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UIUC / Psychology / PSYC 210 / What is collateral sprouting?

What is collateral sprouting?

What is collateral sprouting?


School: University of Illinois at Urbana - Champaign
Department: Psychology
Course: Social Psychology
Professor: Galvez
Term: Fall 2016
Tags: neuroscience, Psychology, Brain and Behavioral Psych, sex, nervous system, aging, Dementia, damage, and Neurological Disorders
Cost: 25
Name: PSYCH 210, Week 6 Notes
Description: These are the notes for week 6 of the class.
Uploaded: 10/08/2017
7 Pages 55 Views 6 Unlocks

Lecture 13 (10/2/17) 

What is collateral sprouting?

Damage to the Nervous System (continued) 

• Collateral Axon Sprouting

o Part of a new circuit solution when anterograde degeneration happens to a  neuron

▪ When axon 2 degenerates, there is not enough synapse from axon 1 for  an action potential causing the cell to not get used as much

• The receptors stay when the axon dies, which is called  

Denervation Super Sensitivity

o Due to a loss of synapses, there is an increase in  

neurotransmitter receptors

o Parkinson’s Disease – loses neurons in the substantia  

nigra, therefore, striatum loses a lot of dopamine in axons

▪ Some causes are blows to the head or pesticides

What are the different types of traumatic brain injury?

▪ Giving more dopamine doesn’t help due to the  

blood-brain barrier, but having supersensitivity  

increases the likelihood to use more dopamine  


o L-DOPA causes an increase in dopamine receptors Don't forget about the age old question of What are the advantages of hedonism?

▪ This happens because L-DOPA can make it through  

the blood-brain barrier

• Has a dedicated transporter

▪ Some patients with Parkinson’s do fine on it for a  

while and other must stop and try again

• This happens since L-DOPA triggers more  

neurons than the targeted ones

▪ The healthy axon 1 will grow branches to replace axon 2

How is fragile x syndrome caused?

If you want to learn more check out What does the lack of craters on io tell us?

• This can potentially cause an action potential and allow the cell to  

be used more

• Can only re-branch with nearby (local) neurons

• Healthy axons do not grow long axons

▪ The new branch along with the old will now only carry partial information

Neurological Disorders (not associated with aging) 

• Traumatic Brain Injury (TBI) – aren’t really known

o A continuum of how bad TBI’s can be or get

o Concussion is on the mild side of TBI’s with a continuum from confusion to o Diaschisis – effects far from the injury  Don't forget about the age old question of Who is lex talionis?

▪ Bleeding (capillary tears), swelling, and local bleeding

• Swelling does not go down with corticosteroids due to the blood

brain barrier

▪ Axons stretched and broken

▪ Necrosis/Apoptosis (cell death)

• Necrosis is death from damage while Apoptosis is death by  

genetic programming

• Necrosis is worse than Apoptosis  

▪ Cannot see damage/swelling with MRI Don't forget about the age old question of Why does innovation matter?

o MRI only shows holes and tumors but not internal damage

• Difficult to treat

• A second injury is more destructive than the first

• Repeat injuries eventually lead to dementia

o Treatments are to rest the brain and stabilize blood  


• Epilepsy

o Recurrent seizures  

o Seizure – imbalance between excitation and inhibition

▪ Too much excitatory transmitter or their receptors are too abundant ▪ Ion channel changes

o Treatment increases inhibitory transmitters

▪ Can get extremely drowsy or unaroused

▪ Sometimes cannot help really strong excitations

o Children can outgrow seizures

▪ Pruning might help this situation  

• Tumors We also discuss several other topics like What are the main types of bonds?

o Occur mostly from gliomas – glia division

▪ Glia cells still divide for life, sometimes too much proliferation

▪ Fast vs. Slow growing

▪ Encapsulated vs. Invasive

• Aren’t in the brain vs. in the brain

• Invasive glioma is fatal

o Can surgically remove most of it but do not know if it’s all  

of it

▪ Can come from other body cancers

▪ Treatment is to stop blood vesicle growth

• This somewhat helps since glia need more blood than regular  


o Multiple Sclerosis (MS) – immune system attacks CNS myelin

▪ Do not know why it happens

▪ Axons can become dysfunctional

• Cannot reproduce same action potential as before

▪ Variable symptoms

• Remission – the immune system will stop attacking and  

remyelinate but then can start again whenever

▪ Treat symptoms If you want to learn more check out What was hamilton's report on public credit?

Lecture 14 (10/4/17) 

Neurological Disorders (continued) 

• Fragile X

o Most common type of developmental mental disability

▪ Continues through life

▪ DNA for Fragile X protein is silenced

• Too many repeats on the chromosome to be used  

o More common in males

▪ It is more obvious to pinpoint in males but harder to notice in females o Behavior: Autism, Hyperactivity, and Short-term memory deficits  

▪ Severity of each varies

▪ Fragile X is not the only cause of Autism

o Brain: dendritic spines are immature in the cortex

▪ Closer to dendrite

▪ Some variability

▪ Dendritic Spines

• A lot of neurons that deal with cognition (cortex and  

hippocampus) have dendritic spines for EPSP

• Spines – excitatory synapses

• Most excitatory synapses are on spines

• Fetal Alcohol Syndrome – prenatal exposure to alcohol

o Variable severity

o Intellectual disabilities and poor muscle tone (always happens)

o Alcohol increases Apoptosis and kills proliferating cells (they are very vulnerable) o Interferes with CAMS (Cell Adhesions Molecules) and other cell signals o There is no safe dosage; it is best to NOT DRINK AT ALL DURING PREGNANCY

Aging (does not involve much neurodegeneration) 

• Normal Aging (vs. neurodegeneration)

o Human Behavior  

▪ Slower, working memory, less flexibility, and sensory decrements (60-90  years old)

▪ Semantic memory is still okay and emotional regulation is better

o Rat Behavior  

▪ Harder to motivate to do things, poorer spatial abilities, and poorer  working memory

• Apathetic

• Human Neural Aging

o Sub cortex is unknown due to not being heavily focused on

o Shrinkage:

▪ Cerebral Cortex

• Neuron loss (10% between 20’s and 90’s cortex)

• Loss of dendrites and synapses in prefrontal cortex (0-50%)

▪ Hippocampus

• Cause of neuron loss is unknown

▪ White Matter

• Myelin, axons?

• Non-Human Neural Aging

o Cortex

▪ Regional neuron loss in cortex (rats and monkeys)

▪ Loss of dendrites, dendritic spines, and synapses (rats and monkeys) o Hippocampus (rats) – still have spatial problems

▪ No loss of neurons

▪ Variable loss of dendrites and synapses

o White Matter – no loss in rats

o Rats have less neural loss during aging than humans

• Dementia

o Global cognitive failure, behavioral disorganization, and loss of memory o 50% of people over 85 years have it

▪ Some are in early stages and will die before its gets worse

o Types:

▪ Alzheimer’s

• Most common form of dementia

• Plaques (Beta Amyloid) and neurofibrally tangles; especially in  

cortex and hippocampus

o Starts with loss of cholinergic input

o Globs up and blocks

• Given some drugs in early stages (acetylcholine) and increases an  

easier time with living with it

• Slightly more females get Alzheimer’s

• Decrease in brain weight

o Mostly in the hippocampus and cortex

o How big the ventricles become is a warning sign

o Hypothesis: neurons stop working and die

• Neurocognitive Reserve 

o More flexibility and awareness

• Healthy people have wide varying brain weight

o Can have smaller brains but no space in ventricles

Lecture 15 (10/6/17) 

Aging (continued) 

• Other Dementias

o Lewy Body Dementia

▪ Second most common

• People afflicted do not live very long

• Medications do not help

▪ Lewy Body – neurofilament clumping that kills cells

▪ Starts with Parkinson’s symptoms but degenerates quickly with dementia  as well

▪ Less obvious neural degeneration than Alzheimer’s

• No obvious shrinkage in the brain

o Vascular Dementia (can be combined with other forms)

▪ Caused by mini-stokes or mini-bleeds

• Either a bleed or block

▪ Variable Symptoms

o Frontal Temporal Dementia – sudden degeneration of frontal and temporal  cortex

▪ Less is known

▪ Can occur at a younger age

▪ Can cause a loss of inhibition

Sex 1 

• Levels of Sex Differences

o Genetic

▪ Male: XY, XXY, or XYY

• The Y chromosome is shorter than X

• Having a Y chromosome always is phenotypically male

• Y chromosomes do not complement the X chromosome

• Males express the X chromosome more so than women, who  

could express both X’s

• Males are more like their mothers

▪ Female: XX, XXX, XO (Turner’s Syndrome)

• XO is phenotypically female

o Fertility is compromised

o Not fatal

▪ XXY, XYY, XXX, and XO are the only triples that are not fatal

o Morphology

▪ Gonads

• Testes – produce sperm and Testosterone (androgen)

o Androgen is the general hormone for Testosterone and  


• Ovaries – produce eggs, Estrogen, and Progesterone

▪ Steroids: Testosterone, Estrogen, and Progesterone

• Testosterone become Estrogen

o Closely similar but one enzyme separates both; Aromatase

• All made from cholesterol  

o Pituitary Output

▪ LH: Luteinizing Hormone

▪ FSH: Follicle Stimulating Hormone

▪ All hormones turn off the organ that is secreting it if there is too much;  except Estrogen

• Feedback Loop

▪ Male

• LH ???? Testes ???? Testosterone  

• FSH + Testosterone ???? Testes ???? Sperm

o Sperm is constantly being produced

o If not released, it is reabsorbed

• If male does not have Testosterone, he will not be behaviorally  aggressive

• Found that winning and good feels increase Testosterone ▪ Female

• Cycle: Estrous or Menstrual

o FSH ???? Ovaries ???? E ???? EE ???? EEE ???? LH ???? Progesterone o Ovaries have the egg

o LH causes ovulation – the release of the egg

▪ Upregulates LH

o Mark of a female hypothalamus

• Estrogen ???? FSH↓ ???? Estrogen↓

• Progesterone ???? LH↓ ???? Progesterone↓

• Start Over: FSH

• Birth Control stops Ovulation

• Menopause has an increase in FSH

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