stress lecs Flashcards

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1
Q

Describe Limbic system and stress?

A

The primary area of the brain that deals with stress is its limbic system.
Because of its enormous influence on emotions and memory, the limbic system is often referred to as the emotional brain.

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2
Q

Describe stressor pathway

A

Stressor->Hypothalamus
then:
Releases CRH-> ant pit -> inc ACTH -> adrenal cortex -> cortisol
posterior Pituitary gland-> incr vasopressin
Goes to : Sympathethic nervos sysrem, adrenaline released trhough medulla, , increasesglucagon, blood decrease through kidneys,

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3
Q

Describe Catcholamine effects/ what happens i sns activated

A

The SNS rapidly prepares to deal with a threat to safety.
Its hormones initiate several metabolic processes that best allow to
cope with danger.
Adrenal glands release adrenaline and other hormones that increase
breathing, heart rate, and blood pressure.
This moves more oxygen-rich blood faster to the brain and to the
muscles needed for fighting or fleeing.
More energy, because adrenaline causes a rapid release of glucose
and fatty acids into your bloodstream.
Senses become keener, memory sharpens, less sensitivity to pain.
Growth, reproduction, and the immune system all go on hold. Blood
flow to the skin is reduced.

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4
Q

Describe Dominance of the SNS

A

Small amounts of noradrenaline isn’t bad. but it is very slow to shut down and allow the
tranquilizing PNS to calm things down

Stress hormones don’t know when to quit acting.
They remain active in the brain for too long –
injuring and even killing cells in the hippocampus.

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5
Q

Describe Inputs into the Amygdala leading to Emotional Responses

A

Auditory, Visual, Tactile GOES into Sensory cortex

Prefrontal cortex- rational

Thalamus->
Hippocampus- memories
Brain Stem-> motivation

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6
Q

Describe the amygdala structures!

A

Sensory info goes into LATERAL nucelues, which goes into BASOLATERAL (hippocampus goes into BASOLAT too) nucleus, which can then go to Basal,

Basal can go to PAG (pain area)

These two can go to ccentral nueclues and then that goes to Hypothalamus

Also:: olfactory to medial N and then to hypothalamus

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7
Q

Overall systems pathway describe from sensory info

A

Sensory->Sensory Thalamus-> Sensory Cortex -> Hippocampus->
Amygdala->
Emotional Response

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8
Q

How do you enhance memory with acute stress?

A
On synapse, increased Glutamate increases Calcium and them AMPA receptors, 
A chronic overreaction to
stress overloads the
brain with powerful
hormones that are
intended
only for short-term duty in
emergency situations.
Their cumulative effect
damages and kills brain
cells
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9
Q

Control of stress how?

A

Cortisol, when it builds up, it neagative feedbacl hypo and ant pit, only works w acute stressor

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10
Q

Chronic stress dendrite what happens?

A

Dendritic length and spine reduced,

Too much CA can have downstream effects

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11
Q

Cortisol and Temporary Memory Loss-Study

A

Rats were stressed by an electrical shock, and then made to go through
a maze that they were already familiar with.
•When the shock was given either four hours before or two minutes before
navigating the maze, the rats had no problem.
•When they were stressed by a shock 30 minutes before, the rats were
unable to remember their way through the maze.
•This time-dependent effect on memory performance correlates with the
levels of circulating cortisol, which are highest at 30 minutes.

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12
Q

Glucocorticoids and Their Adverse Effects on

Hippocampal-Dependent Cognition

A

Hippocampus, a primary GC target, with ample quantities of
corticosteroid receptors
sustained stress or exposure to GCs can impair aspects of
hippocampal-dependent cognition
It’s the retrieval component that is most sensitive to the disruptive
effects of GCs
GCs can disrupt hippocampal-dependent declarative memory
performance
Declarative memory performance in Cushing’s syndrome patients (in
which GCs are hypersecreted secondary to any of a number of
types of tumours) is impaired

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13
Q

describe Schematic representation of neural redox reactions

A

dff

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14
Q

describe A schematic representation of the nitrergic system and
its downstream effects in hippocampal neurons
following stress exposure.

A

fff

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15
Q

Cortisol and the Degenerative Cascade

A

When levels of cortisol rise to a certain level, several areas of the
brain especially the hippocampus tell the hypothalamus to turn off
the cortisol-producing mechanism.
Lots of stress or exposure to cortisol accelerates the degeneration
of the aging hippocampus.
Damaged hippocampus causes cortisol levels to get out of control
– further compromising memory and cognitive function.

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16
Q

What happens with neuron size with chronic stress?

A

Hippocamus shrinks- especially CA3
Amydala increases
The mistake is in figure 1, it should be CA3 pyramidal neurons that have the decrease in dendritic arborization and numbers of spine. CA1 which are downstream from CA3 seem to compensate for the reduction in activity coming from CA3. This was a surprising finding by my previous PhD student. Over sstimulation of CA3 neurons leads to a decrease in dendrite arborization and a decrease in spine numbers (to reduce over stimulation), this reduction in flow to CA1 neurons may be responsible for the no change in dendrite morphology and slight increase in spine density.

17
Q

Link between amygdala and hippocampus and memories

A

Amygdala can hijack hippocampus w memories.
Amyhdala -> implicit memories, autonomically driven
Amydala thrives in excess gluccocorticoids

Amygdala, another limbic structure rich in corticosteroid receptors, plays a
critical role in fear conditioning and in its potentiation by stress
Under circumstances in which stress causes atrophy of dendritic processes in
the hippocampus, the same stressor causes extension of processes by
neurons in the amygdala and in the bed nucleus of the stria terminalis, an
amygdaloid projection site central to anxiety

18
Q

Stress and Plasticity in the Limbic System

A

Stress can alter plasticity in the nervous system, particularly in the
limbic system
Prolonged stress impairs hippocampal-dependent explicit learning and
plasticity
Prolonged stress enhances implicit fear conditioning by amygdaloid
plasticity

19
Q

Summary of stressor effect on body

A
Sensory Information
>>>>
Release of Adrenaline & Cortisol
>>>>
Increased Heart Rate and Blood Pressure
Increased levels of Glucose and Lipids in Blood
Increased activity of Neurons in Brain
Suppression of Immune System
Suppression of Reproductive System
Increased levels of Oxidants
>>>>
Threat removed
Release of Acetylcholine
If not controlled:
Hypertension
Diabetes
Loss of Neurons
Infections & Cancer
Infertility
Cell & DNA Damage
20
Q

SMell and limbic system

A

Very quick, even if you dont know

first libic system and then thalamus

21
Q

Green smell and hippocampus

A

Induces LTP. yeah and works

reduces stress

22
Q

Stress Compromises the Blood-Brain Barrier

A

Stress can dramatically increase the ability of chemicals
to pass through the blood-brain barrier. Eg Gulf War, Israeli
soldiers.
The primary BBB is formed by cerebral capillaries that
are different from those elsewhere in the body. They
contain no “slit pores” that permit molecules to diffuse
easily into the surrounding tissue.
The secondary BBB surrounds the cerebral capillaries. It
is composed of “glial” cells, the other family of brain cells
that outnumber neurons by a factor of ten. Certain types
of glial cells form a buffer between the brain’s capillaries
and its neurons. These support cells further obstruct
toxins from the bloodstream, while regulating the correct
flow of necessary nutrients.