Brain + behaviour

• What are the topics + the studies which link to it?

  Localisation - Maguire 2000.

  
  

  Neuroplasticity - Maguire 2000.

  
  

  neurotransmitters:

  Excitatory - Seigel 2021.

  
  

  Inhibitory - Crockett 2010.

  
  

  Techniques - Maguire 2000.
• What does biological approach say?

  There is a biological reason for behaviour - with a focus on nature
• Maguire 2000


  Looks at localisation of function + neuroplasticity for spatial memory.

  
  

  Aim - Investigate brains of London taxi drivers to look at the structure of their hippocampus which links to spatial abilities.

  
  

  Controls = no females, all right handed, no health issues,

  
  

  Procedure - 16, right-handed male taxi drivers, who had spent 2 years in training and 14.2 years in experience.

  
  

  - MRI brain scans taken. Compared scans to 50 right-handed males who did not drive a taxi.

  
  

  Findings - Increase brain matter volume in posterior hippocampus of the taxi drivers. However controls had greater volume in anterior hippocampus.

  - No difference in terms of size of hippocampus, just the distribution of grey matter (anterior and posterior).

  
  

  Conclusion - Spatial mem is localised to hippocampus as taxi drivers had a larger posterior hippocampus. Support for neuroplasticity = environment changing connections between hippocampus.

  
  

  +

  Quasi - did not randomly assign them to groups as already was pre-existing.

  
  

  Compared to control group which were not taxi drivers to measure cause and control.

  
  

  -

  Just cause they all have a high volume of grey matter in their hippocampus does not mean it is because they are a taxi driver. They may be naturally predisposed to choose a profession which has high spatial memory.
• Evaluation for the localisation of theory?

  Unbiased - Ignores individual differences - e.g., women have small size brain than men with women having a larger hippocampus.

  
  

  Reductionist - Only looks at the hippocampus as don't know that other brain regions could have an impact too.

  
  

  Assumption - overgeneralisation saying that one area of the brain is responsible for behaviour.
• What is neuroplasticity + the procedure?

  Brains ability to rearrange connections between neurons.

  
  

  When we learn someone new the neurons fire leading to an increase in dendric branching. With the more neurons, the more connections which lead to an increase in synapse. The more synapses the stronger the pathway. If synapse is not used then synaptic pruning occures.
• Linking Maguire to neuroplasticity?

  Environmental stimulation occurs in the form of the spatial memory of taxi drivers, leading to an increase in volume of the posterior hippocampus through dendric branching.

  
  

  The taxi drivers had less grey matter in their anterior hippocampi compared to others. Showing that brains are not the same and environmental inputs can cause neural networks to change. As well as cognitive functions (e.g., memory) can change over time (e.g., adulthood).
• Evaluation for neuroplasticity?

  Neuroplasticity has lead to the research into neurorehabilitation which uses motor therapy and electrical stimulation to fix negative effects of cognitive functions. Is amazing for those who have been in accidents, injuries or those who have had strokes.

  
  

  Neuroplasticity has strengthened the idea of localisation and given research into how this happens.
• What is neurotransmitters? Excitatory and Inhibitory?

  Excitatory: Glutamate (Siegel).

  - Stimulates the brain by 'firing' action potential. Released from the neuron and travels up the synapse where it connects to the receptor site.

  
  

  - Glutamate = most common neurotransmitter.

  
  

  
  

  Inhibitory: Serotonin (Arnone).

  
  

  Neurotransmitters released from neuron and travel down synapse where they connect to receptor sites. Less likely to fire an active potential.

  
  

  - Serotonin is an inhibitory neurotransmitter as it inhibits the neuron decreasing action potential through the balancing of excessive neurotransmitters.
• What is serotonin?

  Neurotransmitter. Linked to cog functions like emotion, memory and sleep. Is linked to mood disorders such as depression.

  
  

  - SSRIs - drug companies to reduce depression and other mood disorders. Due to correlation of depression and low levels of serotonin.
• What is an agonist? What is an antagonist and what studies am I using for them?

  Agonist (Siegel) - binds to receptor site on post-synaptic neuron which causes firing of action potential.

  
  

  Antagonist (Arnone) - fits into receptor site on the post-synaptic neuron which prevents the neuron from firing.
• What is ketamine + glutamate? And what is the issue??

  Most common neurotransmitter. Facilitates neural network connection and the 'turning on' of neurons, fuelling neuroplasticity (strengthening of synapse).

  
  

  Newest and most effective to treat mood disorders (depression) for treatment resistant (2SSRIs) individuals.

  
  

  Glutamate = facilitates neural network communication.

  
  

  High doses = glutamate antagonist = blocks glutamate making it good for anaesthetic causing immobility.

  
  

  Low doses = Glutamate production enhanced, therefore good to treat depression due to links to neuroplasticity and dendric branching as it is a 'sub-anaesthetic'.
• Siegel 2021?


  Aim - investigate effectiveness of a long infusion (96h) of ketamine to reduce depressive symptoms and neural network activity.

  
  

  Procedure - University, 23 treatment resistant depression with 27 non-depressed controls.

  
  

  Measured depressive symptoms using MADRS (diagnostic questionnaire) at baseline, 24h, 2weeks and 8 weeks later.

  
  

  Findings - all had reduced scores on MARDS.

  
  

  Ket condition = lower hyperconnectivity (too many neural connections causing a heighten in emotions) in the limbic system. But an increase in connectivity from the limbic system (amygdala) and the frontal lobe (thinking+decision making). Connecting rational thoughts to our emotions.

  
  

  Small hippocampus = largest reduction in depression.

  
  

  Conclusion - single pro-longed infusion of ket reduced depression in treatment resistant individuals with the normalisation of hyperconnectivity within the limbic system and the frontal lobe.

  
  

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  Temporal validity.

  Follow up of 8 weeks later.

  Insight into neural network linking to depression.

  
  

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  8 weeks - not long enough, could relapse?

  Only 23 individuals.

  Students -YAVIS
• What are SSRIs?

  Most common form to treat depression. With the reduction in symptoms.

  
  

  Increase serotonin in brain with the block of reuptake making more serotonin available to stimulate the post-synaptic neuron.

  
  

  -> if depression caused by lack of serotonin, then serotonin should be increased to reduce symptoms.
• Arnone 2013?


  Aim - Investigate role of SSRIs in neurogenesis and reducing depressive symptoms.

  
  

  Procedure - Lab, Uni, 64 unmedicated depressed individuals, compared to 66 healthy controls. Was an 8 week trial.

  
  

  1) 1/2 prescribed citalopram.

  2) 1/2 no treatment.

  
  

  MRI scans to measure grey matter in hippocampus.

  
  

  - After 8 weeks the grey matter was measured again.

  
  

  Findings - Citalopram individuals had an increase in grey matter and less symptoms.

  
  

  Conclusion - citalopram increases grey matter linked to decrease in depressive symptoms. Therefore SSRIs are useful in treating depression.

  
  

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  Lab - controlled.

  MRI scans - scientific + good

  cause of measure.

  Control group.

  
  

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  Unethical - withhold treatment.

  Small sample - low generalisability.

  Not all had reduction in symptoms after 8 weeks.
• Discussion para for neurotransmitters?

  SSRIs overhyped - big Pharma, making $7B in US.

  
  

  Empirical support from animal research.

  
  

  Depression cannot be because of biological factors. Ignores cultural differences (collectivist/individualist).
• What study am i going to use for techniques? What used to happen to patients in 1880s?

  Maguire 2000. - MRI

  
  

  Doctors manipulated brain to calm/treat patients in 1880s (e.g., cortex = schizophrenia).

  
  

  First procedure - labotomy where they used an ice pick and inserted through the eye socket with a hammer to separate frontal lobes.
• What is an MRI scan? How does it work? Strengths/weaknesses?

  Magnetic Resonance Imaging - scanning of human body with use of magnetic and radio waves to create images. Mainly used for brain however can be used for internal body to find tumours and strokes.

  
  

  Due to body being made of water, water has protons which align in magnetic field. MRIs make the protons spin due to absorption of energy therefore allowing images.

  
  

  Made in 1977 used to diagnose cancer.

  
  

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  Helps diagnose conditions, can look at any part of body.

  
  

  Is non-invasive and does not harm pregnant women.

  
  

  No evidence to say is harmful - seen as one of the safest medical procedures.

  
  

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  Expensive to purchase + operate.

  
  

  Can experience claustrophobia - some obese patients cannot use. Harm?

  
  

  Exposure to magnesium = bad for people with metal inserted (metal knee), or those with pacemakers.
• Define localisation of function.

  The theory which states that each specific area of the brain has a certain function.
• What is the limbic system?


  The centre of the brain. Has a role in memory, motivation + emotion.
• What brain parts are in the limbic system?

  Amygdala, Hippocampus, Ventral striatum, Hypothalmus.
• Define the amygdala, hippocampus + the hypothalamus.

  Amygdala - Associated with fear + memory.

  
  

  Hippocampus - Associated with memory.

  
  

  Hypothalamus - regulates the nervous system. Communicates with the endocrine system.
• How do researchers observe brain activity in localised areas while performing tasks on the patient?

  Brain scans - PET, MRI + FMRI
• Key study of localisation of function?

  HM - Corkin et al 1997
• What is the background information of HM?

  He fell off his bike + sustained a head injury which caused him to have serious epileptic attacks from the age of 10. At 27 he had become so incapacitated by his seizures that he couldn't lead a 'normal' life + medication didn't help.
• Who studied HM?

  Scoville -> operated on him - removed his hippocampus.

  Milner -> Cognitive processing tasks (star).

  Corkin -> further tests.
• What did scoville + milner do to HM?

  Observed his behaviour, conducted interviews with HM, did cognitive testing = memory recall test, learning tasks (reverse mirror drawing).
• What did Scoville + Milner conclude?


  That the hippocampus + hippocampal gyrus are critical for the retention of experience (memory).
• What did Corkin et al 1997 aim to do?

  Aimed to determine the extent of HM's amnesia + to understand what this meant for his daily life.
• What is triangulation?

  The use of multiple methods of research to study one person/question.
• What was Corkin et al 1997 method of research?

  Used data from the previous data (testing + observations, interviews + cognitive task. Used MRI's to show the damage of the hippocampus + amygdala + areas close to it. Then tested areas of the brain also linked to memory.
• What was the results of Corkin et al 1997?

  Found that the lesion in his brain was much smaller than reported by the original surgeon (5cm not 8cm), HM could not aquire any new episodic knowledge + same for semantic knowledge -> Suggests that the brain strutires that were removed are important for LTM. However procedural memories were still maintained. Also showed improvements on the performance of new skills (hand - eye coordination's).
• Conclusion of Corkin et al 1997 study on HM.

  concluded that the hippocampus plays a critical role in converting memories from STM to LTM.