CJH332H1 Study Guide - Winter 2018, Comprehensive Midterm Notes - Neuron, Wireless Access Point, Protein
CJH332H1
MIDTERM EXAM
STUDY GUIDE
Fall 2018
Lecture 1: Introduction to Synaptic Neurobiology
Neurobiology of stress
• Stress is processed at the level of cerebral cortex, activating the medial prefrontal, anterior cingulate cortex,
amygdala and hypothalamus (produces physiological response)
- Important in anxiety and depression
• Short term stress is good – release of NE from locus coeruleus
Animal models of stress
• Acute (beneficial) and chronic (detrimental) forms of stress and both physical and psychosocial forms of stress
cause release of glucocorticoids (stress hormone)
• Various forms of stress and the duration of stress on different animals cause changes in the synapse, neurons in
various areas of the brain, their circuits and behavior
- Physical stress (immobilization or restrainer)
- Psychosocial stress (predator odor, elevated platform, social defeat or maternal separation)
• Different circuits have different weakening effects
Stress affects multiple brain areas
• Interplay between NAc (influenced by VTA) and mPFC
• Amygdala – spiny neurons most dominant
• NAc – medium spiny neurons (respond in the same way as amygdala spiny neurons?)
• VTA – dopaminergic neurons
• CA3 (hippocampus) – pyramidal
neuron respond to anxiety and
stress
• mPFC – pyramidal neuron
• Do they respond in the same way
even in same classification?
Depends on the location?
Affects on morphology/function
• Growing of neurons means an over-
activation of the neurons
(hypervigilant) after exposure to
stress
• Dopaminergic neurons shrinks –
losing interest
• Hippocampus neurons shrinkage –
memory affected in bad way
- Some individuals undergoing
anxiety makes association with
traumatic events (PTSD
relation?)
- Cannot concentrate as well (mPFC)
find more resources at oneclass.com
find more resources at oneclass.com
Remembering the synapse
• Dendritic spines can have different phenotypes (short/stubby spines or thin or mushroom spines)
• Stress not only affects the overall morphology of various neurons but also the synapses that each of the neurons
would make
• While post-synaptic portion of the synapse is most commonly affected, pre-synapse does as well
Effects of stress pre-synaptically
• With acute stress, SNAREs increase – same stimulus will release 10-20 times more neurotransmitters
• Receptors respond to stress molecules (corticosterone) and increase release of neurotransmitter pre-
synaptically
• Acute food shock produces a stress-induced depolarization-evoked release of glutamate from presynaptic
terminals of neurons in the prefrontal and frontal cortex
• Corticosterone mediates this effects as this presynaptic enhancement can be blocked by glucocorticoid receptor
blocker RU486
• If corticosterone is elevated, it causes rapid glucocorticoid receptor-mediated increase of presynaptic SNARE
protein complexes (mediates fusion of synaptic vesicles) in the presynaptic membrane
Post-synaptic spines also affected
Why the complicated stress response?
• Steroids can interact and cause genomic changes that are difficult to track in individuals
- Although the same genomic makeup in bred rats, they still all have different genomic response
• Basal release of glucocorticoids varies in a diurnal pattern (eg. trend to get higher during the day and lowest
while sleeping)
- Sleeping habits are different from previous generation – levels of cortisol in pattern directly affects chronic
level of cortisol your brain is exposed to)
• Adrenal steroids can have multiple effects because of complexities in signaling
The cumulative effects of stress
• In the hippocampus, glucocorticoids mediate classic biphasic effect on structure and function
• Acutely, moderate physiological levels of adrenal steroids enhance synaptic function and types of memory
• Chronically, corticosterone mediates adaptive plasticity involving spine synapse turnown, dendritic shrinkage
and suppression of adult neurogenesis in dentate gyrus
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Neurobiology of stress: stress is processed at the level of cerebral cortex, activating the medial prefrontal, anterior cingulate cortex, amygdala and hypothalamus (produces physiological response) Important in anxiety and depression: short term stress is good release of ne from locus coeruleus. Psychosocial stress (predator odor, elevated platform, social defeat or maternal separation: different circuits have different weakening effects. Affects on morphology/function: growing of neurons means an over- activation of the neurons (hypervigilant) after exposure to stress, dopaminergic neurons shrinks losing interest, hippocampus neurons shrinkage memory affected in bad way. Some individuals undergoing anxiety makes association with traumatic events (ptsd relation?) If corticosterone is elevated, it causes rapid glucocorticoid receptor-mediated increase of presynaptic snare protein complexes (mediates fusion of synaptic vesicles) in the presynaptic membrane. Why the complicated stress response: steroids can interact and cause genomic changes that are difficult to track in individuals.
