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neural plate
nursery of stem cells that becomes neurons
notochord
embryonic/primitive midline
becomes SC & vertebrae
spokes
radial glial cells only present during development
guide newly born neurons
leading & trailing processes of neuron wrap around radial cells to move
neural crest striations
telencephalon
becomes neocortex of frontal lobe
diencephalon
becomes thalamus & hypothalamus
mesencephalon
becomes midbrain
rhombencephalon
becomes hindbrain (medulla, pons)
neurogenesis
mitotic division of non-neuronal cells (stem cells) to produce neurons
neurons born near central canal
cell migration
movements of cells to establish distinct neuronal populations
differentiation
stem cells specialize into different types of neurons or glial cells in different areas of the brain
synaptogenesis
establishment of synaptic connections
apoptosis
cell death after not connecting
synapse rearrangement
loss of some and development of other synaptic connections
ventricular zone
near central canal (eventually ventricular system)
neurons & glial cells form up until birth (a little after)
dentate gyrus
part of hippocampus
1 place in the brain with continuous neurogenesis through its lifespan
memory formation, maintaining memories, resilient against effects of stress & trauma
cell adhesion molecules
AKA CAMS
released by spokes part to stick & climb to migrate
Migration Failiures
reduced cell populations, disorderly arrangements, and behavioral disorders
autism, down syndrome, fragile x syndrome, schizophrenia
cell autonomous
gene itself in neuron gets expressed and become that neuron no matter where it is
independent of neighboring cells
predetermined migration
ex. Cerebellar Purkinje Cells
induction
differentiation (fate) dependent upon neighboring cells
needs signal from outside the cell to tell it what to become
ex. spinal motor neurons.- influenced by chemicals (ex. sonic hedgehog-protein)
growth cone
extends and has chemical sensors
lamellipodia
thin, flat, sheet-like membrane protrusions found at the leading edge of migrating cells
filopodia
projections of growth cone like “sniffers” looking for chemical signals
chemoattractants
“grow near me”
chemorepellents
“grow around me”
central canal becomes ___ ___, central canal = ____ ____
neural tube, lateral ventricles
embryonic layer that the NS originates in
ectoderm
18 days
neural stem cells
notochord
neural plate
20 days
central canal
neural crest
22 days
canal becomes neural tube
central canal —> lateral ventricles
24 days
telencephalon - becomes neocortex of frontal lobe
diencephalon - thalamus & hypothalamus
mesencephalon - midbrain
rhombencephalon - hindbrain (medulla & pons)
41 weeks
term pregnancy
brain structure of a 1 week old newborn
full structures & gyri and sulci
Postnatal Synapse Development
1st year - tremendous synaptic growth
First 5 years - most important for developing connections in the brain
microdimene
calcium channels & receptors that compartmentalize the functions of calcium
calcium
signal for apoptosis
cell destroys its own membrane
membrane collapses
microglia (etc) gobble up waste
proteases - 3 caspases ready to go but with a “parking break” on
IAP proteins
inhibitor of apoptosis proteins
“parking breaks” for proteases
diablo protein
release IAPs and allows apoptosis to continue
activated by calcium release from mitochondria
caspases
proteases which are protein-dissolving
3 types
neurotrophic factor
chemicals that promote cell survival and growth
support life
Types: nerve growth factor, brain-derived nerve growth factor, neurotrophin
nerve growth factor
type of neurotrophic factor
discovered by Rita Levi-Montalcini
spinal ganglia and sympathetic nerve ganglia
amount NGF released correlated with amount of innervation
brain-derived NTF
type of nerve growth factor
important in neural plasticity, learning, memory, normal function
involved in anxiety & depression disorders
important for life
neurotropins
type of nerve growth factor
family of NGF-like molecules
fluid mosaic model
describes the structure of the plasma membrane as a flexible lipid bilayer with protein, cholesterol, and carbohydrate molecules floating and moving laterally within it
2-way communication
presynaptic neuron takes in neurotropic factors from postsynaptic neuron, and vide versa
failing of neurotropic factors can trigger ___
apoptosis
intrinsic
factors within a cell
genes
extrinsic
factors outside the cell
nutrients, cell-to-cell interactions
genotype
sum of all genetic information
NATURE
phenotype
sum of all physical characteristics
interaction of genotype and extrinsic factor
NURTURE
epigenetics
nature vs nurture to shape a whole person
environmental factors (internal/external) interacting with genetics
life experiences can switch on/off certain genes at certain times to affect phenotype
mutations
sudden usually random change in genetic structure
related to marked anatomical/physiological change
could’ve been induced by chemicals or radiation
mutants
animals with altered genes
great subjects: links genes, proteins to anatomy, physiology, & behavior
trasnsgenic and knock-out mice
site-directed mutagenesis (mutation in 1 gene)
critical developmental periods
sensitive periods of time for development (like a window)
visual deprivation
blindness
amblyopia
double-vision in one eye caused by misalignment of the eye in the orbit
AKA lazy-eye
can be surgically corrected if sone before 7-8 y/o
realignment in adulthood does not restore normal vision because of reduced plasticity
binocular deprivation
causes loss of dendritic spines and reduction in synaptic density in visual cortex
monocular deprivation
caused profound structural and functional changes in the thalamus and visual cortex (in cats)
Hubel & Wiesel’s Experiments
altered ocular dominance
response strength of a visual neuron to stimuli presented to either the L or R eye
predominance of neurons that respond to input from one eye
cells: usually equally excited by either eye
need sustained light activity eyes
loss of NTF - some cats had BDNF injected and this resulted in a healing effect
primary visual cortex
in the occipital lobe
ocular-dominance columns
neurons respond preferentially to one eye
arranged like columns
all receive input from L & R eye
- left column dominant left eye input (& vice versa)
collateral sprouting
axon grows more axons and connects more
Phenylketonuria (PKU)
recessive hereditary disorders of protein metabolism
may cause mental retardation
Preventative measures
diet low in phenylalamine, especially before age 2 (gene can be found, single-gene issue)
Mechanism
aa (phenylalanine) —> protein —> clearance mechanisms can have too much or if they fail, accumulation of excess aa/protein —> clump & clog, push on neurons/glia —> kill cells
enzyme lacking to break down phenylalanine
Down Syndrome
trisomy 21 (extra chromosome 21)
related to age of mother (>45 = 1/40)
IQ ~80, sometimes higher
cortical abnormalities - brain looks older, resembling Alzheimer’s
abnormal dendritic spine formation
physical abnormalities
Fragile X Syndrome
inherited mental retardation (mild - severe)
long arm of X chromosome breaks off
Features: elongated face, large ears, prominent chin
more common in males (penetrance bc of 1 available X)
Fragile sites = CGG (trinucleotide repeat)
Autism
life-long developmental disorder with impaired social competence
language and a narrow range of activities and interests
spectrum disorder
low functioning/nonverbal —> high functioning/IQ (Aspberger’s)
Brain differences in Autism
smaller corpus callosum & cerebellar regions = delays in motor development & cognitive skills, gait
developmental differences in hippocampus (smaller)
developmental differences in amygdala (bigger)
ASD Rise in Diagnoses (possibly) Caused by…
overdiagnosis in recent times
underdiagnosis in previous times
environmental changes
vaccines (no)
age of parent
Neural Changes During Aging
myelin thickening
slower processing/memory
hippocampus shrinkage
Alzheimer’s Disease - type of dementia
Alzheimer’s Disease
type of dementia
faliure of cognitive abilities: memory, orientation, identity loss
probability increases with ages above 85
no definitive diagnoses until autopsy
Causes & Mechanism of Alzheimer’s Diseas
loss of dopaminergic and cholinergic neurons, receptors, or connections throughout the cortex
3 major characteristics
senile plaques
neurofibrillary tangles
basal forebrain nuclei disappear
senile plaques
build-up of a protein called beta-amyloid
beta-amyloid
protein at which normal levels healthy for a brain
neurofibrillary tangles
abnormal twisting and binding of neurofilaments, including tau proteins
basal forebrain nuclei
disappear in Alzheimer’s due to plaques and tangles
Pathology of Alzheimer’s Disease
ApoE binds & clears excess amyloid
if too much excess beta-amyloid, plaques form and make neurofibrillary tangles
loss of basal forebrain produce acetylcholine
dementia
hormones
chemical messengers
released into bloodstream to circulate into the body
only act on tissues that have specific receptors
endocrine glands
organs that make and release hormones
autocrine
release chemical that feeds back to itself to regulate
paracrine
group of cells in system that release chemical messenger that only affects nearby cells
endocrine function
make hormone, release it into bloodstream, bloodstream delivers to target organ/receptor for hormonal action
Principles of Hormone Action
gradual time course - hours to weeks
a little goes a long way, gene transcription/translation occurs
Changing intensity/probability of behavior
does not direct behavior, more like a dimmer switch
type and amount of hormone depends on environment
reciprocal relationship
each hormone has multiple effects on various tissues, organs, and behaviors
diametrically opposed actions on the same organ are possible
produced in small amounts & secreted in bursts
levels vary rhythmically during the day
hormones interact with other hormones
chemical stricture may be similar across species but function may vary
can only affect cells that have specific receptors for that hormone
protein horomones
hormones made of long aa chains
FSH, LH, TSH, GH, prolactin, insulin, oxytocin, vasopressin
protein receptors embedded into plasma membrane that activate 2nd messengers
amine hormones
hormones made of a N-H group
epi, norepi, melatonin
protein receptors embedded into plasma membrane that activate 2nd messengers
steroid hormones
gonadal hormones
cortisol (glucocorticoid)
lipid soluble, pass directly into membrane, interact with intracellular steroid receptors → change gene transcription
autocrine feedback
endocrine cell makes & releases hormone
makes target cell
endocrine cell says '“enough”
shuts down until needed again
target cell feedback
endocrine cell makes hormone
makes effect on target cell
target cell makes secondary biological response that feeds back onto endocrine cell to
shuts endocrine cell down
brain & pituitary regulation
hypothalamus has releasing hormones—neurons that release hormones into blood stream by pituitary gland
activates & releases tropic hormone
tells other glands to make & release their main hormone
released to target cell
response
hypothalamus, pituitary gland, and double-mechanism shuts down hormone release
pituitary gland
primary hormone is oxytocin
oxytocin
primary hormone of pituitary
milk-letdown reflex
bond between mom & child
milk-letdown reflex
nerve impulse to brain to release oxytocin
causes cells of mammary glands to contract/milk release, baby continues suckling
posterior pituitary gland
neurohypophysis & hypothalamus axons extend to posterior pituitary, make and release hormones that release directly into the local bloodstream —> body
anterior pituitary gland
adenohypophysis; neurons shorted axon, pump hormone into local blood supply and corticotropic releasing hormones direct pituitary cells to release trophic hormones
GNRH
releasing hormone of hypothalamus
release LH & FSH tell cells to release sperm & egg