Human NeuroPsych Exam 2

Ganglia

cluster of cells found in the PNS

Diseases when you damage basal ganglia

Huntington's disease and Tourette's syndrome

Huntington's disease

genetic disease that causes dance like movements or tics you can't control

What is the repeat in Huntington's disease

trinucleotide repeat on chromosome 4

Huntington's disease and the striatum

massive death in the striatum—lose 90% of it, causes enlarged ventricles, enlarged ventricles lead to atrophy of other parts of the brain

Tourette's syndrome

more subtle damage to the basal ganglia, causes coprolalia and copropraxia, the less socially appropriate the situation the more likely to engage in these behaviors

Damage to hippocampus

can only keep memory for a short amount of time

H.M. case study

had hippocampus removed on both sides of brain to prevent seizure focus from growing, lead to him developing sever anterograde amnesia

Cortisol and the hippocampus

hippocampus has highest density of cortisol receptors of any brain structure, part of negative feedback loop (stress thermostat), if cortisol levels get too high the hippocampus sends message to hypothalamus to turn down cortisol levels

High levels of cortisol

can lead to shrinking of the hippocampus, can harm the ability to shut of the stress response

Damage to amygdala

people cannot feel fear, don't remember what fear felt like before the damage, can't recognize fear in others

Kluver-bucy syndrome

no fear, memory problems, oral tendencies, hypersexuality

Thalamus

diencephalic structure, best known for being sensory relay station for nearly all sensory modalities, also has motor nuclei and nuclei for emotion

Sensory modalities in thalamus

sight, touch, hearing, taste, vestibular function (sense of balance), and proprioception (knowing where your body parts in space and having a sense of ownership over them)

Only sensory modality that doesn't go to the thalamus

olfaction—it goes straight to the cortex

Corpus callosum

biggest fiber bundle that crosses from one side of the brain to another

When would you cut the corpus callosum

to prevent a seizure focus from growing to the other hemisphere—you can develop a seizure focus perfectly symmetrical to the first so cut the corpus callosum to prevent this

Fornix

white matter tract that connects hippocampus to mammillary bodies, structure is part of the hypothalamus

Korsakov's syndrome

caused by damage to the mamillary body, usually from chronic alcoholism, arrives from a thiamine (vitamin B) deficiency, causes the person to develop anterograde amnesia and confabulation (making up stuff that's not true)

Jimmy from Man Who Mistook His Wife for a Hat

had anterograde amnesia from Korsakov's, was shocked when he saw his brother—thought he looked so old

NA case study

military man who turned into letter opener, it went in through his nose and into the brain, damaged his anterior nuclei of thalamus causing anterograde amnesia

Phantoms from Man Who Mistook His Wife for a Hat

phantom sensation in his prosthetic—for him it made prosthetic use easier, could use his prosthetic better when he had phantom sensations

Thalamic Nuclei

divided into 3 parts by white matter—sensory, motor, and limbic nuclei

Internal Capsule

made up of reciprocal fibers between the thalamus and cortex

3 hypothalamic zones

lateral, medial, periventricular

Lateral hypothalamic zone

not well defined nuclei, cells involved in cardiovascular function and regulation of food and water

Medial hypothalamic zone

has well defined nuclei—chiasmatic region, tuberal region, mammillary region

Chiasmatic region

important in hormone release and cardiac function

Tuberal region

nuclei affect hormone release and feeding

Mammillary region

cells doing temperature regulation, blood pressure, feeding, and memory formation

Where does the hypothalamus speak to much of the body

pituitary gland

Anterior pituitary hormones

FLAT PG, Follicle stimulating hormone, Luteinizing hormone, Adrenocorticotropic hormone, Thyroid stimulating hormone, Prolactin, Growth hormone

Posterior pituitary hormones

vasopressin and oxytocin

Who came up with the idea of limbic

Broca

Broca's limbic system

limbic = bordering the brain stem, thought the structures in the system had to do with olfaction

Limbic system now

refers to a group of structures that affect emotions, refers to a unity that doesn't exist and people don't agree on what should be considered part of the limbic system

Papez Circuit

circle of structure that were originally part of a circuit that Papez defined as an emotion structure

Structures of the Papez circuit

neocortex, cingulate cortex, hippocampus, hypothalamus, anterior nuclei of thalamus

Dentate gyrus

one of the hotspots for adult neurogenesis

Lentiform nucleus

putamen and globus pallidus

Striatum

caudate nucleus and putamen

Where is the insular lobe

beneath the sylvian fissure

Sylvian fissure

divides temporal lobe from frontal and parietal lobe (lies horizontally)

Brodmann's map

most famous cytoarchitectural map, found that layer patterns were different from one area of the brain to another

Brodmann's area 14

primary motor cortex

Brodmann's area 1,2,3

primary somatosensory cortex

Brodmann's area 17

primary visual cortex

Brodmann's area 41

primary auditory cortex

Wilder Penfield

would get informed consent from patients to take an electrode and stimulate parts of the brain around the place he was operating on, stimulated parts of the brain and had the patient tell him what they were feeling, created a map of body on the sensory and motor cortexes—motor and sensory homunculi

What happens to the part of the cortex that controls the hand if the hand is amputated

it gets taken over by the cortex around it that is in charge of different body parts—can explain phantom sensations

Crossings in the brain

right side of body controlled by left side of the brain, we don't know why the crossings are there

How to make an axon faster

myelination or bigger

Most commonly used excitatory neurotransmitter

glutamate

Most commonly used inhibitory neurotransmitter

gaba

Autoreceptor

neurotransmitter binds to the same synapse it is being released from, negative feedback loop that inhibits further release

What happens if a neurotransmitter stays in the synaptic cleft

death, the receptor becomes desensitized and doesn't respond to neurotransmitters

Ways for neurotransmitter to get out of the cleft

reuptake, enzymatic breakdown, glial cells

Reuptake

transporter proteins pulls the neurotransmitter back inside

Enzymatic breakdown

enzymes chop up neurotransmitter so its no longer functional

Glial cells

astrocytes that take up excess ions that could cause too much excitation

Astrocytes

most plentiful type of glial cell, star shaped cells that provide structural and chemical support for neurons, creates the blood brain barrier

Glial scars

astrocytes proliferate and create a scar on damaged part of the brain making it hard to create proper connections

Oligodendrocytes

provide myelin sheath for axons in the CNS

Schwann Cells

provide myelin sheath for axons in the PNS

Microglial cells

cleans up invaders and prunes aways unwanted synapses, does this when you sleep

How can microglial cells be villainous

can accentuate inflammation—like in Alzheimer's

How many Alzeheimer's cases are the familial (genetic) kind

~5% have the genetic kind (also called early onset)

How many Alzeheimer's cases are the sporadic kind

~95%

What are the 2 main pathologies in Alzheimer's disease

beta amyloid plaques and neurofibrillary tangles

Beta amyloid plaques

glom up inside the neuron, cells get clogged and can longer transport things leading to neuronal death; beta amyloid derives from cleaved amyloid precursor protein

What areas of the brain are hit hardest by Alzeheimer's

the medial temporal lobe and cholinergic cells; they are the hardest hit and first to go

apo E gene epsilon 4

allele increases risk of Alzeheimer's

apo E gene epsilon 2

allele decreases risk of Alzeheimer's

a-macroglobulin gene

2 allele increases risk of Alzeheimer's

TREM2 gene mutation

rare-decreases microglial cell's ability to clear amyloid beta increasing risk for Alzeheimer's

Presenilin 1 gene

defect in APP

Presenilin 2 gene

defect in genes that cut APP

How to treat symptoms of Alzehiemer's

drug that stops the enzymatic breakdown of acetylcholine-maximize how long acetylcholine sticks around, this will not cure the disease just help symptoms

Examples of prion disease

mad cow disease, scrapie, kuru

What is a prion

protein that has normal and abnormal morphs, abnormal morph makes the infectious protein

How prions work

bad prions convert normal prions, the "bad" prions aggregate and form clumps causing cell death that leads to holes in the brain (spongiform tissue)

How can you get prion disease

genetic mutation that leads to natural formation of prions, eating infected meat-especially brains and spinal cord

Scrapie

in sheep, started with selective breeding gone wrong, caused behavioral changes, tremors, and uncoordinated movements, when the sheep would die farmers would grind up the beef and feed it to other animals as extra protein, caused other cattle to be infected with the bad prions

Kuru

found in cannibal tribes in New Guinea, symptoms included headaches, laughing, coordination problems

Mad cow disease

bovine spongiform encephalopathy

Prion disease in white tail deers

hunters would keep deer captive and feed them food laced with animal proteins, the deer eventually got loose and spread prion disease in the wild

Adaptive prion like proteins

help turn short term memory into long term memory

CPEB

cytoplasmic polyadenylation element binding protein, important in transcriptional process, helps stabilize and awaken sleeping mRNAs

Draw an action potential

see diagram in notebook

What uses a lot of ATP to keep resting potential

ion pumps

Where do action potentials occur

mainly in axons

Why do action potentials occur mainly in axons

high density of voltage gated channels

What is the role of Calcium in an action potential

helps with release of small molecule neurotransmitters in the amazon terminal and helps with exocytosis

MS vs Guillain-Barré

MS affects the brain and spinal cord, GB affects the PNS; GB usually goes away, MS does not

Why demyelination is bad in MS and Guillain-Barré

it renders the neuron ineffective because the the voltage gated ion channels are clustered at the nodes, without myelin the nerve cannot start an action potential

Small molecule neurotransmitters

amino acids or chemically modified versions of amino acids

Neuropeptides

brief chain of amino acids

Two types of neurotransmitter receptor types

ligand gated ion channels and g-protein coupled receptors

nACH receptor

ligand gated ion channel-see diagram in notebook

mACh receptor

g protein coupled receptor-see diagram in notebook