Brain plasticity

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Brain changes

Cell development in 8 stages: birth, migration, differentiation & maturation, synaptogenesis, death, rearrangement, and myelination.

Pioneer axons lay down a path, follower axons use this path to form multiple connections. Agenesis of the corpus callosum is when the corpus callosum fails to develop normally. It's either partly or completely missing. Fibres may be present but do not cross the inter-hemispheric fissure. Outcomes are very variable, from severe disability to no symptoms.

In humans, the brain continues to grow at the foetal rate for 2 years after birth (Bogin, 1997). It only reaches 90% of an adult size brain by 5 years of age (Dekaban & Sadowsky, 1978). Synaptic pruning continues after birth.

There is some neuronal plasticity, i.e cell death, synaptic shedding, synaptic rearrangement and myelination start before but continue after birth. This plasticity is limited. Cells aren't free to migrate to new areas, or make large changes in long-distance connectivity

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Sensitive/critical periods

Sensitive periods are generally observed through behaviour, but they are due to neural circuits, e.g filial imprinting, visual system, language. Not all circuits are shaped during sensitive periods, some are innate and robust (spinal cord). Some circuits demonstrate plasticity throughout life (CA1 of hippocampus). May require prerequisite stages or be influenced by experience.

After sensitive periods, circuits become resistant to change. Change may still occur, but may require more energy to maintain "less stable" connections. Complex behaviours may rely on hierarchies of circuits. These circuits operate in parallel and are able to compensate for abnormal processing. There are species specific sensitive periods.

Filial imprinting: common in birds. Chicks imprint on some constant in the environment. Sensitive period differs between species but generally happens within 32 hours of birth. Restricted area of forebrain seems to be important for imprinting

Visual deprivation: kitten's eyes sewn shut for the first 4-6 weeks of life. After the stitches were taken out the cells that owuld usually process visual information were unable to do so. After the sensitive period however, sewing the eyes shut had no effect. Visual development needs environmental input during a sensitive period of neural development

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Sensitive/critical periods pt. 2

Language: exposure to language before babies can speak influences language development. There is a systematic decline in ability to learn new languages after age 7. At 6 months, babies can differentiate the key phonetic units in all languages. By 10 months, babies show a preference for their own language (Kuhl et al, 2010). In addition to this, there's an environmental component - social interaction. American 9 month olds had 12 sessions with a Mandarin Chinese speaker. There was significant learning of Chinese phonemes months later, but no effect occurred if the children just watched video/audio of learning Mandarin (Kuhl et al, 2010).

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Environmental influences: early life

It is suggested that the environment and environmental stimuli impact brain and behaviour. Stimulation may occur by processing information in the environment or social interaction. The effect of the environment may be especially impactful in development.

Diamond et al (1987): Rats aged 60 days placed in enriched or impoverished environments. Rats in enriched environments had more, thicker dendritic connections than rats in impoverished environments (9,400 compared to 7,600 connections). They also had greater cortical depth (6.4% greater) and an increase in glia (14%). Nilsson et al (1999) placed 3 month old rats in standard or enriched environments. In the enriched condition, the rats showed greater cell proliferation in the dentate gyrus, and there was evidence for the affect it had on the brain.

In humans: Rutter et al (1998) & Beckett et al (2006) studied Romanian orphans. Those who were adopted very young, at under 4 months showed improvements in IQ. Those adopted later, after 19 months, largely remained in the impaired range.

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Adult plasticity

Bruel-Jungerman et al (2005): adult rats placed in enriched environment showed enhanced neurogenesis in the dentate gyrus. Enhanced environment impacts memory - recognition memory was measured as time spent exploring new or old objects. No group differences at short delay but at longer delay, enriched rats showed better recognition.

Adult plasticity refers to the capacity to adapt to changing demands by altering structure. Leads to changes in the brain and behaviour/cognition. As adults, we learn new things, and this learning involves changes in synaptic weights between neurons. So, there must be funcitonal plasticity in the adult brain.

Although neurons don't divide in the adult brain, stem cells exist and give rise to new neurons. In the hippocampus lost neurons aren't replaced but there's an exchange of neurons at a population level. The majority of hippocampal neurons aren't exchanged, approximately 35% of neurons do a "turnover". There are approximately 700 new neurons per day in each hippocampus (Eriksson et al, 1998; Spalding et al, 2013).

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Adult plasticity in taxi drivers

Maguire et al (2000) - classic taxi drivers study: the hippocampus is known to be important for spatial memory. There is evidence for plasticity in the hippocampus. Maguire et al conducted a study on 50 licensed London taxi drivers. Participants were male, 32-62 years and healthy. All had completed the "knowledge" taxi exam. Compared against non-taxi driver controls. There were no differences in the hippocampi as a whole, but taxi drivers had

  • increased grey matter volume in posterior regions
  • smaller anterior grey matter volumes than controls
  • significant correlation between size of hippocampi and time as a taxi driver

Posterior hippocampus stores spatial representation, and can expand when required.

Woollett & Maguire (2011): no difference between qualifiers and non-qualifiers of taxi exam in terms of age, IQ, memory, or brain volume. Qualifiers spent more time training, and were better at a spatial relations test. However, they were worse at a recall of a complex figure. MRI imaging showed larger posterior hippocampi volume at follow-up compared to baseline, but no other volume changes.

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Environmental influences: protective

Thuret et al (2009): "at risk" mice (low amounts of adult neurogenesis) - produce 75% fewer new neurons in dentate gyrus than other mice. Provided an environment with a running wheel.

When the at risk mice had unlimited access to a running wheel, neurogenesis was equal to no risk. At risk mice spatial learning and visual recognition equalled that of the no risk mice after running, and improved memory and performance on a water maze.

Passineau et al (2001): after traumatic brain injury (TBI), rats were placed in standard or enriched environments - provided with motor and tactile stimuli (toys, running wheel, tunnels) and olfactory stimuli (different bedding types).

2 weeks post-TBI, enriched animals had approximately twofold smaller lesion areas. Conclusions: environment can improve recovery after injury.

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Exercise in humans

Environment (exercise through running wheel) has been shown to protect at risk mice; can it do the same for humans?

Hwang et al (2017): 87 young adults. Their aerobic fitness, sustained attention, and working memory was measured. Those who had excellent fitness had faster reaction time and more accurate reactions compared to those with very poor/poor fitness. Physical fitness may lead to a better ability to focus attention

Churchill et al (2002): 124 sedentary adults 60-75 years, assigned to either walking or toning for 6 months. Walking group showed significant improvements in reaction time after exercise.

Voss et al (2013): 70 sedentary adults 55-85, assigned to either walking or stretching group for 1 year. Change in fitness through walking correlated with improvement on a working memory test - maybe having an effect through cardiovascular factors

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Plasticity: gradual or sudden

Bugos et al (2007): 31 adults aged 60-85 years, assigned to no intervention or 6 months piano training, which included 30 mins lesson and 3 hours practice per week. There were changes in executive function in the piano group only.

All studies are conducted on "typical" people; are there differences when brain or behaviour is "atypical"? Do we always know if there is something different about the brain? Case of a 24 year old woman in China: reported at hospital with nausea and dizziness where it was eventually found she had no cerebellum. As well as this, a population study (Vernooij et al, 2007) of 2000 people found asymptomatic brain infarcts in 7.2% of people. This tells us that the brain often adapts to gradual changes. What happens when the change is not gradual?

Phantom limbs: this pain sensation appears to come from an amputated limb, but can also be felt when there is nerve damage and thus no sensory input. Areas of sensory cortex for the amputated limb no longer receive input. Sensory input from adjacent areas "spreads" into areas no longer receiving signals.

Gradual change may allow for compensation to occur.

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Adult plasticity in musicians

Sluming et al (2002): 26 male symphony orchestra musicians. Average around 36 hours playing per week. Voxel-based analysis showed musicians have increased grey matter density in left Broca's area. Broca's area is important for language, but also action and spatial information. There was a significant negative correlation between left inferior frontal gyrus volume and age in controls only - is musical training protective against age-related decline?

Bengtsson et al (2005): study of white matter tracts in musicians, 8 concert pianists and 8 controls. There were differences between musicians and controls in the right internal capsule, which includes cortico-spinal and thalamocortical tracts. They also found that childhood practice correlated with white matter in internal capsule and isthmus. Adolescent practice correlated with white matter in splenium, and adult practice correlated with white matter in arcuate fasciculus.

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