High levels of somatostatin bring about a multitude of problems.  Its close relationship with microglia (a natural macrophage) is important as it buffers in synaptic pruning.  This is a normal and essential process as microglia would strip the brain of most synapses without its presence.  However too much somatostatin impedes the healthy pruning and does not allow the brain to remove connections that are no longer needed.  This is thought to happen between early childhood and adulthood.  If this process doesn’t occur normal learning is certainly disadvantaged.

Somatostatin can activate a cytokine response which can cause widespread inflammation of the brain.  AS Somatostatin is very high in autism this could very well be the reason why this is so.

For further reading: *Astrocytes and Microglia and their Potential Link with Autism Spectrum Disorders-Frontiers *https://pubmed.ncbi.nlm.nih.gov/34059669/

While there is general dysfunction with astrocytes in the autistic brain (formation and maturation) there is a number of factors which are contributing to the problems they harbour.  Failure of synaptic pruning and low dopamine two contributors.  It must be said if there is a malfunctioning event happening another process in the brain may react to directly alleviate the problem or overcompensate causing more problems.  This tit for tat activity makes the original low dopamine/high somatostatin levels continue to produce highly complex irregularities within the central nervous system over the lifetime of an individual.

Dopamine modulates glia cells and there is no surprise that there are irregular activities also in oligodendrocytes and myelin as a whole.

For further reading: *Role of Oligodendrocytes and Myelin in the Pathophysiology of Autism Spectrum Disorder – Pub Med

Because of this development, there are abnormalities in pivotal areas of the brain (frontal lobe, limbic areas, putamen area).

Across the board glial cells are affected and thus present a multitude of problems.

Restricted or Repetitive Behaviours or Interests

1. Lines up toys or other objects and gets upset when order is changed.  Because of limited dopamine and abundant somatostatin, the channels of concentration are limited and flawed.  The ensembles that are formed in early childhood are confined and repetition is a haven for the autistic brain.  Tasks that can be formed repeatedly lock out other stimulations from other pants of the brain where synapse are abundant.  A small alteration can be disruptive as this requires additional dopamine which may or may not be on offer.  Adaptability is something that more than likely will bring discomfort to someone on the spectrum especially the more challenged.

2. Repeats words or phrases.  By doing this it attracts more dopamine.  Eventually it may register or associate with something else.  Its like a learning.  Go over and over a fact or paragraph of literature until it becomes a memory trace.  At night and with sleep it becomes more substantiated being thrown between the hippocampus and locus coeruleus.

3. Plays with toys the same way every time.  Basically, it’s in an individual’s comfort zone.  The dopamine has been allocated before so it’s a matter of re-engaging with it which is a lot easier than creating a new activity.  Repetition like this may seem simplistic but this can create highly detailed observations which is different type of reward.  Slowly but surely a higher level of dopamine is achieved.  Thus, it gets revisited.  This process can’t be done to every activity so there are limited pet projects.

4. Gets upset by minor changes.

5. Has obsessive interests.

As explained above reward and comfort essentially dictate where the autistic brain becomes obsessive and minor changes derail this process.

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The human brain and its associations in the body has always intrigued me and I continue to enjoy learning more.  The complexities of this subject is nothing new to those who are like-minded and I hope the information I provide is helpful and inspires further thought for people who read my material on this website.

Cameron Dyer

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