exam 2 Flashcards
first stage of neuron development
proliferation
second stage of neuron development
migration
third stage of neuron development
differentiation
fourth stage of neuron development
myelination
fifth stage of neuron development
synaptogenesis
proliferation
what is it?
when does it occur?
(1)
production of new cells in brain
occurs mostly in early life
when do stem cells begin to develop
after 20 weeks
migration
what is it?
what happens if harm occurs?
(2)
movement of the newly formed neurons/glia to their eventual locations
harm = permanent deformations
what chemicals guide neuron migration?
immunoglobulins and chemokines
radial glia aid
homeobox genes
what do they do?
what do mutations here do?
influence migration patterns
regulate expression and control start of anatomical development
mutation = brain disorders, physical deformities
differentiation
what is it?
order?
(3)
forming of the axon and dendrites that give the neuron its distinct shape
1. axon (during migration or after reaching target)
2. dendrites
myelination
what is it?
when does it occur?
where does it occur?
(4)
process by which glia produce the fatty sheath that covers the axons of some neurons
occurs: gradually for decades
occurs: spinal cord to hindbrain to midbrain to forebrain
glia important for myelination
oligodendrocytes (CNS)
Schwann cells (PNS)
synaptogenesis
what is it?
when does it occur?
when does it slow?
(5)
formation of synapses between neurons
occurs: throughout life
slows: in later life (significantly)
stem cells
undifferentiated cells found in the interior of the brain that generate daughter cells that can transform into glia or neurons
where are new neurons formed most primarily throughout life? why?
basal ganglia and hippocampus
because these areas are linked with memory and facilitate learning
diaschisis
decreased activity of surviving neurons after damage to other neurons – thus disrupts patterns of normal stimulation because of connection losses
recovery mechanisms for brain damage
axon regrowth and axon sprouting
axon regrowth
facilitated by glia cells
axons can only grow from cell-body side
axon sprouting
uses neurotrophins to lead axons to form collateral sprouts
what steers axons towards their targets?
chemical gradients
neural darwinism
we start with many neurons & synapses, but over time we keep & reject specific combos
the brain wires itself
neurotrophins
chemicals that promote the survival and activity of neurons
(essential for for axon/dendrite growth)
nerve growth factors (NGFs)
proteins sent from target regions back to the neuron attached to it to promote survival and growth
sensation
(sensory systems model)
input for receptors
sent to thalamus
sent to primary sensory cortex
perception
(sensory systems model)
input from primary sensory cortex sent to secondary sensory cortex
sent to association cortex
descending pathways
(in our current sensory model!)
higher levels of sensory systems can influence sensory input
rods
where?
used in what light?
detects what?
where: periphery
light: faint/dim light (bright bleaches them)
detects: patterns
cones
where?
used in what light?
essential for?
where: in/near fovea
light: bright
essential for: color vision
photopigments
what are they?
where are they?
present in both rods and cones
chemicals that release energy when exposed to light
bipolar cells
important for?
connects to?
where?
important for perceiving detail
receptors connects to bipolar which in turn connects to ganglion (the mid-layer)
located near center of eye
the visual path within the eye
net effect?
receptors send their messages to bipolar and horizontal cells, which in turn send messages to amacrine and ganglion cells. The axons of the ganglion cells form the optic nerve
net effect: excitation of the bipolar cell and inhibition of the surrounding bipolar cells
ganglion cells
important for?
connects to?
where?
important for perceiving detail
connects to bipolar cells (the deepest layer)
located near the fovea
horizontal cells
excited by?
inhibits?
why are they considered local?
where are they?
excited by light
inhibits the surrounding bipolar cells
they are local: no axon, no action potentials, therefore the depolarization decays with distance
located between receptors and bipolar cells, perpendicular
lateral inhibition
explained concisely?
used for?
the reduction of activity in one neuron by activity in neighboring neurons
used for heightening contrast
circular receptive fields
occur where?
describe?
in ganglion cells (retina), LGN cells (thalamus)
bullseye of excitation, surrounding circle is inhibitory
bar receptive fields
occur where?
what kinds of zones?
in simple cells (visual cortex)
zones: fixed excitatory and inhibitory – specific orientation
what are amacrine cells for
fine-tuning
retina
where?
how many receptors?
located at the back of the eye
has most of the cells (lined with receptors)
fovea
purpose?
kind of axons?
cones or rods?
for acute/detailed vision
axons are thin/unmyelinated, and go directly to the brain (receptors use just one axon)
high concentration of cones
blindspot
where?
why?
receptors?
located at the optic nerve
created by axons leaving & blood vessels blocking
no receptors here
magnocellular pathway
dorsal or ventral?
through which lobe?
where or what?
for (elaborate)?
large or small ganglion?
dorsal
parietal lobe
the “where” path
for visually guided movements
large ganglion cells go to LGN
parvocellular pathway
dorsal or ventral?
through which lobe?
where or what?
for (elaborate)?
large or small ganglion?
ventral
temporal lobe
the “what” path
for fine detail (color), recognizing objects
small ganglion cells go to LGN
primary visual cortex
where?
role in visual pathways?
in occipital lobe
pathways from retina go here
information may get sent back to thalamus for refining, then sent back to PVC
LGN
what is it?
where?
role in visual pathway?
lateral geniculate nucleus
in thalamus
most ganglion cell axons go here
superior colliculus
role in vision?
where?
some ganglion cell axons go here
in the midbrain
physics : amplitude
perception : ?
loudness
physics : frequency
perception : ?
pitch
physics : complexity
perception : ?
timbre
steps of auditory perception
- sound enters
- sound strikes tympanic membrane
- auditory ossicles
- displace hair cells on cochlea
- action potentials on auditory nerve
pitch perception
low frequencies: basilar membrane vibrations in synchrony with waves
high frequencies: neurons fire at some of the waves, but are phase-locked at the peak of cells
volley principle
the auditory nerve as a whole can have volleys of impulses up to about 4,000 Hz per second
primary auditory cortex
organized how?
damage?
tonotopically organized
damage = issues with speech/music
secondary auditory cortex
what does it do?
neurons respond to complex combinations of sound
posterior speech cortex
what does it do?
which Area is here?
finalizes speech processing
Wernicke’s Area (speech comprehension)
middle-ear deafness
another way to describe?
can’t hear others well but…?
role of auditory ossicles?
temporary or permanent?
what can help?
conductive deafness - can hear themselves clearly
auditory ossicles fail to transmit sound waves
sometimes temporary
sometimes hearing-aids help, or even surgery
inner-ear deafness
results from damage to what?
what happens to perception?
how is this obtained?
what can help?
damage to cochlea, hair cells, or auditory nerve
impairs hearing of certain frequencies
can be inherited, from disease, or exposure to loud noises
hearing aids can help
flavor
taste and smell
taste receptors
modified __?
excitable or inhibitory?
modified skin cells
excitable
release neurotransmitters
transmit information
taste buds
what are they?
where are they found?
how many papillae?
name the papillae
bundles of 50+ taste receptors
found mostly along sides of tongue – none in center
3 papillae
1. circumvallate
2. foliate
3. fungiform
medial superior olives
what are they for?
what do they do?
for sound localization
they respond to the difference in time of arrival between ears
lateral superior olives
what are they for?
what do they do?
for sound localization
they respond to the difference in amplitude of sound between ears
superior colliculus
role in audition?
where?
map of auditory space, directs head and eye movement
located in midbrain
pathway of taste that uses cranial nerve 7
and is it first or second?
damage here?
another name for cranial nerve 7’s branch?
from the anterior part of tongue to the brain
the first path
damage = inability to taste saltiness
branch: chords tympani
pathway of taste that uses cranial nerves 4 & 5
and is it first or second?
from cranial nerves 4&5 to tractus soliatirus (the NTS in medulla), then to many other places (such as pons, hypothalamus, thalamus, insult, etc.)
the second path
olfactory cells
responsible for?
where?
where are dendrites?
responsible for smell
line the olfactory epithelium, at the rear of the nasal passage
dendrites are in the mucous surface of the nasal cavity (like cilia)
olfactory receptors
where?
how often do they change out?
how fast is the adaptation?
located on the dendrites/cilia of olf. cells
they replace monthly (about)
adapts to scents rapidly
circumvallate
what and where?
papillae for bitter
located at posterior central of tongue
foliate
what and where?
papillae for salty
located at lateral sides of tongue
fungiform
what and where?
papillae for sweet and sour
located at anterior of tongue
(highest density of buds at tip)
main olfactory detection signaling
present in who?
how fast does it adapt?
present in both humans and animals
adapts quickly to continuous odors
uses olfactory bulb
vomeronasal olfactory detection signaling
purpose?
present in who?
how fast does it adapt?
for responding to pheromones
present in mostly animals
does not adapt to odors
list all (4) skin sensory receptors
free nerve endings, pacinian corpuscles, Merkel disks, Ruffini endings
free nerve endings
what kind of cell?
senses what, specifically?
skin receptor
simple cell
for pain and temperature
pacinian corpuscles
what kind of cell, and fast or slow?
senses what, specifically?
skin receptor
large, fast-adapting
for understanding surface texture
merkel disks
fast or slow?
senses what, specifically?
skin receptor
slow-adapting
for light touch, detecting shapes/textures
Ruffini endings
fast or slow
senses what, specifically?
skin receptors
slow-adapting
for shapes and textures
spinal cord nerves
where?
route of sensory info?
touch receptors below the head
carries info through dermatomes (spinal cord to thalamus to primary cortex)
cranial nerves
where?
touch receptors in the head
final destination of sensory information
primary cortex
dorsal columns-medial lemniscus tract
what senses does it detect?
describe the axons?
when does the info cross over?
detects touch, vibration, and pressure
axons are thick and myelinated, for quick signals
info crosses over in the medulla after entering the dorsal spine
spinothalamic (anterolateral) tract
what senses does it detect?
describe the axons?
when does the info cross over?
detects pain, itch, and temperature
axons are a combination: thin and unmyelinated are for dull pain, thick and myelinated are for sharp pain
info crosses over immediately in the spinal cord after entering the dorsal spine
what neurotransmitter(s) are used for dull pain?
glutamate
what neurotransmitter(s) are used for sharp pain?
glutamate and substance P
which part of your body do opioids affect?
central nervous system (the brain primarily)
opioids..
release __:
block __:
release endorphins
block substance P
what are endorphins
endogenous morphines
gate theory
non-pain stimuli can reduce pain
in other words: spinal cord input from the brain and touch receptors can close the gates on pain messages – done partly by releasing endorphins
cannabinoids
use what neurotransmitter?
affects which part of your body?
uses capsaicin
affects the PNS
motor cortex is where in relation to the somatosensory cortex?
directly anterior
somatosensory cortex
how many cell layers for touch?
for sensation or experience?
4 cell layers
for the experience of touch
secondary somatosensory cortex
two primary uses:
tactile object recognition
memory
motor cortex
axons from here go where?
for what kinds of actions?
active when moving AND ALSO…
axons go directly to brainstem/spinal cord
for complex actions (walking, talking, etc.)
some actions have less control (laughing, coughing, etc.)
active even when imagining/remembering movements
all 3 cortices for planning movement are ___ cortices
secondary
3 cortices known for planning movement
prefrontal cortex, premotor cortex, posterior parietal cortex
prefrontal cortex and planning movement (3)
damage?
organizes rapid sequences of movements
considers probable outcomes
stores past sensory info
damage = disorganized movement
(includes supplementary motor cortex)
supplementary motor cortex
in what main cortex
does what in regard to planning movement
in the prefrontal cortex
inhibits habitual actions
premotor cortex and planning movement (1)
when is it active?
integrates information about the body and the target
active right before movement
posterior parietal cortex and planning movement (2)
damage?
monitors position of body relative to the world
active with intention to move
damage = can’t find obstacles in space
what are the 2 corticospinal tracts and what exactly are these pathways
medial and lateral
these are pathways from the cerebral cortex to the spinal cord
lateral corticospinal tract
axons from motor cortex to?
do the axons cross over? why or why not?
movement of?
axons to target neurons in spinal cord
crosses over in medulla pyramids, because the movement is on only one side of the body (ex: your right arm)
movement of extremities (hands, feet)
medial corticospinal tract
axons from motor cortex to?
do the axons cross over? why or why not?
movement of?
axons to midbrain/vestibular system
axons do not cross over, because the movement is on both sides of the body
movement of trunk, neck, shoulders
cerebellum (little brain)
what does it control?
damage?
(has the most neurons here than anywhere else in the brain)
controls aim, timing, start/stop movement, balance, coordination
plays a role in movement duration
damage = impairs rhythmic movement, difficulty pointing at moving objects
what is Parkinson’s disease?
spontaneous/involunatry movements are slow/weak
parkinson’s disease cause and treatments
28 gene variants in the substantia nigra (part of the basal ganglia)
there’s a gradual loss of dopamine-releasing axons from the substantia nigra to the striatum
this leads to the striatum to decrease inhibition of globus pallidus
this then increases inhibitory input to the thalamus
treatments include: L-Dopa (a precursor to dopamine) and gene therapy
circadian rhythm
how long is this rhythm?
regulates what?
purpose?
controlled and sharpened by?
about 24 hours long
regulates: sleep/wakefulness, body temperature, hormone secretion, frequency of eating
purpose: keep our internal workings in phase with the outside world
controlled by genetics (innate) and sharpened by light
zeitgebers
and examples?
a stimulus that resets our internal clock
ex: light, exercise, noise, meals, temperature
suprachiasmatic nucleus (SCN)
what is it?
where?
purpose?
our biological clock
located in thalamus
for driving rhythms in sleep and body temperature
does our body temperature increase or decrease at night
decrease
is phase advancement or phase delay easier for us
phase advancement
jet lag, going forward in time
what 2 areas are involved in the retinohypothalamic path?
optic nerve and SCN
retinohypothalamic path
what is the path?
created with?
what is unique with ^?
light travels directly from retina to the SCN via a small branch in the optic nerve called the retinohypothalamic path
created with ganglion cells
these cells have a unique photopigment called melanopsin (does not require input from rods/cones)
the 2 genes involved in sleep
Period and Timeless
when are Period and Timeless upregulated
throughout the day, peaking just after sunset
what proteins does Period create?
describe their daily pattern?
protein PER
concentration of PER increases after sunset, falling at sunrise
what proteins does Timeless create?
describe their daily pattern?
protein TIM
concentration of TIM increases after sunset, falling at sunrise
melatonin
what is it?
secreted and regulated where?
secreted when?
hormone that increases sleepiness
secreted through the pineal gland and regulated by the SCN
secreted 2-3 hours before bedtime (taking melatonin in afternoon is optimal)
what are the 6 stages of sleep in order
awake, stage 1, stage 2, stage 3, stage 4, REM
awake stage of sleep
describe the brainwaves?
describe the brainwaves during relaxation?
beta waves: fast frequency, low amplitude (15-20 Hz)
relaxed = alpha waves: 8-12 Hz
stage 1 of sleep
heart rate slow or fast?
describe brainwaves?
length?
heart rate begins to slow
waves: irregular frequency, smaller amplitude, vertex spikes
about 1-7 minutes long
stage 2 of sleep
occurrence of what 2 phenomenons?
length?
sleep spindles (12-14 Hz): occur in bursts, increase after new learning, correlated with improved memory
k complexes: sharp negative EEG potentials, temporary inhibition of neuron firing
about 10-25 minutes long
stage 3 of sleep
describe brainwaves?
length?
beginnings of delta waves: large amplitude, slow waves – occur about once per second
sleep spindles continue
several minutes long
stage 4 of sleep
describe brainwaves?
delta waves: large amplitude, slow waves – occur about half the time
night terrors
what are they?
when do they occur?
sudden arousal from stages 3 and 4 of sleep due to fear and autonomic activity
when does sleep walking occur?
stages 3 or 4
stage REM of sleep
describe brainwaves?
describe dreams?
waves: small amplitude, high frequency – like being awake
relaxed muscles – “paradoxical sleep”
dreams are vivid
nightmares
what are they?
when do they occur?
waking during REM due to a frightening dream
when does sleep talking occur?
REM
what are the 4 reasons for why we sleep
energy conservation, predator avoidance, body restoration, memory consolidation
ascending reticular activation system (ARAS)
what is reticular formation?
axons go where?
pontomesencephalon?
structure in midbrain that extends from the medulla into the forebrain
axons go to both brain and spinal cord
pontomesencephalon area maintains arousal in wide regions of cerebral cortex
damage to the basal forebrain?
decreased arousal (can be caused by electrical stimulation)
impaired learning and memory
induced insomnia (from a lesion)
severe damage = Alzheimer’s disease
damage to hypothalamus?
disorganized sleep (from loss of hypocretin, a neurotransmitter, that regulates sleep patterns— narcolepsy)
antihistamines cross blood-brain brain and cause drowsiness
symptoms of narcolepsy?
gradual or sudden attack of sleepiness
occasional cataplexy
sleep paralysis
hypnagogic hallucinations
cataplexy
muscle weakness caused by strong emotions
hypnagogic hallucinations
dreamlike experiences, difficulty distinguishing from reality
causes of narcolepsy?
lack of hypothalamic cells that release and produce orexin
treatments of narcolepsy?
stimulant drugs that increase wakefulness by enhancing dopamine and norepinephrine activity
homeostasis
any self-regulating biological process that keeps the body variables within a fixed range
set point
a single value that the body works to maintain
negative feedback
processes that reduce discrepancies from the set point
allostasis
the adaptive ways in which the body anticipates needs depending on situation
advantages of a 98.6 degree F set point
warmth benefits muscle activity
ready for vigorous activity
why is our body temperature set point (98.6) not higher?
it would require more energy
proteins would denature
our reproductive cells need cooler temperatures
what 2 areas regulate our temperature?
pre-optic area (POA) and anterior hypothalamus (AH)
what do the POA and AH do?
receive input from temperature receptors throughout body
(primary for shivering and sweating)
fevers
directed by?
decrease __?
increase __?
directed by hypothalamus
decreases bacterial growth
increases immune system activity
what does the insulin & glucagon system regulate?
the I&G system regulates the flow of glucose into liver and fat cells
where is insulin and glucagon synthesized?
pancreas
as blood glucose increases…
insulin increases
insulin helps…
so then hunger…
glucose enter cells for use or storage.
… hunger decreases
as blood glucose levels decline…
insulin levels decrease
as insulin levels decrease…
glucagon increases
hunger increases
if stored supplies of glucose (glycogen) are brought into the blood (as glucagon increases), what does this affect?
it slows the return of hunger
lateral hypothalamus (LH)
damage?
lesion to the tracts?
lesion to the nucleus?
stimulation?
damage = refuse to eat, may survive if force-fed
lesion to tracts = stops eating/looking for food
lesion to nucleus = loss of feeding entirely
stimulation = increase of feeding and food seeking
ventromedial hypothalamus (VMH)
damage?
damage = overeating and weight gain, increase of insulin
frequent snacking
damage to ventral noradrenergic bundle leads to the greatest excess of eating
paraventricular nucleus (PVN)
damage?
damage = overeat during meals, insensitive to signals that end meals
arcuate nucleus (ARC)
damage?
damage = disrupts energy homeostasis; extreme weight loss or gain
damage hunger neurons = weight loss
damage satiety neurons = weight gain
hunger is guided by which neurons?
NPY/AgRP neurons
hunger cells inhibit what?
they inhibit PVN, and PVN inhibits LH, leading to a net excitation that gives us hunger
satiety is guided by which neurons?
POMC/CART neurons
satiety hormones (3)
CCK, insulin, leptin
rhodopsin is where
what is it
in rods
it’s a photopigment
photopsin is where and what is it
in cones and it’s a photopigment
optic chiasm
where the axons cross over in the optic nerve
what are the auditory ossicles
tiny bones in ear
