Author Archives: Kenzo Le Vaillant

The two stress response components

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Introduction

This page is the first part of a study of articles.

An overview on stress neurobiology: Fundamental concepts and its consequences by Rumi Iqbal Doewes, Lekshmi Gangadhar and Saranyadevi Subburaj

Context

Stress is as much an issue for humans as it is necessary.

It may prevent us from performing at our best or in some cases make us sick. However, it is what helped us identify the dangers around us and prepared our bodies to fight or run.

It is so important that several brain regions are involved in it.

When we detect something, the combined response from these brain regions is what will determine if it is a stressor and what kind of stressor it is.

Stressor

What causes a stress response in an individual

The stress system

When faced with a stressor, the body will react in two ways.

A rapid, short way by the SAM axis and

SAM axis

Sympathetic Adrenal-medullary axis

The rapid but short term component of the stress response done by the releasing of noradrenaline.

A slower but longer lasting way by the HPA axis.

HPA axis

Hypothalamic pituitary adrenal axis

The slow but long term component of the stress response done by the releasing of glucocorticoids.

The chemicals produced by these responses will bind to various cells causing the stress response.

The stress response will generally block or change some functions that are needed in everyday life but not when facing danger such as digestion, growth, the immune system and the metabolism.

These are why chronic stress can block growth and make people sick.

In the brain, the stress response will usually inhibit the outer regions of the brain where higher level functions such as rational thinking are done and activate the limbic regions.

Limbic region

The lower, inner part of the brain consisting of the hypothalamus, thalamus, hippocampus, amygdala and the cingulate gyrus.

It is involved in emotions, memories and learning, reproductive behaviours, feeding behaviours and stress responses.

This is especially in the fast SAM axis which is mainly triggered by the hypothalamus.

Next part : The amygdalas reaction to two different stressors

Part 3 : The hippocampus, genetics and molecules of stress

Alcohol can improve memory ?!

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This is the second part of a study of the article

THE PSYCHOLOGY AND NEUROSCIENCE OF FORGETTING by John T. Wixted

Alcohol and other drugs

When having consumed too much alcohol, it is possible to not remember anything about that time.

That is because alcohol, like a drug called benzodiazepines and some others, block information from reaching the hippocampus.

However, although they may seem bad to memory, they actually don’t disturb the consolidation process.

This, in addition to the blocking of retroactive interference they create, helps the information before the consumption to be better retained.

This phenomenon where alcohol and these drugs can improve retention of things learnt before consumption is called retrograde facilitation.

However, this effect doesn’t work on old memories and it also doesn’t mean it’s better to drink alcohol after studying etc…

Also, this is a hypothesis and other theories do exist.

One of them is that they improve the consolidation process although this should then do the same for memories after or during consumption.

Sleep

Another similar thing we do on a regular basis is sleep.

Experiments have found information learnt right before going to sleep were better remembered. This may be in part due to the lack of retroactive interference but also due to the mechanism of sleep.

The formation of memory

The main theory of the formation of a memory is LTP.

Similarly to memory, LTP is blocked in the hippocampus by alcohol and benzodiazepines. NMDA receptor antagonists, which also impair learning tasks that require the use of the hippocampus, and non-REM sleep also have the same effect.

Antagonist

A chemical that will block another from functioning or reduce its activity.

However, these effects didn’t happen when the LTP in the hippocampus was induced one hour before the consumption or non-REM state, showing another similarity to memory as learning before the consumption wasn’t blocked at all.

Unlike non-REM sleep, LTP can be induced during REM sleep.

REM sleep is said to contain lively mental images and facilitates memories such as procedural memories that don’t need the hippocampus.

The images can also be remembered, which is something that can’t be done in non-REM sleep that contains a lot of mental activity which can’t be retained.

This may lower the demands in the hippocampus allowing it to coordinate the memory circuits it holds to the neo-cortex to store for a longer time.

Neo-cortex

The outermost layer of our brains with grooves and ridges that is involved in most higher cognitive functioning.

This could also be done at anytime when the hippocampus isn’t busy such as during quiet wakefulness.

Although again, LTP seems to be a great solution to the question of “where are our memories stored?”, they are only artificial now and don’t seem to be permanent.

It’s easy induction in the hippocampus suggests that it may be more of an initial storage for memory before a completely different storage for long term ones.

Related posts

Part 1