Epigenetics and psychology- neuroepigenetics (People who has abusive…
Epigenetics and psychology- neuroepigenetics
People who has abusive childhoods had higher levels of cortisol
Cortisol is the stress hormone.
Experiments done on rats suggest nurturing babies means offspring have lower stress levels
Rats which had been nurtured as offspring had higher levels of the happy hormone, serotonin, which upregulated epigenetic enzymes resulting in reduced DNA methylation of cortisol receptors, so the cortisol could more easliy bind to receptor and keep the rats relaxed.
Rats which had little or no nurturing responsed aggressivley to small annoyanced whereas nurtured rates were more calm.
Adults who had abusive childhoods had there cortisol levels taken and these were much higher than normal, even if they were healthy and content at the time of the measurement.
There are a quadrillion neuronal connections.
Studies on mice suggest mice which had not been well nurtured had chronic stress as adults.
Just like the rats, well nurtured mice responded aggressively to small annoyances
Arginine vasopressin had decreased methylation on stressed rats so was more expressed.
There are more than one type of gene involved in adult stress.
Separation from the mother in mide triggered neuron activity in the hypothalamus
This stimulated a signalling cascade, affecting the MeCp2 protein.
The MeCp2 protein is highly expressed in neurones- it helps repress gene expression.
The addition of a phosphate group to MeCp2 causes MeCp2 to become unattached to arginine vasopressin so it can no longer act as a flag, recruiting repressive modifications to bind to DNA leading to modifications that upregualte to be put on genes like acetylation.
Mice showed high levels of stress throughout their life.
A particular modification itself is not bad, but where the modification is makes big difference.
Studies done on people who had committed suicide revealed that DNA methylation on the cortisol receptors was higher for those who had abusive childhoods and lower in those who did not.
Methylation on cortisol receptors meant they were expressed less, and were less able to detect cortisol, meaning cortisol remained in blood for longer.
Over 120 million people worldwide are affected by depression with 850,000 depression related suicides a year and these figures are expected to increase according to the World Health Organisation.
SSRIs introduced in the 90's (selective serotonin reuptake inhibitors) were a big step forward in treating depression.
The name is self explanatory, but serotonin levels remain high in the brain.
Depression is not just caused by one chemical having its levels dropped. There are much longer term changes in the brain as depression develops which includes changes to synapses.
Research on depression is less focused on individually researching neurotransmintter levels but now takes into account the network of connections between neurones.
The system must be in balance in order to remain healthy
Nucleus accumbens in the brain is important in aggression, fear, pleasure and reward.
Gdnf (glial cell-derived neurotrophic factor) was had increased expression in response to stress in the humpy mice
Experiments were done on two strains of mice: one was 'jumpy' and the other was 'chilled'. They imitated depressed and non depressed humans respectively.
The Gdnf promoter was identical in the chilled and jump mice but their epigneomes were different.
Jumpy mice had fewer acetyl groups than chilled mice so had lower levels of Gdnf expression.
The reason for this was HDAC2 was more highly expressed in jumpy mice than chilled mice.
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The jumpy mice had increased HDAC2 expression and decreased Gdnf expression. Treating mice with SAHA, an HDAC leads to increased Gdnf expression and stops mice from being so stressed and keeps them more chilled.
Changing histone acetylation changes their behaviour.
Mice normally love sugared water but depressed mice do not- analogous to depressed humans no longer enjoying activities they used to.
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Neuroepigenetics is highly controversial
Sceptics of epigenetics argue that since the epigenetic modifications are so small but there is a very bid difference in phenotype, that this cannot be the answer,
They also alrgue correlation does not mean causation
Counter arguments include: molecular biologists are not good at interpretation of real world experiments,
The brain has lots of highly specialized regions that are affected differently by epigenetics. Cells are targeted in ways scientists dont know how they work. Skeptics think that epigenetic modifications differing with one stimulus in different parts of the brain is a reason fro skepticism.
How is DNA methylation removed in long lived cells like neurones?
Demethylation (not by gradual fade out as DNA is replicated but not methyalation) is called active demethylation. Its mechanisms is unknown.
In trying to find a a way to remove methyaltion, scientists found a way to add something on (an OH group) and has the same effect as demethylation. Addition of OH forms 5-hydroxymethylcytosine.
MeCp2 can no longer recognise 5-hydroxymethycytosine as it has the OH attached and is therefore read like unmethylated DNA,
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Experiments on memory are hard to conduct as it is hard to know which part of the memory you are studying.
Memory has been hypothsised to be controlled maybe not all but t least partially by epigenetics.