My Return To Blogging

It has been a long time since I wrote a post on this blog. 2013 has been an extremely busy year for me, mainly due to the fact that it was my final year of university. I am ecstatic to report that I have graduated with a 2.1 BSc in Forensic Psychology (from the University of Leeds) and am about to begin the next chapter of my life.

Now that I am no longer a full-time student I am realizing how difficult it can be to keep up to date with learning new things. As a result, I am now going to use this blog to post about things I am learning both for academic reasons and out of general interest.

My first course of action was to sign up for several FutureLearn courses. FutureLearn.com is a website which offers a wide variety of free short online courses from some of the world's top universities. It is quite a new scheme run by a private company and for 2013/14 all of the courses are pilots which will allow feedback and editing for the courses for the following years. New courses are unveiled regularly on the site and I have signed up for several of them including: England in the time of King Richard III (which started last week), Introduction to Forensic Science, Good Brain Bad Brain: Basics, Shakespeare's Hamlet: text, performance and culture, and finally Good Brain Bad Brain: Parkinson's Disease. Many of these courses begin in the new year, I will try my best to complete all of them although this will obviously depend on my work schedule.

I have also recently been offered a full-time job with the NHS as a Medical Illustration Support Worker. The job is within the National Diabetic Eye Screening Programme (NDESP) and so I have been reading a lot of related research and hope to learn much more along about the programme itself and diabetes along the way.

I am really looking forward to picking up where I left off with these blog posts and hope that they are both interesting and informative.

Thank you for reading.

Rose. X

Internal Regulation

     This next revision blog is all about internal regulation i.e. eating and drinking.

The Brainstem

     The brainstem is ancient. All our ancestors ate and drank (chewed and swallowed). The brainstem links to the heart and lungs (blood and air) and also monitors glucose levels.
     The brainstem receives data from the digestive system (and elsewhere):
* tongue
* stomach
* duodenum
* liver
     It then transmits this information further into the brain i.e. to the hypothalamus.


Fluid Regulation

Extracellular fluid is like seawater.

Daily Water Balance
* Intake of water - from water itself and from food (about 2.5 litres)
* Output of water - through urine, evaporative loss and faeces (about 2.5 litres)
There is a balance here.

Fluid Balance
     Intracellular fluid accounts for about 67%. Extracellular fluid accounts for the rest. There are different types of extracellular fluid:
* Interstitial fluid (26%)
* Blood plasma (7%)
* Cerebrospinal fluid in the brain (approximately 1%)
     If the levels of these drop, you get thirsty. Intracellular fluid and blood plasma are the most important.

     Osmosis ensures that there is an equal salt concentration on both sides of the membrane. This is shown in the diagram below.

     With plenty of water, cells work well. If they have too much, they rupture as chemical reactions fail. Little water = lots of salt.
     Outside of a cell there is lots of water and few solutes. Osmosis brings the water into the cell and ensures there is the same concentration on both the inside and the outside.

Blood Plasma
     Blood plasma is critical to the heart. Without enough blood, the heart is unable to pump effectively. There is some flexibility however this is limited. Too much plasma (and therefore pressure) causes blood vessels to burst.
     A hangover is losing cerebrospinal fluid in the brain, therefore you need lots of water!

Two types of thirst
     There are two types of thirst. These are called volumetric thirst and osmometric thirst. Volumetric thirst is caused by loss of blood plasma, whilst osmometric thirst is caused by the loss of intracellular water. Feeling thirsty leads you to seek out water - this a behavioural.

     In volumetric thirst you lose water through serious blood loss and diarrhoea. Osmometric thirst is caused by lack of water e.g. through a salty meal.

Osmometric Thirst
     Osmometric thirst is caused by not having enough water in your cells. The cells begin to shrink. Specialist neurons are able to spot this. These are called osmoreceptors. Cell shrinkage leads to a change in the rate of neuron firing, this is shown in the diagram below.

The diagram below shows circumventricular organs. Note the lamina terminalis.

     The anterior cingulate cortex is the most primitive cortex in the limbic system. It is responsible for the sense of thirst. This area of the brain gives you the feeling of a dry throat even though you're throat isn't actually dry. This is also known has motivational unpleasantness.

     In the image above look at view B. The anterior cingulate is situated between the pink bit and the frontal lobe just under the letters 'ob'. The lamina terminalis is just above (but slightly to the left) the pituitary gland.
     When you are running short of water, the anterior cingulate is aware. It gets more active which makes you thirsty. Once you have had a drink, the lamina terminalis settles down after about 20 minutes.


Volumetric Thirst


     Volumetric thirst is caused by a lack of blood plasma. This occurs through loss of blood (and blood pressure), diarrhoea and vomiting. It means you have a lack of salt within your bodily fluid.

     Atrial Baroreceptors detect the stretchiness (or lack of) of arteries. They release atrial natriuretic peptide (ANP). When blood pressure drops, less is produced. This inhibits drinking and boosts the kidneys. The less ANP there is, the thirstier you get.

     Vasopressin is a peptide hormone released by the posterior pituitary gland. It is an anti-diuretic hormone (ADH) which instructs the kidneys to reduce the flow of water to the bladder.

     Volumetric thirst means a reduced flow of blood to the kidneys. The kidneys secrete a chemical known as Renin.

     The diagram above shows hormones, their relationship with enzymes and the effects caused. Remember that the circumventricular organs is the lamina terminalis! The lamina terminalis spots thirst.

     Both types of thirst (volumetric and osmometric) activate thirst in the same place/area. This is shown in the diagram below.

Food Regulation

     The average American eats 3,800 calories a day. Half of the US is clinically obese whilse 3% of US adolescents suffer from anorexia or bulimia nervosa.

     Although food provides energy, about 33% of energy is food is lost during digestion. 55% is consumed by metabolism e.g. maintaining membrane potentials and heat production etc. The last 12% is used for active behaviour.

Long-term satiety

     Fluctuating body weight adjusts over a long-term basis. Force-fed rats will reduce their food intake once they are permitted to do so. This shows that it can't be weight that is measured - how does your body know? Your body knows when your hormones and fat cells are full.

Energy Storage

     Glucose is the principle sugar, therefore it must be stored inertly. Glucose is converted into glycogen. This is called glycogenesis. You don't keep glucose in your system as it is unhealthy. Glycogen is stored in the liver and muscles. Every time you convert glucose into glycogen, you lose some - it is not a perfectly efficient process. Glycogenesis involves insulin which is a peptide.

Insulin and Satiety

     Newly released insulin allows for the instant use of glucose (and storage of the rest). Glucodetectors in the liver, signal the 'nucleus of solitary tract' (NST) which is in the hypothalamus. Too much glucose causes you to secrete insulin.

See the diagram above. Leptin is released by fat cells, ghrelin by the stomach and PYY by the gut. A combination of all of these, drives apetite. The signals produced go to the brainstem or hypothalamus.

     The dual-centre hypothesis states that there is one area for hunger and one for satiety. This hypothesis is far too simplistic.

     In the lateral hypothalamus, lesions cause Aphagia (refusal to eat). Whereas lesions/damage in the ventromedial hypothalamus cause obesity. The latter has been found in research involving rats, dogs and humans.

     The diagram below, shows what occurs when there are lesions in the ventromedial hypothalamus.

The satiety centre is where the arrow points. The satiety centre is the part that tells you that you are full. Therefore the arrow points to the fact that the lesion has destroyed this.

     It is not just insulin that effects satiety. All four hormones listed previously are important (leptin, ghrelin and PYY). Ghrelin releases growth hormones.

Leptin

     Leptin is a chemical secreted by well-nourished fat cells i.e. it tells you not to eat anymore. Certain mice are unable to produce leptin this makes them obese.

     Both mice in the picture above are obese due to being unable to produce leptin. The mouse on the right however is injected with leptin on a daily basis. The mouse on the left weighs 67g whilst the one on the right only weighs 35g.

     However, when injecting leptin into rats it increases their aggression.

Ghrelin

     Ghrelin releases growth hormones. When the stomach is empty then it secretes ghrelin but when it is full it secretes hydrochloric acid. Ghrelin increases before meals and the levels drop immediately after a meal is eaten. It is only when the stomach is empty that you need to eat.

     If you inject ghrelin into the cerebral ventricles you get a massive increase in apetite.

PYY3-36

     PYY is secreted by both the small and large intestines. You have low blood levels prior to meals. Injecting PYY curbs apetite in both humans and rats. Therefore it has the opposite effect to ghrelin.

     When the hypothalamus picks up on PYY it knows that you have food in your gut/intestine. The diagram below shows peptic hormones.

     Leptin and insulin are longer term chemicals. They deal with the consequences of your reserve e.g. leptin - how much fat you have. They activate appetite-suppression areas and inhibit appetite-increasing areas.
     Ghrelin and PYY are short-term chemicals which are based entirely on whether you have eaten (immediate).

Over/under eating
     Starvation is worse than overeating (it is fatal in short-term) and is evolutionarily more likely. We have evolved to obtain/store food - we eat when empty, not when hungry. Everyone eats more than they need to. We enjoy high calorie foods therefore are predisposed to putting weight on.

What stops eating?
1) Short-term satiety - feedback from food you have yet to swallow, eyes, nose, mouth and the contents of
                                   your gut.
2) Long-term satiety - fatty tissue (eating more has an effect - build fatty tissue).

The image above shows a study by Weingarten & Kulikovsky (1989). Rats were given one of two diets:
1) usual diet - gradually eat more
2) completely new diet - ate more from the start

The diagram shows that those on the unfamiliar diet ate more than those on the normal diet.

The hypothalamus monitors peptide hormones in the blood.

Weight Loss
    Most programs are unsuccessful. Weight loss is rapid, then it declines, then halts. When the diet ends you then rapidly gain weight and you are back to the starting point.

Who gains weight?
     Some prefer high calorie foods, some cultures are more prone. Output such as exercise is important.

Eating Disorders
     50% of the US are obese. Anorexia Nervosa accounts for 1.5% - here there is evidence of abnormal peptide levels. Anorexics find it hard to increase their desire to eat more. Bulimia Nervosa also accounts for 1.5% and relates to a lack of nutrient reserves.



So, fluid and food intake is now done. Just over 9 hours till the exam so best get cracking on the next topic (reproductive behaviour).

xoxo

Neurological Diseases

     This revision blog post concerns neurological diseases such as tumours, seizures, strokes and degenerative disorders such as Alzheimer's and Parkinson's.


     Neurogenesis (cells growing back) is possible in adults although it is very limited. The diagram below shows the brain in relation to the limbic system.

     The hippocampus and the olfactory bulb are the only areas which can replace neurons. The image below shows the site of most adult neurogenesis. This integrates into hippocampal functioning.

     There are several things which encourage neurogenesis i.e. help to grow neurons:
* Enriched experiences - e.g. learning (lectures is an example)
* Physical exercise (this has been shown in rat studies)


Tumours (cancer)


    Tumours develop through neoplasm or 'new growth' and the duplication of malfunctioning cells. Benign tumours mean that there is no chemical damage but they kills cells through compression. Malignant tumours travel everywhere.
     Encapsulation - does a border exist between the tumour and the brain? If so, the tumour is easier to remove. If not, it is hard to say whether or not all of the tumour has been removed.

The diagram below shows a scan of a benign brain tumour. In the image there is a clear boundary between the brain and the tumour.

The diagram below shows a scan of a malignant brain tumour (the one on the left). The tumour is shown in the form of dark mass, this type of tumour is much more dangerous as bits could break off meaning that there could be small parts of the tumour all over the brain.

Metastases
     Malignant tumours shed cells. These travel through the blood stream as 'seeds'. Being stressed increases cancer as the sugars produced feed it.

Tumours and Damage

Compression - is when the tumour pushes brain tissue aside. Benign tumours occupy space and directly
                       destroy brain tissue. They also indirectly block the flow of cerebrospinal fluid (CSF) and
                       affect normal brain functioning.

Infiltration - occurs with malignant tumours. This is when the tumour invades the surrounding areas,
                   destroying other cells.

     Malignant tumours grow fast, but are sensitive to radiation. Astrocytes (a type of glial cell) are key in making mistakes in duplication.



Epilepsy


     Epilepsy is the manifestation of the electrical nature of the nervous system. Normal activity is desynchronised.
     Seizures are a wave of excitation that is carried across the brain. i.e. lots of neurons fire (almost like a mexican wave). Sometimes it is hard to tell if someone is having a seizure.

     Epilepsy is self-generated and affects approximately 1% of the population. It is more common in children, however they tend to grow out of it. Not only does epilepsy cause convulsions (motor seizures) it also has more subtle effects on things such as:
* thought, mood and behaviour
* viruses, blows to the head and toxins

Categories of Seizure
1) Generalised - whole brain, causes loss of consciousness and symmetrical muscle spasms in both halves of
                          the brain at the same time.
2) Complex Partial Seizures - affect specific areas of the brain

The diagram above shows abnormal EEG (electroencephalogram) activity across the brain.

Grand Mal


     A grand mal seizure is a generalised, tonic-clonic seizure which results in a convulsion. The tonic phase is the first phase of a grand mal seizure in which all of the patients muscles are contracted and rigid. The clonic phase is the second phase of a grand mal seizure in which the patient shows rhythmic jerking movements.
     Grand mal seizures usually either constrict or stop breathing. They also cause the patients' eyes to roll, their face to contort and they often bite their tongue. There is also intense sweating and/or salivation.
     Soon after the seizure, breathing returns and the patient goes into an unresponsive sleep (15 minutes) followed by normal sleep (2 hours).

Petit Mal


     A petit mal (little trouble) seizure occurs in a different type of epilepsy. There are no convulsions and it is most common in children and ceases around puberty. When the patient suffers from a petit mal seizure (sometimes called an absence seizure) they appear to be absent or daydreaming.
     Petit mal seizures a very brief - lasting only 15 seconds or less. When they occur, the patient may simply stop talking momentarily. It may also interfere with school, particularly because the child may be viewed as just having a lack of attention. The patient has no memory of the event although you can sometimes get a sense of when one is about to occur. It has been found that calling the persons name can help to stop the seizure occurring.

Complex Partial Seizures
      Complex partial seizures only involve part of the brain and are associated with the bilateral cerebral hemisphere. There are a wide variety of symptoms and they are usually preceded by an unusual sensation.




Strokes


     Strokes produce permanent brain damage, but depending on the size of the affected blood vessel, the amount of damage can vary from negligible to massive.


Cerebral Haemorrhage - blood vessels burst in the brain and the sufferer has very high blood pressure.

Cerebral Ischemia - the disruption of blood supply to the brain (blockage).

The diagram below shows bifurcation (splitting). The bifurcation occurs where the dark shadow is. When a person has high blood pressure it is hit at a high speed which creates damage. Epinephrine (adrenaline) stimulates sugar release. Sticky sugar gets stuck in the crates.

     Atherosclerotic Plaque can also lead to strokes and is shown in the diagram below. Oestrogen helps to stop plaque forming which is one reason why men die earlier than women.

     A thrombus is a blood clot that forms within a blood vessel particularly when their walls are already damaged. Sometimes thrombi become so large that blood cannot flow through the vessel causing a stroke. If a thrombus blocks coronary artery it causes a heart attack.

Alzheimer's Disease


     Alzheimer's disease is a degenerative brain disorder of unknown origin. It causes progressive memory loss, motor deficits and eventual death. It is a type of senile dementia which appears before the age of 65. It's frequency increases until the age of about 85 years, after that chances fall.

     The diagram above shows brain shrinkage with age. Only hippocampul shrinkage correlates with loss of memory. Alzheimer's Disease causes severe degeneration in the hippocampus but the amygdala and many areas of the cortex are also affected (frontal and temporal).

     Extensive use of brain makes Alzheimer's less likely.

     Early signs of Alzheimer's disease include memory loss of recent events, memory impairment and an inability to follow conversation. In the early stages, some people make up stories in order to fill in the gaps in their memory.
     People who have Alzheimer's are unable to answer questions such as:
* who is prime minister?
* what year is it?
* where are you now?
     They are also unable to care for themselves.

     The diagram above shows the Cholinergic Pathways (ACh). In Alzheimer's disease, problems occur in the area shown as the basal forebrain. In this area there is a mutation in the production of proteins.

Changes associated with Alzheimer's Disease
* Amyloid Plaques - extracellular deposits that consist of a dense core of a protein called B-amyloid.
* Neurofibrillary Tangles - are due to whorls of proteins, caused by plaques and consist of dying neurons.

     These changes cause the basal forebrain to stop producing acetylcholine.

The diagram below shows a normal human brain.

This image shows a brain affected by Alzheimer's Disease. Note how dry and crusty (my lecturer's terms) this is.

The next three diagrams shows the brains degeneration in Alzheimer's Disease. Diagram 1 shows a preclinical brain. Diagram 2 shows a brain with mild Alzheimer's Disease. Diagram 3 shows severe Alzheimer's Disease.

Delusions


     Delusions are a false belief which are firmly maintained in spite of incontrovertible and obvious proof to the contrary. Delusions can be symptomatic of other conditions such as dementia and one can have  more than one type at the same time.

Here are some examples:
* "My neighbour steals from me" - this is a persecutory delusion

* "My husband is an imposter. He looks like him and acts like him, but it isn't him" - this is called capgrass
    syndrome. There is no emotional link.


Confabulation


     Confabulation is a 'filling in' of memory gaps through fabrication. If patients are unable to remember, it is tempting to invent stories. Not all Alzheimer's patients do this.

The graph below shows research by Feinburg and Keenan (2004). They found that people with delusions tend to have right hemisphere damage.

Below is an image from a fMRI scan showing semantic memory i.e. recalling the name of a previous school. Just to point out - it is the orange coloured bits at the top (front) of the brain which you should be looking at.

The image below shows episodic memory i.e. recalling something that happened to you at primary school. If this area is damaged, you won't be able to remember what happened at school.

It is important to note that Alzheimer's Disease is not dementia. It is one cause, however dementia is also caused by strokes and dehydration.




Parkinson's Disease


     Parkinson's Disease is to a great extent, a movement disorder. It affects 1% of those over the age of 65 and is most prevalent in males (x2.5). Parkinson's Disease causes widespread neural degeneration in the substantia nigra (nigrostriatal system).

     When treating Schizophrenia, if a patient is given too much dopamine it can lead to Parkinson's Disease and vice-versa.

This diagram shows the Dopaminergic Pathways. The mesostriatal pathway is also called the nigrostriatal pathway/system. Parkinson's Disease is caused by a lack of dopamine.

Substantia Nigra
     The substantia nigra secretes dopamine which is an important neurotransmitter. When the substantia nigra is 80% degraded, Parkinson's Disease occurs.

Nigrostriatal Pathway
     The nigrostriatal pathway to Caudate Nucleus and Putamen (called striatem when together) is a basal ganglia motor loop.
     When an individual is affected by Parkinson's Disease they have difficulty controlling and planning their movement.

The diagram above shows the Basal Ganglia. The moderation of activities however is initiated elsewhere.

The diagram above shows the links between the primary motor cortex and the nonprimary motor cortex. Messages are sent along the arrows shown. The basal ganglia is in trouble when you have Parkinson's Disease. The cerebellum is in trouble when you are drunk.

This next diagram looks at the link between movement and Parkinson's Disease:

     When you initiate movement, the basal ganglia sends its opinion very quickly - later the cerebellum does the same thing. The cerebellum joins movements e.g. if you reach for a cup, the cerebellum gets you to grip it.

     The image above shows the typical posture of someone with Parkinson's Disease. They suffer from instability and have difficulties in starting and stopping movement. They are also unable to catch themselves if they fall.
     Parkinson's is normally shown in a resting tremor (which diminishes during purposeful movement). It also causes rigidity of the joints - this however, is not the cause of slow movement! In Parkinson's Disease, nigrostriatal neurons disappear or mutate.

Damaged Basal Ganglia
     When the basal ganglia is damaged, an individual has a lack of internal cues to help with movement. Therefore when someone is suffering from Parkinson's Disease, external cues provide helpful feedback e.g. having a line to their bedroom. This helps them to walk around normally. The basal ganglia is important for implicit skill learning and new associations.

The diagram above shows episodic recall ability. This shows that it is not affected by Parkinson's Disease.



So. That was my revision for neurological disorders. It has made me feel slightly depressed. Particularly as I now have 11 and a half hours to go until my biological psychology exam. It is 2.30am and I am definitely in need of some food and some more coffee!!!

xoxo

Neurodevelopment (Brain Development)

Genie

     The case study of Genie is well-known throughout psychology. The case begins with Genie's parents. Her mother (Irene) banged her head as a child, was blind in one eye and was 90% blind in the other eye. Genie's father (Clark) was twenty years older than her mother and was described as being 'overprotective'.

     Genie's father did not want children, two of his children with Irene died at early ages and a third child was looked after by the paternal grandmother. Yet, in 1957 Genie was born.

     Shortly after Genie's birth, her grandmother died in a hit-and-run. This incident left Clark feeling very depressed and outraged. He grew isolated and deemed society to be 'evil'.

     When Genie was discovered, she had spent all thirteen years of her life in a tiny bedroom. She had mainly been restrained on a potty, but also with a sleeping bag acting like a straight-jacket. All her life, Genie had been actively discouraged from making any sounds at all. When in contact with her, Genie's father merely growled. Alongside this, Genie's mother and brother only spoke in whispers for fear of the father - therefore Genie heard next-to-nothing in her first thirteen years of life.

     Genie's visual stimuli was also limited as her bedroom contained two small windows which had been taped up. The only thing she had been allowed to occasionally play with was a plastic raincoat. When it came to food, Genie was fed either baby food or a hard-boiled egg in complete silence and if she choked or spat any out, it would be rubbed in her face. Apparently, her father had said that she would not live beyond twelve years old, and that if she did, only then could her mother seek help.

     Genie was discovered and taken into care in 1970. Her father committed suicide on the day he was due in court for abuse charges. When she was found, Genie weighed only 59lbs and was 4' 5" tall. She was incontinent, unable to chew solid food and couldn't swallow properly. If Genie got excited she she would urinate and she was unable to focus her eyes beyond 12ft. Due to the conditions she had been kept in, Genie was unable to extend her limbs properly which made walking difficult. The lack of speech and noise that she had experienced, meant that she knew very few words.

     When she was first taken into care, some progress was made. For example: she was toilet trained within three days. She also began to hoard plastic objects and held people's hands to stop them from leaving. Unfortunately, years later Genie still had no reaction to warmth/cold, was easily terrified, was still unable to chew food and was still limited to just a few words of vocabulary.

     This unique case greatly emphasises the importance of experience in our development!

Neurodevelopment

There are two stages:

1) Nature - growth of the embryo

2) Nurture - experience of life

     The photo above shows X and Y chromosomes. The X chromosome contains 1000 genes, whilst the Y chromosome contains 80 (the latter is due to 300 million years of chemical attack).

     XX: makes a female

     XY: makes a male

     1-2% of men are infertile due to the malfunctioning of the Y chromosome. The Y chromosome also contains things which are harmful to women.

The Zygote

     The male's sperm is X/Y while the female's egg is X only. In terms of sperm, X is hardier and Y is faster.

Mortality Rates

     Males experience higher mortality rates at all stages of life (Dodson, 2007). When it comes to conception the mortality rates are: 100 girls/125 boys. At birth the rates are: 100 girls/105 boys - almost 20% don't make it.

     Upon conception the zygote continually divides - by the 5th day there are 16 cells. Is this zygote simply an amorphous mass (shapeless mass of protoplasm)? No:

1) You can differentiate between cells e.g. muscles, glial cells, bones

2) Cells must be able to get to where they need to be, then align correctly

3) Can establish the relationships between them

     The mesoderm is one of the three primary germ cell layers in the very early embryo. The other two layers are the endoderm (inside layer) and ectoderm (outside layer). The mesoderm relates to the circulatory system, gonads, muscle, bone and cartilage. The endoderm relates to the digestive organs and the lungs.

Names for zygote:

* Zygote at fertilisation (up to 2 weeks)

* Embryo (2 to 8 weeks)

* Foetus (9 weeks to birth)

Neural Plate

     There neural plate develops three weeks after conception. This is the first stage of development in all vertebrates. The vertebrate brain includes the forebrain, midbrain and hindbrain. The next images show interesting stages in the development of a human embryo.

This next picture shows the development of the human face during weeks 10-14.

This diagram shows what the human embryo looks like at approximately 28 days. Note the presence of the forebrain, midbrain and hindbrain (the latter of which are the beginning of the brainstem).

Stem Cells

     Stem cells are able to self-renew. They are also undifferentiated meaning that they can develop into anything. When in the nervous system, some become neurons but most become glial cells.

Migration

     Once created, cells have to move to their correct location. There are two types: glia-mediated translocation (diagram) and somal translocation (chemical attraction).

Neural Proliferation

      Neural proliferation is the massive expansion of cell numbers in the neural tube. Not all areas grow at the same rate, this is determined by species e.g. birds and fish have larger areas responsible for 3D.

What happens on arrival in the correct location?

Aggregation - thanks to certain chemicals, similar cells bind together.

     Once neurons have migrated to the right place and have aggregated into structures, axons and dendrites grow out from them. Some neurons extend finger-like growth cones or filopodia.

The French Flag Model below shows the ZPA (Zone of Polarising Activity).

Synapse Formation

     Once the axons are in the correct place, a network needs to be built. Most neurons are connected to at least a thousand others (the average is around 7,000). One neuron can build an axon, but two are needed to build a synapse. This is called synaptogenesis. Connections are made with the best available cells, this is shown in the diagram below.

The graph below shows synapse levels in postnatal development:

     Alcohol readily passes into the placenta, disrupting synaptogenesis. It causes Foetal Alcohol Syndrome (FAS) which can lead to brain damage, deformity and poor coordination.

Infant Development

     Between birth and adulthood, the brain quadruples in size. There are however, no additional neurons being developed. This brain growth is due to myelination, further branching out etc.

     Linking back to Genie, early experience is vital as unactivated neurons will die (apoptosis).

     According to Spear (2000), the brain only achieves maturity in late adolescence. After birth the focus of development is mainly on the pre-frontal cortex.

     Myelination is required for adult function. Most myelination is done by 3-4 years.

So there you have it! Basic neurodevelopment!

xoxo