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Brain and thought

QuestionAnswer
brainstem region of brain that connects to spinal cord; comprised of midbrain, pons, medulla
hypothalamus located below the thalamus; regulates homeostatic, circadian, reproductive functions.
cortex the outermost later of the cerebrum
sulci vs. gyri sulci are the grooves in the cortex; gyri are the ridges
somatosensory cortex in parietal lobe
visual cortex in occipital lobe
auditory cortex in temporal lobe
nucleus group of neurons with similar funcitons
glia non-neuronal cell. ratio of 1:1 with neurons in the human brain; ratio of 1:2 in gray matter
soma cell body
dendritic spines protrusion from a dendrite that recieves info from a SINGLE synapse
axon hillock also called the "initial segment" -- the part of the axon that connects to the soma
presynaptic terminals the termination of the axon; also called bouton
synapse the junction of two neurons
synaptic cleft the physical space between the presynaptic and postsynaptic membrane
ligand-gated channel IONOTROPIC, channel-linked receptor (the neurotransmitter binds directly to the channel to open it)
motor cortex "president" -- sends the signal to motor neurons to move muscles.
cerebellum provides feedback on the state of your muscles; sensitive to alcohol
thalamus deciding which information (e.g. sensory) goes where; shuts off during sleep
basal ganglia group of structures (caudate, putamen, GPi and GPe, nucleus accumbens) that is connected to the thalamus and regulates habits
autonomic nervous system part of the nervous system that is responsible for subconscious (involuntary) functions
parietal cortex integrates SPATIAL information -- tells you where you are
temporal cortex associations between things
prefrontal cortex planning, inhibiting inappropriate actions
amygdala crucial role in emotions; such as feeling fear and pleasure
hippocampus responsible for laying down memories. cortex here only has 2 layers!
pituitary gland master gland of the endocrine (hormone) system
suprachaismatic nucleus controls circadian rhythms
pyramidal cell excitatory, long-reaching, spiny
stellate cels excitatory, local, spiny
interneurons inhibitory, local, aspiny
glutamate most common excitatory neurotransmitter
GABA most common inhibitory neurotransmitter; works by opening Chlorine channels on the postsynaptic membrane, thereby allowing Chlorine to enter the cell along with sodium, inducing much less net change in voltage
commisure
meninges
dura protective cover on outside of brain
arachnoid just beneath dura
pia one-cell membrane under the arachnoid
reticulum
Golgi stain reveals neuronal cell bodies
Column functional unit of the cortex
Brodmann he discovered many different Cytoarchitechonic areas
Cytoarchitechture distinct areas of cortex that are slightly different; specialized for diff purposes
heirarchical vs. parallel circuits
networks
olfactory cortex in temporal lobe; has projections to sensory cortex that does NOT go through thalamus. cortex here only has 3 layers
nissl stain reveals and proximal dendrites
voltage difference in electrical charge between the inside and outside of the neuron
conductance
resistance
propagation
reversal potential the voltage at which there is no net flow of an ion across the membrane
myelin series of Schwann cells that wrap around a neuron's axon, insulating it and allowing the action potential to travel much faster. in between the cells there are nodes of ranvier where there is a high concentration of sodium channels.
saltatory conduction the process by which the action potential jumps from node to node
gap junction a space between two neurons that does not use neurotransmitters to relay the message; if the first one fires an action potential, the other does as well
norepinephrine neurotransmitter; catecholamine; binds to alpha2a, alpha1a, and beta receptors. important in the regulation of stress, sleep, feeding, attention. Locus coeruleus.
acetylcholine the neurotransmitter found at neuromuscular junctions
dopamine neurotransmitter; catecholamine; regulates reward/motivation, coordination of movement (basal ganglia!). Substantia nigra, ventral tegmental area.
serotonin neurotransmitter; regulates sleep, important in depression. Raphe nuclei.
neuropeptides a peptide (large molecule) that functions as a neurotransmitter
synthesis creation of new neurotransmitters by specific enzymes
second messengers
EPSP vs. IPSP EPSP is a neurotransmitter-induced change in postsynaptic potential that INCREASES the likelihood the postsynaptic neuron will fire; IPSP is a postsynaptic potential change that DECREASES the likelihood the neuron will fire
summation the idea that whether or not a neuron fires an action potential depends on whether there are enough signals within a short time (temporal summation) or whether other cells synapse simultaneously (spatial tuning)
histamine neurotransmitter; regulates attention and arousal. Hypothalamus.
CT scan shine xrays through head at many different angles; receptors on the other side pick up what it passed through and create a 3d image
PET scan inject radioisotopes with very short 1/2 life; they go to parts of brain that are active and decay; the decay collides with an electron, producing 2 opposite gamma rays
SPECT scan radioisotopes bind to blood cells, go to active areas; decay, and emit 1 gamma ray
X ray 2-d scan of brain produced by shining x-ray through the brain to see what it passed through
MRI use a magnet to line up water protons; then shake them up. they emit energy which is picked up by a radio detector
fMRI deoxygenated vs oxygenated hemoglobin has different magnetic field; therefore, the radio receptors can pick up changes in magnetic field due to changes in blood flow
dorsal horn afferents come into the dorsal horn
ventral horn efferents go out of the ventral horn
afferents nerve pathways going TO the spinal cord/brainstem
efferent nerve pathways going AWAY from the spinal cord/brainstem
cervical arm/back/head/neck
thoracic trunk
lumbar front of legs
sacral back of legs
lower motor neurons (alpha motor neurons) these motor neurons go to the muscles themselves; they are under voluntary control.
gamma motor neurons (gamma loop) these go to the muscle spindles and tell them to keep being sensitive to stretch even if the muscle gets bigger and more contracted. allows you to build muscle
muscle spindles inside the muscle; tells if the muscle is stretched
1a spindle afferent wraps around the muscle; if under passive stretch, it sends info to the
golgi tendon organ fire when your muscle is contracted
synergist vs. antagonist muscles synergist muscle is the muscle that contracts when under passive stretch; antagonist is the muscle that is told to relax. on the other hand, when the GTO tells the synergist muscle to relax and the antagonist muscle to contract
reflex a signal that is sent just to the dorsal horn of the spinal cord, not all the way to brainstem
cortico-spinal tract the nerve tract that runs up and down the spinal cord
upper motor neurons
central sulcus divides the frontal and the parietal lobes
primary motor cortex controls your own actions; sends signal to do something
premotor cortex fire when someone else does something or when you think about doing something
homonculus the image of the man with big lips and hands to show that they are overrepresented in the PMC
topographic organization the primary motor cortex is topographically organized, with the lips and hands being overrepresented bc there are the most receptors there
population response the average response of a group of neurons, not just one neuron
plasticity the connections and functions of many parts of the nervous system change based on experience; e.g. violin player's maps of his hands in SI changed as he played more and more
dorsal root ganglia the part of the dorsal root (afferent from nerve endings to dorsal horn of spinal cord) that contains the cell bodies of the nerves
transduction of mechanical energy into neural signals
proprioception part of the sensory system that gives feedback about the state of YOUR OWN muscles
joint receptors
mechanosensory
rapidly adapting receptors touch receptors that rapidly adjust to a stimulus and stop firing; these highlight changes in your environment. Meissner (superficial) and Pacinian (deep)
slow adapting receptors touch receptors that do not become adjusted; they keep firing if there is constant pressure. Merkel (superficial) and Ruffini (deep)
2 point discrimination
receptive field how spread out a receptor's dendrites are; if it has a small RF, activation gives very specific information; if large RF, doesn't really know where in the RF it was activated; less specific
somatosensory fovea
free nerve ending these are the receptors for nociception; they go to the dorsal horn, crossing right away, and then to thalamus
gating of pain by fine touch your AB fiber for fine touch has a synapse on the dorsal horn projection neuron for the nociceptor, which, when fires, inhibits the nociceptor. so when you activate your AB fiber mechanically, it lessens the amount of pain you feel
opiate peptides, analgesia drugs that lessen pain; e.g. enkephalin. they regulate experience of pain by inhibiting nociceptors. morphine mimics this
thalamic projections to VPL and VPM thalamic projections to VPL give information about the body; projections to VPM convey information about the face
primary somatosensory cortex areas 1, 2, 3a (proprioception), 3b (mechanosensory). information comes to the somatosensory cortices by LABELED LINE
higher order somatosensory cortex SII: first place where both sides are integrated; area 5 (integrates conception about entire body parts), 7b (integrates conception of ENTIRE body -- lesion here in Man Who Fell Out of Bed)
olfactory bulb place in temporal cortex where the axons from the OSNs converge
olfactory sensory neuron bipolar receptor neurons located in the nose. they have cilia that extend from them, and they project to the olfactory bulb. each one expresses only ONE odorant receptor
odorant receptor 7-transmembrane G-protein coupled receptors. each OSN expresses only ONE of these receptors. humans have 350
local circuits
primary afferent synapse
glomeruli located in the Olfactory bulb; the target of the OSNs. it is here that the pattern of activation is read.
external plexiform layer
mitral cell projeciton neurons that recieve sensory information and project it to higher cortical areas (the olfactory bulb)
periglomerular cell regulate (inhibit) input to mitral cells
granule cell regulate output of mitral cells to higher cortical regions
combinatorial code the idea that what scent you're smelling is read as an overall PATTERN of activation in the glomeruli rather than as individual ORs
piriform cortex very simple, 3-layer cortex to which the olfactory bulb projects.
odor ligand odorants are ligands for the odorant receptors
7-transmembrane receptor ORs are this type of receptor
dendrodendritic synapse
cilia microvilli that come out from the odorant receptors that increase the surface area of the receptor
sustentacular cell supporting cell to olfactory system, detoxifies the surrounding environment
basal cells stem cells of the olfactory system; produce new OSNs if some of them die. it's the only sensory neurons that regenerate
5 major categories of taste salty, savory, sour, sweet, bitter (and umami -- unknown)
chemotopy an INCORRECT view of how taste works -- that different parts of the tongue sense different tastes.
taste bud onion shaped structures on tongue and pharynx that contain taste cells
papillae elevations on tongue on which taste buds are: 3 types: fungiform, foliate, circumvallate
taste receptor cells clustered in taste buds. can sense all 5 tastes. send information to the Nucleus of the Solitary Tract
cranial nerves in gustation facial nerve, vagus nerve, glossopharyngeal nerve
amplitude loudness of a sound
frequency pitch of a sound
hair cells the first cells that fire an action potential if mechanically activated
auditory nerve fibers the nerve fibers that are efferent from the hair cells
tonotopy there is a tonotopic organization of frequencies, with labeled lines up to the primary auditory cortex
tympanic membrane ear drum
oval window where the ossicles connect to the cochlea
ossibles the three bones in your middle ear
conductive hearing loss damage to inner ear or middle ear
sensorineural hearing loss damage to inner hair cells
cochlea the most important structure in the ear; snail shaped; filled with fluid. the fluid in the scala media is HIGH in K+; this is where transduction happens. it can also make sound which allows
basilar membrane a membrane in the center of the cochlea; it differs in thickness from the apex (wide, flexible, low frequency) to the base (thin, stiff, high frequency)
tectorial membrane the membrane on top of the hair cells.
stereocilia the actual hair-like protrusions coming off the hair cells. all stereocilia are diffeerent link
tip links the little links between each stereocilium. when the hair cells are moving back and forth, the tip links stretch. when the movement is toward the LONGest stereocilium, the tip links OPEN the channels and K+ rushes into the cell, depolarizing it
endolymph the K+ fluid that is on the top division of the cochlea
perilymph the K+ poor fluid that is on the bottom division of the cochlea
Inner Hair Cell the cells that send 95% of information to the auditory nerve fiber. these are the actual sensory receptors
Outer Hair Cell recieve efferent signals, help with tuning by actively contracting and relaxing
tuning curves for a specific auditory nerve fiber, it shows all the different intensities for different frequencies
characteristic frequency the lowest frequency that an auditory nerve fiber can sense
medial superior olive allows you to localize sounds of low frequency by the time difference it takes to reach the MSO
lateral superior olive allows you to localize sounds of high frequency by the intensity difference or
medial nucleus of the trapezoid body the structure that inhibits the contralateral LSO
primary auditory cortex the part of the cortex that consciously processes sounds
belt areas the parts of the cortex around the primary auditory cortex that process complex sounds (e.g. speech)
visual field what you can see; everything that is hitting your V1 (but NOT everything that you are consciously seeing)
retina the innermost layer of the eye, containing the rods and the cones
cornea outermost covering of the eye
lens the little disk that focuses light
macula the area surrounding the fovea on the retina
fovea the area at the direct center of the retina; rods are pushed away.
photoreceptors (rods and cones) rods are very sensitive to light but they are not very high clarity; cones are very high clarity and can also detect color
ganglion cells the first cell in the visual system that actually fires an action potential. it is synapsed by the bipolar cells and amacrine cells
bipolar cells the cells that receive input from the rods and cones. they respond opposite to glutamate that normal cells do (glutamate is inhibitory)
amacrine cells the inhibitory interneurons of the bipolar - ganglion cell synapse
horizontal cells the inhibitory interneuron on the rods and cones.
lateral inhibition the idea that the photoreceptors surrounding a specific photoreceptor will affect how light or dark it seems, due to the lateral communication between photoreceptors due to horizontal cells
phototransduction photorhodopsin changes shape under light --> transducin --> photodisasterase --> destroys cGMP which was holding sodium channels open --> they slam shut --> cell hyperpolarizes, cell releases less glutamate, BP cell fires more, ganglion cell fires more
rhodopsin the light sensitive photopigment in photoreceptors
On center cell the on center bipolar cell becomes depolarized in response to light because the light hyperpolarizes the photoreceptor, releasing less (here-inhibitory) glutamate, leaving the on-center bp cell free to fire
Off center cell off center bp cell decreases its firing in response to light because hyperpolarization of the photoreceptor means it releases less (here-excitatory) glutamate, meaning that the on-center cell is firing less.
magnocellular cells the big cells in the visual pathway for detecting motion. located in layers 1 and 2 of the LGN of the thalamus.
parvocellular cells the relatively small cells in the visual pathway for detecting color. small visual fields. located in layers 3-6 of the LGN of the thalamus.
Where (M pathway) the pathway ending up in the dorsal parietal cortex, helping you tell where you are / spatial relations.
What (p pathway) the visual pathway ending up in the ventral inferior temporal cortex, helping you make associations / make sense of what you're seeing.
color: single and double opponent ganglion cells
Porjections of the retina ganglion cells to the suprachiasmatic nucleus of hypothalamus for control of circadian rhythms it helps regulate circadium rhythms.
superior colliculcus the superior colliculus is in charge of regulating small eye movements
lateral geniculate nucleus of the thalamus eye information goes here
optic chiasm the first place where the nerves in the optic nerve go
***???*** blobs and stripes ***???*** ***???*** blob detection are specialized for detecting points in the visual field that differ from surrounding ***???***
ocular dominance columns certain neurons respond selectively to input from only one eye or the other; some respond to the difference between the two eyes. ocular dominance columns are crucial for accurately pouncing on your prey!
orientation columns certain neurons in the visual cortex respond selectively to edges of a specific orientation
visual cortical areas V1, V2, V3, V4, MT/V5, 7, IT V1=primary visual cortex. V4=color MT=motion
visual cortical areas v2, v3, 7, IT v3=form 7a=maps of the world with reference points. 7b=integrates visual and somatosensory information
V4 crucial for color processing. color and form are processed separately
IT inferior temporal cortex --> majorly important in recognition. it's recognition independent of spatial location or orientation... like olfactory bulb!!. the IT cortex fires less when something is familiar, and amnesic patients retain this "familiarity"
STS
fusiform gyrus crucial for face recognition. lesions here resulted in prosopagnosia. some people think it is the "face" area, but some people think it is just the "expertise" area, because some people who are experts in "cars" -- this lights up.
parahippocampal gyrus
binocular rivalry different stimuli shown to two different eyes
binding two different aspects of a stimulus are bound together into "object 1." although separate recognition of color and shape happens in temporal lobe, the binding of the two happens in the parietal lobe.
geon a theory that says that all objects are broken down into simple geometric shapes. there are <40 geons, but billions of combinations. this is a "combinatorial" solution to the olfactory problem of billions of smells
degraded image
visual agnosia any deficit in recognition, resulting from damage to temporal lobe. you are AWARE of a stimulus, but you can't say what it IS.
prosopagnosia inability to recognize faces. due to a lesion to your temporal lobe (patient LH)
Mr. P: musicologist in Man Who Mistook, he had severe agnosia. he could not see things, but could not recognize them. learned to recognize by their smell and sound
Rey Osterich figure a complicated image that a patient has to copy correctly. good performance on this task relies on many abilities; much parietal cortex but also PFC; allows assesment of parietal cortex lesions.
V2 depth stripes these compare the difference between the images presented by your two eyes in order to give you a sense of depth
MT area in the parietal cortex that processes movement (by temporal summation??). operates even if anesthetised or asleep. lesion causes you to see things like a slideshow. different columns are for different directions of motion. you have a map of near/far
parietal area 7a area 7a makes maps of the world with reference points -- where things are in relation to each other. need to be conscious
LIP area LIP makes maps that are body-based. need to be conscious
Posner's test of covert visual spatial attention orienting raise your hand if you see a blue square on one side. if you have just seen a red circle, it takes longer to do this bc your attn has been shifted away. this is MAPPED in area 7a!!!
retrograde amnesia forgetting memories you have already made
antereograde amnesia inability to make new memories
declarative memory memory of THINGS: words, events, history
procedural/habit memory priming cues, procedural memory/puzzles, habits, associations
priming when a circuit is used in cortex, more likely to use it again given a specific stimuli
HM and dr. scoville "most instructive man in neuroscience" --> showed that without your hippocampus/medial temporal lobe you CANNOT form new memories
medial temporal lobe located deep inside the temporal lobe. crucial for creating new memories, because it contains the hippocampi
hippocampus cruical for forming new memories bc it amplifies information from the entorhinal cortex
CA1 part of the hippocampus that shows much LTP
dentate gyrus part of the hippocampus that the perforant path from the ER talks to
subiculum
fornix
perforant path the path from the ER to the hippocampus.
entorhinal and perirhinal cortex the ER talks to the hippocampus by way of the perforant pathway. the perirhinal cortex talks to the ER about OBJECT recognition
parahippocampal gyrus the parahippocampal gyrus talks to the ER about SPATIAL recognition
prefrontal cortex the frontmost part of the frontal cortex. crucial for planning, inhibiting inappropriate responses
associative learning a type of LTP which strenthens a synapse if two synapses are fired together (by summation)
LTP and LTD LTP=strengthening of the synapse due to much activation. it is bc new AMPA receptors are inserted into the membrane. also, new spines can form too. LTD=opposite
intralaminar thalamic nuclei and medialdorsal thalamus these project to the medial temporal lobe and put it in "awake" mode. destroyed in korsakoff's amnesia.
mamilary bodies of hypothalamus
Korsakoff's amnesia type of amnesia caused by destruction of the intralaminar nuclei of the thalamus. it is caused by a vitamin B1 (aka THIAMINE) deficiency, most likely seen in chronic alcoholics. causes both antereograde and retrograde amnesia. results in CONFABULATION.
Alzheimer's disease disease in which plaques and tangles affect the ER, disconnecting the hippocamps from the cortex. affects object recognition, spatial recognition, language, pfc. eventually spreads to cortex, destroying retrograde memories as well. VIDEO PATIENT "BOB"
NMDA and AMPA receptors glutamate receptors; new ones are inserted into the postsynaptic membrane in hippocampus in LTP
confabulation telling a story as fact that did not actually happen; you don't know what happened so you sort of "guess" what must have happened.
dementia severe loss of cognitive ability, more than normal aging. to be "dementia" it must have impaired SOCIAL functioning.
apolipoprotein E risk factor for developing early onset AD. depends on number of alleles you have.
beta-amyloid plaques affect ER
neurofibrillary tangles affect ER
immunization experimental treatments
mini-mental status exam ask patient to remember words over a short time; could not do it. ask to tell current events, past events. what day it is. subtract from 100s by 7s.
habit memory
basal ganglia caudate/putamen/globus pallidus/substantia nigra/nucleus accumbens
parallel circuits there is a direct and indirect circuit for regulating habits; they occur in parallel
cognitive loop pfc to caudate to SNpr to thalamus; pfc to caudate to GPe to subthalam to SNpr to thal
motor loop motor cortex to putamen to GPi to thal; motor cortex to putamen to GPe to subthal to GPi to thal
affective loop amygdala to nuc accumbens to ventral palladum to SNpr to thal
subthalamic nucleus this excites the SNpr and GPi, which inhibit the thal. therefore, when it is firing, the thalamus is more excited
Globus pallidus the structures in the basal ganglia that project to the thalamus (direct loop) or to the subthalamic nucleus (indirect loop)
substantia nigra pars compacta dopamine making cells
substantia nigra pars reticulata connected to the GPi; input to thalamus
direct pathway stimulated by dopamine D1 receptors; drives input to thalamus
indirect pathway stimulated by dopaminergic D2 receptors; inhibits input to thal
parkinsons disease the cells that produce dopamine die; too little dopamine. therefore, your BG is not active enough and you have trouble initiating movements
Huntington's disease selective death of the D2 receptors for the indirect pathway. there is not enough fine tuning of your movements; you make jerky movements
Dopamine D1 and D2 receptors D1 is for direct; D2 is for indirect
ventral tegmental area base of midbrain; another place that makes dopamine
amygdala small structure in brain that is responsible for regulating much of our emotional experience; such as fear or pleasure
PTSD a disorder caused by chronic stress, and therefore increased amygdala and NE
central nucleus of the amygdala
stria terminalis
conditioned fear paradigm the idea that you can condition someone to be scared of something even if it was previously neutral, by consistently pairing it with an affective stimulus. LTP in hippocamus: building new spines associated with the stimulus.
extinction if you no longer pair the simulus with the affective one, the condition will go away (LTD)
fear-potential startle
norepinephrine neurotransmitter. made in the locus coerulus. important in governing memory retention and stress response. increased in emotions and stress. fine tunes spatial tuning. alpha1a, 2a, and beta2 receptors
beta adrenergic receptors the highest threshold for NE activation. it acts as a chemical switch to strengthen amygdala under stress conditions. blocker is propranolo
alpha1a receptor second highest threshold for NE activation. also chemical switch. blocker is prazosin
alpha2a receptor low threshold for NE activation. if stimulated, acts as a swich OFF for amygdala function.
propranolol blocker for beta 2 receptors
prazosin blocker for alpha1a receptor
guanfacine stimulator for alpha2a receptor
Reversal learning
Extinction
Orbital PFC
Frontal pole
SSRI
ketamine
Created by: catikinz
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