P1 - Biological Approach - Brain and Behaviour Flashcards

techniques, localisation, neuroplasicity, neurotransmitters

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1
Q

what does localisation of function mean?

A

specific parts of the brain are responsible for specific behaviours or cognitive processes

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2
Q

what is the study used for localisation of function?

A

Maguire et al (2000)

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3
Q

what does the hippocampus control?

A
  • critical memory formation
  • helps consolidate or reorganise and stabilise memory
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4
Q

what is the aim of Maguire et al (2000)

A

to investigate the brains of London taxi drivers and if the structure of their hippocampus would be different due to spatial memory

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5
Q

why were london taxi drivers used in Maguire et al (2000)

A

because they undergo an intensive training programme on how to navigate the city and have to pass a set of exams to be licensed.

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6
Q

what was the procedure of Maguire et al (2000)

A

16 right handed male taxi drivers, their average experience as a driver was 14.2 years

MRI brain scans of control subjects were taken from a databased

subjects below 32 and above 62 were excluded, females, left handed were eliminated

this meant comparison sample was 50 healthy right-handed male subjects who did not drive a taxi

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7
Q

what were the findings of Maguire et al (2000)

A

increased brain matter volume in the brains of taxi drivers

control subjects had greater volumes of grey matter in the anterior hippocampus.

no significant difference between general volume of hippocampus, but significant distribution of grey matter from anterior to posterior hippocampus in the brains of taxi drivers

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8
Q

What was the conclusion of Maguire et al (2000)?

A

The researchers concluded that spatial memory is localised to the hippocampus as the taxi drivers, who have to remember large amounts of information, had bigger parts of the posterior hippocampus.

Link back: environmental stimulus in the form of intense spatial memory of taxi drivers, led to an increase in density in the posterior hippocampus.

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9
Q

What is neuroplasicity?

A

Brains ability to rearrange the connections between its neurons as a result of learning or experience

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10
Q

Explain the process of neuroplasicity

A
  • every time we learn something new, neurons repeatedly fire, this is known as long-term potentiation
  • leads to an increase in dendritic branching
  • dendrites of the neurons grow in numbers and connect with other neurons
  • leads to increased number of synapses
  • more synapses - stronger the pathway
  • when a synapse is not used, it may go through synaptic pruning
  • this is our body’s way of maintaining more efficient brain function as we get older and learn more complex information
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11
Q

What study do we use for neuroplasicity?

A

Maguire et al (2000)

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12
Q

How is maguire linked to neuroplasicity?

A

Environmental stiumulus in the form of the intense spatial memory of taxi drivers, led to an increase in density in the posterior hippocampus through the process of dendritic branching.

This shows that not everyone’s brain is not the same and that individuals neural networks can change based on environmental inputs.

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13
Q

what is a neurotransmitter?

A

chemicals that allow neurons to communicate with each other

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14
Q

what is an excitatory neurotransmitter?

A

neurotransmitters which make the target neuron more likely to “fire” an action potential

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15
Q

what is an example of an excitatory neurotransmitter?

A

glutamate

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16
Q

what is glutamate?

A
  • one of the most common neurotransmitters
  • facilitates neural connections and the “turning on” of neurons
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17
Q

what is an inhibitory neurotransmitter?

A

neurotransmitters which make the target neuron less likely to “fire”

18
Q

what is an example of an inhibitory neurotransmitter?

A

serotonin as it has inhibitory effects on neurons, decreasing the likelihood of neurons firing an action potential.

it does not stimulate the brain, but balances out the excessive effects of other neurotransmitters

19
Q

what is serotonin??

A

inhibitrory neurotransmitter

  • plays a role in emotion, sleep and memory
  • links to mood disorders such as depression
20
Q

what is an agonist molecule?

A

any chemical that binds to a receptor site on a post-synaptic neuron causing the neuron to fire

21
Q

what is an antagonist molecule?

A

any substance that fits into a receptor site on the post-synaptic neuron, inhibiting the neuron

22
Q

what is ketamine?

A

high doses - glutamate antagonist, its an excitatory neurotransmitter that facilitates neural network connection making it an anaesthetic

low doses - ketamine acts as a glutamate agonist, enhances stimulation of AMPA glutamate receptors

23
Q

what study do we use for agonist molecules?

A

siegel et al 2021

24
Q

what study do we use for antagonist molecules?

A

arnone et al 2013

25
Q

what study do we use for inhibitory neurotransmitters?

A

arnone et al 2013

26
Q

what study do we use for excitatory neurotransmitters?

A

siegel et al 2021

27
Q

what is the aim of siegel et al 2021

A

to investigate the effiacy of a longer infusion of ketamine in regard to reducing depressive symptoms and link to neural network activity

28
Q

what is the procedure of siegel et al 2021

A
  • University of Washington School of Medicine
  • 23 individuals from treatment resistant depression
  • 27 matched non-depressed controls

MADRS at baseline, 24hrs, 2 weeks, 8 weeks and resting state fMRI

29
Q

what were the findings of Siegel et al 2021

A

participants had significantly reduced scores

ketamine - decrease in hyperconnectivity within limbic system and increase in connectivity between limbic system and frontal areas

smaller right hippocampus at baseline had largest reduction

30
Q

what was the conclusion of Siegel 2021

A

infusion of ketamine provides a sustained response and normalises depression related hyperconnectivity in the limbic system and frontal lobe

31
Q

link siegel to excitatory and agonist questions

A
  • demonstrates how glutamate has a role in encouraging neurogenesis and treating depression. Participants demonstrated increased connectivity between limbic system and frontal lobe as ketamine would have increased levels of glutamate

excitatory - facilitates neural network connections and turning ‘on’ neurons resulting in decrease of depressive symptoms

agonist - ketamine caused neurons to fire encouraging production and passing of glutamate receptors in the brain

32
Q

what was the aim of arnone 2013

A

to investigate the role of SSRIs in neurogenesis and role in reducing symptoms of depression

33
Q

what was the procedure of arnone 2013

A

lab experiment
uni of manchester
64 unipolar depressed participants with half having citalopram and half not
compared to 66 healthy controls
all had MRI scans to measure grey matter concentration in hippocampi

34
Q

what were the findings of arnone 2013

A

after 8 weeks, participants with depression who were assigned to the citalopram had an increase in grey matter and decrease in depressive symptoms

35
Q

what was the conclusions of arnone 2013

A

citalopram increases grey matter which correlates with a decrease in depressive symptoms

36
Q

link arnone with inhibitory/antagonist molecules

A

inhibitory - serotonin in SSRIs are inhibitory neurotransmitters decreasing the neurons will fire actiion potential. it balances out excessive excitatory effects

antagonist - inhibits neurons to fire, which stops reuptake of transmitter leaving more available in the synaptic gap

37
Q

what are MRIs used for?

A
  • creating detailed images of human body
  • used in research to measure brain structure and function
  • can be used to diagnose strokes, tumours etc
38
Q

how does the human body work?

A
  • human body is mostly water
  • protons become aligned in a magnetic field
  • MRI scanner applies a strong magnetic field which aligns the protons ‘spins’
  • scanner produces a radio frequency
  • protons absorb this from the magnetic field and flip their spins
  • when field is off, protons return to normal spin called precession
  • return process produces a radio signal that can be measured
39
Q

what study do we use for scanning?

A

Maguire 2000

40
Q

link scanning to Maguire

A
  • provides evidence for both neuroplasicity and localisation of function
  • achieved through comparison of MRIs between taxi drivers and control group
  • can be inferred the differences in the hippocampi could be attributed to the use of spatial memory by studying change in structure through MRI