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Transmission of Early Life Adversity/ Individual Differences - Coggle…
Transmission of Early Life Adversity/
Individual Differences
General Transmission of
Early Life Adversity
Transmission of olfactory memories across generations
Olfactory system and learning
Olfactory sensory neurons (OSNs) in the main olfactory epithelium (MOE; in the nose) respond to different neurons.
The projections of the OSN converge back onto specific glomeruli in the olfactory bulb.
The distribution of OSNs that respond to most odours are overlapping, BUT the OSNs that respond to acetophenone and propranolol are non-overlapping (as are the glomeruli that process each odour.
Jones et al (2008): olfactory learning in adult transgenic mice
what they did:
Some trained to associate acetophenone with shock, and others trained to associate propranolol with shock. They were tested for FPS in the presence of each odour.
what they found:
increased FPS for those Ace trained when in the presence of Ace but not Pro.
increased FPS for those Pro trained when in the presence of Pro but not Ace.
Brains were extracted to check glomeruli > Trained are twice the size of the controls
Dias & Ressler (2014) studied whether the olfactory memory in adult mice could be transgenerationally transmitted.
what they did:
olfactory fear conditioning of F0 generation.
what they found:
When tested the next day, these animals exhibited odour-potentiated startle (OPS) to acetophenone but not propranolol.
Exhibited the same pronounced increase in glomeruli size.
F1 and F2: Subsequent generations were not ever exposed to acetophenone (until test) or given any fear conditioning (not ever shocked until test)
Offspring of trained animals (F1-Ace-M71) responded to odours like their fathers had.
Also observed a clear change in the structure of glomeruli in the acetophenone area of the olfactory bulb.
Measured with a place aversion task > chamber with 2 compartments, in the corner of one they put the odour.
Both F1 Ace and F1 Prop rats are similarly sensitive at a concentration of 0.01% and 0.06%, but and 0.03%, Ace rats are MUCH more sensitive than Prop rats
How is the experience transmitted?
Inheritance via gametes
Transmission via a social route of some sort (behaviour)
You can avoid this with IVF > getting sperm from F0 father and fertilising an egg and implanting it in a female rat > no contact at all with bio parents.
Controversy is that epigenetic changes CANNOT be transmitted across generations > somatic cells don’t pass changes to germ
Generational transmission of survival skills
Deshe et al (2023): role of associative learning in survival
what they did:
Used c.elegans (roundworm lifespan of ~3 days)
Trained (during one day) some worms to associate a preferred odour with stressful starvation conditions.
what they found:
Those worms subsequently avoided the odour, and so did their offspring.
Avoidance could be extinguished in parent, but the offspring still avoided it > extinction does not get rid of transgenerational learning.
The learned association led to increased survival. Animals re-exposed to odour (would have activated stress response in trained worms) and then exposed to high heat were more likely to survive (observed in F0, F1 but not F2).
Evidence of epigenetic changes in sperm but not eggs > seems to be a pattern
Individual Differences
Evidence of epigenetic changes in sperm but not eggs > seems to be a pattern
Ideographic research: looking at individual differences.
Massive individual differences in response to trauma in humans.
McCallum et al 2015: looked at levels of depression in response to the loss of a loved one.
Pre-existing (7.4%): depressed beforehand
Chronic grief (13.2%): not depressed before, but chronic after
Depressed improved (11.2%): depressed before but not after
Resilient (68.2%): not depressed before or after
As a species we are shown to be resilient.
Individual differences in human
stress reaction and memory
Andreano and Cahill (2006)
what they did:
Exposed human participants (male and female) to a story “The War of the Ghost” (very sad and famous).
After reading the story they do the “cold pressor” task > sticking hand in cold water, and then try and recall the story.
Controls did room temp water.
what they found:
There is an effect of stress > those with cold water remembered more.
More effective in males > i think cause females have a higher pain tolerance?
Almost 40% of variance in memory is explained by cortisol levels (IN MEN) (due to ice water) > there is an inverted u-shape function > too much or not enough stress is not good for memory.
adult neurogenesis
male meadow voles have larger hippocampuses due to being polygamous and needing to remember more home ranges > puzzling because the sexual dimorphism comes and goes as a function of breeding season.
Is it true that we must make do with a fixed number of neurons?
Questioned by Altman (1962) > finding that adult neurogenesis happened, but people largely disagree
Re-discovered in 1999 (Gould et al) and was cited way more.
Still controversial rn but there was a shift in perspective.
From the perspective that all neurons in the brains of vertebrates are formed early in development, learning/memory in adulthood must occur only through modifications of existing memory.
If there are new neurons being born in adulthood, might they play a role in learning/memory?
We now know that neurons are being made all the time, especially in the hippocampus and the olfactory bulb.
The cell cycle:
Process by which a cell divides and reproduces.
DNA is copied during synthesis phase
Bromodeoxyuridine (BrdU) is a thymidine analogue that is incorporated into the DNA in place of thymidine during the synthesis phase.
Can stain for BrdU since it was injected > any cells with BrdU would have been created after the injection > staining for neurogenesis.
Drapeau et al (2003) examined neurogenesis in aged rats (10-11 months old)
what they did:
Animals injected with BrdU and then trained on a MWM (with hidden platform) > some were impaired and some were not- performing just as well as younger rats (on spatial memory).
what they found:
More BrdU-IR cells (in the granule cell layer-hippocampus), less latency in finding platform > better memory.
Animals with preserved spatial memory exhibited a higher level of cell proliferation in comparison with animals displaying spatial memory impairments.
Somewhat similar result occurs in human
Pudas et al (2013) examined brain differences during episodic memory task in “successful” vs “average” aging humans (mean age 68.8 years for both groups) and young adults
what they did:
Longitudinal > started at 40, took memory test every 5 years.
memory tests every 5 years for 20 years
what they found:
episodic memory score went up as successful agers got older, but went down as average agers got older.
successful older people and young people had similar neural activity (in the left hc cluster) on a paired associates task, while average older people had way less
Nassif et at (2022) looking at “superagers”
Defined as individuals aged 80 or older who appear to be resistant to the deleterious effects of aging on memory function
what they did:
Examined if the neuronal integrity in the entorhinal cortex (ERC; a part of the hippocampus) is different in identified Superagers (n=6) compared to (1) cognitively-healthy younger individuals and (2) cognitively average peers (normal elderly n=7) and (3) individuals with amnesic mild cognitive impairment (n=5)
Used neuronal size in the ERC as a proxy for cellular integrity.
what they found:
superagers had the biggest neurons, young people slightly smaller, and normal elderly smaller still.
Bigger the neuron, better the memory
Nassif et al (2022) examined neurofibrillary tangles (NFTs) in the brains
Not known why, but cells in the ERC are particularly susceptible to the formation of NFTs typically observed in normal aging and in alzheimer’s disease.
they cause neuronal shrinkage and death
Superagers resist the development of NFTs in the ERC > my also be resilient to cognitive impairment even when demonstrating pathological brain changes.
individual differences in extinction of learned fear
Extinction is the empirical basis for exposure-based therapy.
General model> there are some animals/people that will eventually be able to extinguish their fear and some that won’t.
Reinstatement approach: King et al (2018)
what they did:
Adult male rats. 5 presentations of noise-shock. Extinction training- not a specific amount of trials, just until each rat had completely extinguished fear.
13 or less extinction trials were considered “fast”, and 16 or more were considered “slow”.
Fast and slow learned at the same rate, and froze just as much when tested for extinction.
Question if fast or slow extinguishers are susceptible to relapse (reinstatement).
1US gets one shock (same extinction context), 2US gets 2 > reinstatement procedure.
also did the same thing as before but with spontaneous recovery