TARGETS. now this means, that the newt now saw the world UPSIDE DOWN AND REVERSED because their vision WAS UPSIDE DOWN AND REVERSED
this tells us that each axon regenerated to the same place it originally was in, presumably bcz they followed a chemical trail!!
so our next question
how does an axon find its target?
well, we found that tehy are attracted and repelled by certain chemicals!!
so development happens in waves, bcz each type of neuron takes a couple days to form
the axons that form earlier, extend axons longer have more branches, more synaptic branches
those forming later connect to less new ones. and those maturing at a particular time with make synapses with other neurons maturing at that time as well
question: can an immature neuron make a synapse with a neuron that has already been developed?
STOP AND CHECK
what was sperry’s evidence that axons grow to a specific target instead of attaching at random?
i mean, the eyes were upside, which means they went to the right places, but since you flipped the eye, they see the opposite. if you didnt flip the eye, they wouldve been fine. if you flipped the eye, and they cnnected to whatever was closest, since its just an eye, it wouldve worked out fine
what the textbook says:
if he cut connections to newt’s eye and inverted the eye, axons grew back to their original targets, even though the connects were inappropriate to their new positions on the eye! so literally what i said! yippiekiyay!
COMPETITION AMONG AXONS
when axons reach targets, chemical gradients steer them to about the right location, but they dont achieve perfect accuracy
in fact, if neuron cant find its normal target, perhaps cause targets ben damged, in many cases it just forms a synpase onto another target
like dating, if you can’t find your perfect mate, you might attach to the best person available.
THIS IS LITERALLY WHATS IN THE TEXTBOOK LMFAOOOOOOOOO
each axon forms synapses onto many cells in about the same location, and each target cell receives synapses from many axons
MATURATION OF THE VERTEBRATE BRAIN
series of genes called homoebox genes are found in a shit ton of things
vertebrates, insects, plants, fungi, and yeast
what they do is they regulate the expression of other genes and control the start of anatomically development
all homeobox genes share a large sequence of dna bases. mutations can result in abnormalities. in insects, they can form legs where anthennas hsould be, or an extra set of wings.
in humans, mutations in homeobox genes have been linked to serious mental and physical disorders
HUMAN CNS
begins forming at 2 weeks
dorsal surface thickens, long thin lips rise, curl and merge
neural tube forms (in the center is the central canal where theres cerebrospinal fluid)
as tube sinks under surface of skin, forward end enlarges and differentiates into hindbrain, midbrain and forebrain, other end becomes spinal cord
neural tube becomes central canal + four ventricles of the brain (all containing four ventricles of brain and csf)
first muscle movemnents at 7.5 weeks DUE TO SPONTANEOUS ACTIVITY IN SPINAL CORD!!!! but sensory organs arent functional yet, so movements actually start first before sensations
in early infancy, primary sensory areas of cortex that are responsible for vision, hearing and other senses are actually more mature than the prefrontal cortex!!!!!!! and areas responsible for attention, memory and deciison making!!!!
these develop super slowly through teenage years as well, which makes a lot of sense lol like your sensory stuff develop first, and theyre so good in infancy, but everything else takes FOREVERRR to develop
GROWTH AND DEVELOPMETN OF NEURONS
proliferation
production of new cells
the cells lining the ventricles divide (in the ventricular zone, the neuroepithelial cells)
stem cells
the ones that remain as they are, and keep dividing
but some others migrate to other parts of the nervous system
in humans most of this migration happens before birth, but some migrate for the first few months after birth
major difference between human and chimpanzee brains is HUMAN NEURONS CONTINUE PROLIFERATING (new fucking cells) FOR LONGER
early in development, primitive cells begin to migrate
chemicals known as immunoglobulins and chemokines guide neuron migration
not enough of these chemicals? well YOUR MIGRATION IS FUCKED, YOUR BRAIN IS SMALLER, YOUR INTELLECTUAL ABILITIES ARE IMPAIRED
cells differentiate into neurons, and when this hapens you can see the dendrites, axons and synapses
birth to age 2.5, dendritic trees EXPAND CRAZY FAST, and literally by age 2.5 theyre close to the adult pattern
based on when and where neurons are developed and what genes they express THEY LITERALLY LOOK DIFFERENT, and also have diff functions (sensoyr, motor, dopaminergic…)
synaptogensis
the formation of synapses!!!
begins in the uterus, continues through lfie as we learn, we form new synapses, and we lose old ones
this process slows down in older ppl, as does hte process of forming new dendritic branches
which results in slower processing speed im assuming.
myelination
a slower stage of neuronal development!!
by which glia produce the insulating fatty sheaths that make neuron communicaiton faster in the axons!!!
myelin first forms in the spinal cord, then in the hindbrain, midbrain, forebrain
it continues slowly thorugh life and is changed by certain types of learning
wait HOLD THE FUCK UP. MYELINATION IS MODIFIED BY CERTAIN TYPES OF LEARNING???????
STOP AND CHECK
what causes the first muscle movements in a developing embryo?
spontaneous activity in the spinal cord!! sensory organs arent developed yet tho, so you cant feel it!
which comes first: migration, synaptogenesis, or myelination
migration!!
neuroepithelial cells migrate from the ventricular zone
synaptigensis
once theyve differntiated into neurons, they will form synapses
myelination
glial cells will myelinate neurons
NEW NEURONS LATER IN LIFE
cajal’s work said that vetebrate brains formed ALL neurons early on in life or in uterus
he said the neurons can change shap since, but NO MORE NEW NEURONS
mostly, this is right!! but in some areas, we absolutely have neurogenesis later in life
first exception is olfactory receptors
nose has stem cells that stay immature throughout life!! periodically they divide
when they divide into two, one of them stays immature, and the other one DIFFERENTIATES to replace a dying olfactory receptor due to toxic chemicals in the environment
this happens like all through life
in songbirds
in the fall, brain area responsible for singing losing neurons, in the spring, it regains them (bcz mating season)
how to see if there are new neurons in adult human brain or not??
CARBON DATING!!
they use radioactive isotope of carbon (the carbon element with 14 neutrons), and they look a the concentration of this isotope in the atmosphere
why? cause dude, the concentration of C14 in the atmosphere was nearly CONSTNAT OVER TIME until NCULEAR BOMB TESTING, WHICH RELEASED A SHIT TON OF RADIOACTIVITY
this was banned in 1963, and the C14 peaked and has been declining since
if you acc look at tree rings, youll find each ring has the C14 content typical of that year
so they do the same thing in human cells, looking at the carbon in the DNA of various human cells
when seeing skin cels, they found a concentration of C14 corresponding to hte year they did the test in. skin cells turn over every year, so its only ever the same as a year ago, skeletal muscles replaced slowly so that makes an average cell there 15 yeras old
they basically measure the level of this radioactive isotope of carbon in your cells to figure out how old that cell is (when i learned about this in grade 9, we used it to carbon date biological material like centuries ago. as far as i can remember)
so basically, with all this, they find that the CEREBRAL CORTEX, forms NO NEW NERUONS after the year of birth
but other parts, we find that new small interneurons acc do form thruogh life in HIPPOCAMPUS, which is MEMORY
so new neurons, keeps hippocampus “young” to learn new tasks
new neurons can be found in the human hippocampus up to about age 7, but beyond that, evidence of neruogenesis is a bit shaky (fwith other findings that mice have greatest number of new neurons, and almost non in humans)
STOP AND CHECK
new receptor neurons form in which sensory system?
olfactory system
what evidence demonstrates that new neurons dont form in the human cerebral cortex?
carbon dating
PATHFINDING BY AXONS
so paul weiss conducted an expeirment where he grafted an extra leg to a salamander and waited for axons to grow into it
salamanders acc do except transplants of extra limbs and do generate new axon branches to these extra limbs!! thats fucking crazy
anyways, so the axons just reach the muscles, the extra leg moved IN SYNCHONY, and weiss was like ‘what no way that each axon found its way the right muscle in the extra limb. its so much more probably that the nerves just attached to muscles at random and then sent messages, and these messages were linked to a different muscle)
like muscles were like radios tuned to diff statios, and each muscles recieved many signals but only responded to one
LATER EVIDENCE SAYS NO!!
that the salamders extra leg moved in synchrony with neighbour BECAUSE EACH AXON ACTUALLY DID FIND THE RIGHT MUSCLE
robert sperry did the crazy ass experiment with the newt’s optic nerves
he did this to see how sensory axons find their way to their correct targets
he said sensory axons find their way in the same way axons to muscles find their way
so basically what did he do?
he cut the optic nerves of newts (they grow back in amphibians which was instrumental bcz he wanted to see if he switched the eyeball around, would the optic nerves regenerate in the same areas as it used to (which was opp), or to the same one?)
what happened was the damaged optic nerve grew back and connected wtih the tectum, where amphibians take in visual info
so first, he acc ust cut them and had them regenerate, and it was all good they could see again!!
and that was great, but he wanted to kjnow, did they grow at random or tdid they grow to a specific target?
so for the next set, he cut the optic nerve then rotated the eye by 180 degrees
when axons grew back to tectum, the axons from what was in dorsal first, grew back in area resposnible fro vision in dorsal retina!!
and axons from other parts ALSO GREW BACK TO ORIGINAL TARGETS. now this means, that the newt now saw the world UPSIDE DOWN AND REVERSED because their vision WAS UPSIDE DOWN AND REVERSED
this tells us that each axon regenerated to the same place it originally was in, presumably bcz they followed a chemical trail!!
so our next question
how does an axon find its target?
well, we found that tehy are attracted and repelled by certain chemicals!!
so development happens in waves, bcz each type of neuron takes a couple days to form
the axons that form earlier, extend axons longer have more branches, more synaptic branches
those forming later connect to less new ones. and those maturing at a particular time with make synapses with other neurons maturing at that time as well
question: can an immature neuron make a synapse with a neuron that has already been developed?
STOP AND CHECK
what was sperry’s evidence that axons grow to a specific target instead of attaching at random?
i mean, the eyes were upside, which means they went to the right places, but since you flipped the eye, they see the opposite. if you didnt flip the eye, they wouldve been fine. if you flipped the eye, and they cnnected to whatever was closest, since its just an eye, it wouldve worked out fine
what the textbook says:
if he cut connections to newt’s eye and inverted the eye, axons grew back to their original targets, even though the connects were inappropriate to their new positions on the eye! so literally what i said! yippiekiyay!
COMPETITION AMONG AXONS
when axons reach targets, chemical gradients steer them to about the right location, but they dont achieve perfect accuracy
in fact, if neuron cant find its normal target, perhaps cause targets ben damged, in many cases it just forms a synpase onto another target
like dating, if you can’t find your perfect mate, you might attach to the best person available.
THIS IS LITERALLY WHATS IN THE TEXTBOOK LMFAOOOOOOOOO
each axon forms synapses onto many cells in about the same location, and each target cell receives synapses from many axons
overtime each postsynaptic cell strenghtens most appropriate synapses and elimaintes others, this adjustment depends on the pattern of input from incoming axon
ex. one part of thalamus recieves input from MANY retinal axons
during dev in womb, bfefore first exposure to light, repeated waves of SPONTANEOUS adctivity go over retina from one side to the other so axons from adjacent areas of retina send almost simultaneous messages to visual area of thalamus
each thalamic neruon selects a gorup of axons that are simultanously active, so receptors from adjacent regions of retina are found and synapess from other locations are dismissed
this suggested a general principle of neural darwinism
in the dev of nervous system, we start with more neruons and synpases thatn we can keep, then through a selection process, we keep the most successful combos of synapses and reject others
the pricniple of competition is importnat, but darwinian evolution is the whole thing
mutations in genes are radnom events, BUTTTT neurotrophins acc play a role by STEERING NEW AXONAL BRANCHES AND SYNAPSES IN APPROX THE RIGHT DIRECTION
if axons from the retina were prevented from showing spontaneous activity during early development, what would be the probably effect on teh development of the thalamus?
the axons would attach based on a chemical gradient, butttt they couldn’t fine-tune adjustment based on experience, so connections would be less precise.
why? because while chemicals take it to where it needs to go, target cells recieve synapses from many axons, and we need to know which ones to strenghten and which ones to get rid of. how do we know which ones to do what with? wellll it depends on teh input we get from incoming axons. so when the thalamus gets incput from etinal axons, thats when it adjusts htings so it knows which neurons to keep and which ones to get rid of for more precise connections!!
DETERMINANTS OF NEURONAL SURVIVAL
each ganglion of sympathetic nervous system has enough axons to supply all muscles and glands in area with no axons left over. ITS FUCKING EXACT. how is it so exact???
wellllllllllllll a long long time ago ppl were like“omg well i thinkj that muscles sent chemical messages to tell the symapthetic anglion how many neurons to form
but Rita Levi-Montalcini, she was like “yeah nah man”
she found that muscles don’t determine how many axons FORM, they determine how many SURVIVE
she found that the sympathetic nervous system (SNS), forms wayyyyyyyy more neurons than it needs, and when any of its neurons form a synapse onto a muscle, that muscle delivers a protein called NGF (nerve growth factor) that promtoes the survival ad growth of teh axon!!
an axon that doenst get this nerve growth factor degenerates, then we have apoptosis, programmed celll death, and the cell just dies
if axon doesnt connect to an appropriate postsynaptic cell by a certain age, thats when cell apoptosis goes on.
if it doesnt match by round 5 it dies!!!!!!!!!1
the textbook literally says “dating with a deadline”. PLEASE HELP ME WHO WROTE T HIS
WHEN SNS begins sending axons towards muslces nad glands it doesnt know eact size, so it makes more neurons than necessary and discards excess, and when you have more axons than muscles, ITS LIKE MINGLE.
nerve growth factor is a neurotrophin
a chemical that promotes survival and activity of neruons
BDNF - brain-derived neurotrophic factor, the nervous system responds to this and several other neurotrophins
neurotrohpines are essential for the growth of axons, dendrites, new synapses, and learning
when cortical neruons reach a certain age in early devleopment a certain percentage die because one factor controlling survival IS THAT NERUONS NEED INPUT FROM INCOMING AXONS. once the bains assembled normal anatomies, neurons started dying rapidly
bcz axons that fail to make synapses, die.
STOP AND CHECK
what process assures that the spinal cord has the right number of axons to innervate all the muscle cells?
apoptosis!!
what class of chemicals prevents apoptosis in the symapthetic nervous system?
neurotrophins!! including brain-derived neurotrophic factor!!
at what age does a person ahve the greatest number of neurons? during early devleopment, during adolescnece, or during adulthood?
during early development!!
THE VULNERABLE DEVELOPING BRAIN
gastrulation, early stage of embryological development
if you mess up early devleopment, youll have problems later on
early brain devleopment vulenrable to damage from malnutrition, toxic chemicals, and infections that would produce milder problems at lter ages
fever as adult? ughh i can’t work on thsi super important proposal i have due this is gonna mess everything up. as a kid? you might die.
well not really immediatley not alays, but it does impair neruon proliferation!!!!!!!!!!
FETAL ALCOHOL SYNDROME
mothers who drink heavily during pregnancy marked wtih this
hyperactivity, impulsiveness, attention deficits, motor problems, heart defects, facial abnormalities, thinning of cerebral cortex
even moderate drinking during pregnancy increaes risks of attention deficits, seperation anxiety..
how does alcohol interfere with developing brain?
interferes with neuron profileraiton, then neruon migration and differntiation, definitely impairs synaptic transmission
kills neurons by apoptosis, bcz it ihbits receptors for glutamate, enhances receptors for GABA, so decrease in net excitation, and hey if neurons arent being excited, they will die!! use it or lose it
develooping brain highly responsive to influences from mother
if mother rat exposed to stressful experiences, becomes more fearful, spends less than usual time licking and grooming offspring offpsirng become permanently more fearful in a variety of situations
also chilren of impoverished women have increased problems in academic and social lives because stress to mother changes her behaviour in ways that change offpsirngs behaviour
STOP AND CHECK
anesthetic drugs and anxiety-reducing drugs increase acitivyt of GABA, decreasing brain excitation. it is possible that extensive exposure to such drugs before birth might interfere with brain development. baesd on what you just read, what is a possible reason for that concern?
well bcz, early on in life, you wanna make neuronal connections and then prune away the unecessary ones. if your neurons arne’t be excited at all, then they will go through cell apoptosis, which is so shitty because they need neurons!!!!!!!1
DIFFERENTIATION OF THE CORTEX
when does neuron decide what type of neuron its gonna be?
well its not sudden!! immature neurons transplants from one part of develping cortex to another, develop properties characteristic of new location
neurons at sightly later stage develop some new properties while keeping old ones
like immigrant children, you enter contry very young, you speak like a native, but you come when youre liek 12, you’re gonna keep a couple bits of the accent
researchers explored what would happen to immature auditory portions of brian if they received input from eyes instead of eras
optic nerves have not yet reached thalamus when born (ferrets)
damaged superior colliculus and occipital cortex, two main targets for optic nerves
also damaged auditory input
optic nerve could not attach to usual target, and auditory area of tahlamus lacked usual inuput
so optic nerve attached to uaditory area
WHICH MEANT. THE WHAT WOULD HAVE BEEN AUDITORY THALAMUS AND CORTEX REORGANIZED, DEVELOPING SOME BUT NOT ALL OF CHARACERISTIC APPEARANCE OF VISUAL AREAS
rewired temporal cortex, receiving input from optic nerve, rpoduced visual responses
In hte ferret study how did the experimenters determine that visual input to the auditory portions of the brain produced a visual sensation?
they trained ferrets to respond to stimuli on the normal side, turning on direction in response to sounds, and the other in response to lights. then they rpesented light to the rewired side, and saw that the ferret again turned in the direction it had associated with lights.
FINE TUNING BY EXPERIENCE
blueprints for house determine overall plan, but brains remodel themsleves in response to expeirence
EXPERIENCE AND DENDRITIC BRANCHING
although central structure of dendrite becomes stable by adolescnece, branhes of a drndrite remain fleixible thorugh life
dale purves injected a dye tht let tehm watch structure of a living mouse neuron over days or weeks, found that some dendiritc branches extended between one viewing adn antoher, some retracted or disappeared. about 6% of dendritic spines appear or disappear withina month, and this turnover of synapses relates to learning
rat in more sitmulating envirronment, thicker cortex, more dendirtic branching, improved learning
more common to keep rats in enriched envronment from this (which are also just normal rat in the wold environments)
might suppose that neuronal changes in an enriched enviornment depend on interesting expeirences and social interactions, no doubt some of them do, but much is produced by enriched environemmtn is due to physical activity
using a running wheel improves neural plasticty and learning,e ven for rodens in social isolation
far transfer
teaching something challenging and hoping studnest get smarter in other ways too
nar transfer, if training on one task produces iprovemnet on a similar task. far transfer, consistnetly a weak effet
many studies have attempted to improve memory or intelligence by omputerized tasks that practice verbal and spatial skills, butttttttttttt little improvement on things aside form what was direclty practiced shows!!
like old people do sudoku, well puzzle practice imrpoves someone’s skills at puzzles but not much else
question:
so doing puzzles, better at puzzles, would it make you better at like visuospatial ksills or reasoning? like it does still ehlp your brain health in a way but exercise is more effective in promoting BDNF!!
STOP AND CHECK
an enriched enviornment promotes growth of axons and dendrites in lab rodens. what is kown to be one improtnat reason for this effect?
well see it hoguth it was cause they were learning a lot
BUT TURNS OUT
they were actually more active, and their EXERCISE is what enahnces the growth of their axons and dendrites!!!!!!
question: is it not that theyre also just fucking around iwth leraning stuff? that they’re just learning?
EFFETS OF SECIAL EXPEIRNECES
brain adapatations after sensory loss
what happens to brain if one sensory system is imparied
like those whho were blind early in life, area in tempral cortex that otherwise repsonds to visaul motion becomes sensitive to movement of sounds
blind ppl better tha n others at localizating sounds
greater sensitivy tin fingers, averae sensitive to touch on lips or other areas they pay no more atteniton than anyone else
question: in the textbook, they talked briefly of how blind people had greater sensitivity to touc in their fingers, but not greater snesitivty to ouch on lips or liek areas they dont pay any ATTENTION TO so i was wondering what sort of role attention plays in which areas get the most cortical space?
blind ppl use occiptial cortex to help identify what they feel, it also responds to langauge and other auditoyr info for those who have been blind since birth
the increased rep of isual info enables deaf people to recognzie emotional rexpressions better than average, teporal corte maintains features that would have been typical of auditry cortex,
after auditory cortex reorganizes to attend to sight (again ltos of emphasis on what you attend to, so like attention?)
so after it attends to sight, it reps ivsual stimuli left to right, detects peripheral sights well instead of concentrating on fovea like visual cortex does
most peoples sensory cortex doesnt distingih lealry between one toe and another, but cortex does for those who were forced to use toes liek fignesr
STOP AND CHECK
name two kinds of evidence that touch info fro the fingers activates the occipial cortex of ppl blind since birth
FOCAL HAND DYSTONIA
musicians cramp, threatens career
brain reorg is the problem
appraoch is to find an appropriate type fo retraining
providing bursts of vibration to affected muslces or trains the person to reach towards tarets
sometimes wearing latex glvoes helps, by increasing seperation between fingers
the chagne in brain responsbiel is that rep of middle fingers expnading, overlapping and displacing rep of index and little finger
so one or more fingers goes into constnatly contraction, and you cant move one finger iwthout moving another
BRAIN DEVLEOPNAD BEHAVIOURAL DEVLEOPMENT
adolescnets like quicker reards than later ones
prefrontal cortex immature in adulescents, but only one reason
most risky behaviours come from those iwth troublesome behaviours
most reisky behaviours are more common towards later teenage years, because brains respones to erwards increasies udirng teenage years
during adolescne adne young adulthood, ppl need to find mates nad compete for sucess adn prosperity
why is immtaurity of the prefrontal cortex not a satisfactory explanation for risky behaviour in adolescents?
as teenage years progress, risky behaviours tend s to increase, even while prefrontal cortex is becoming more mature
OLD AGE
reaosning tends to decline
neurons lose synapses
remaining synapses change more slowly tahn before in esponse to experiences'
thickenss of temporal cortex shrinks by 0.5% a year
ivolume of hippocamps also gradually declines, certain aspects of memory decline in propertion to lss of hippocampus
one factor that increases chance in retaining strong intellect in old age is a genetic predisposition
consistent physical activity, helps
brief intense activity aslo good
STOP AND CHECK
why are reports of declining intellect in old age somewhat misleading?
reports present average, but averag performance is depressed by ppl who are in early stages of alzheimers or other disorders, doesnt include healt age
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