week 5 Flashcards

Associating brain and behaviour Describe stages of CNS development Discuss how experience changes the brain Describe basics of genetics and relation to behaviour Identify methods of testing genetic contribution to behaviour

1
Q

How do we correlate the brain with behaviour?

A

Postmortem Examination [Analysis of the brain after death]
Lesion/Ablation Studies [Removing part of brain]
Brain Stimulation [Structural and Functional]
Imaging Studies [Structural and Functional]

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2
Q

What is the only definitive way to diagnose Alzheimer’s disease? What are some critiques of this examination?

A

Postmortem, we have to compare Alzheimers disease with Neurotypical brains. persons of the same age, sex and died of similar reasons

Critiques;

  • Convenience sampling
  • Issues of consent
  • Issues of confounding (e.g., other trauma causing behaviour)
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3
Q

What is the goal of Lesion of Ablation studies?

A

the goal of lesion studies is to reveal what functions are performed by different regions of the brain then to understand how those functions are combined to accomplish particular behaviors and so you can remove or destroy parts of the brain and then observed subsequent behaviour

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4
Q

How is Lesion or Ablation Studies used with animals?

A

Animal research using a stereotaxic instrument

  • Stereotaxis: ability to locate objects in space
    • Electrical current through stainless steel wire using a radio frequency which kills the cells in the region of the brain, but not super accurate, kills cells around
  • Excitotoxic lesion by injecting a compound, kills cells in that region while sparing cells around it, more accurate
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5
Q

What is the importance of lesion or ablation studies?

A

Ablation studies can be effective using particular techniques to minimize or to improve the quality of life of some patients … seizures

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6
Q

Can we create lesions in a healthy human brain?

A

No, instead we stimulate and deactivate parts of the brain instead - TMS

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7
Q

What is Transcranial magnetic Stimulation (TMS)?

A

Inactivation of neurons using magnetic field placed on the scalp – coil produces small electrical current over the brain
Important to ensure not lesioning important structures during surgery

Not precise, but provided interesting way to map function along the cortical surface of the brain to behaviour

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8
Q

How can we correlate the brain and behaviour in real time, not waiting for the person to die?

A

Computerised Axial Tomography (CT/CAT) Scan

Magnetic Resonance Imaging (MRI)

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9
Q

What are the 3 different way s we can “slice the brain” when imaging? (CT/CAT and MRI)

A

Coronal section; dorsal and ventral split
Horizontal section; posterior and anterior
Mid-sagittal; along the mid-section

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10
Q

What does a CAT scan do?

A

Injection of contrast agent
3D image created by rotating X-ray scans
Series of slices that are put together to form a 3-D image of the brain
good for bones

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11
Q

What does an MRI scan do?

A

good for soft tissue
this machine assesses this interaction between the human body and a powerful magnetic field
Use of static Magnetic field (1.5 Tesla - 11T)
60% of our body is made up of water, the magnetic field is going to interact with the H20 in the brain
Water molecules (hydrogen atoms) align with the magnetic field
Add radiofrequency/electromagnetic pulse (coils) to perturb oscillation
Turn pulse off and atoms to create ENERGY (radio wave)
- Frequency of these waves show the image

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12
Q

Why can a CAT scan be considered dangerous?

A

Too many CAT scans within a year involves a lot of radiation throughout the body

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13
Q

How can we record brain acidity during behaviour?

A

Positron emission tomography (PET)
Electroencephalograph (EEG)
Functional MRI (fMRI)

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14
Q

What is a Positron emission tomography (PET)?

A

Record brain activity during behaviour

Injection of radioactive tracer.

  • participants are injected with a tracer that’s analog to glucose, glucose is a primary source of energy in the brain and so brain parts of the brain that are highly active will have more energy or more glucose.
  • Metabolic activity.
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15
Q

What is a Electroencephalograph (EEG)?

A

Record brain activity during behaviour

Record from scalp, low resolution.
- Looking at cortical structures
Voltage fluctuations - ERP, movement of neurons

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16
Q

What is a Functional MRI (fMRI)?

A

Record brain activity during behaviour

Change in blood flow to activated areas.
BOLD (blood oxygenation level dependent) response

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17
Q

What tissue does the CNS develop from? And name the other 2 germ layers.

A

16 days post fertilisation the embryo’s cells belong to one of 3 germ layers:
Endoderm[lining tissues of spaces in the body], Mesoderm [muscle and connective tissues], Ectoderm [outer layer, skin and nervous system]

Nervous system develops from ectoderm tissue

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18
Q

Describe the development of the CNS during the primary neurulation.

A

Primary neurulation: ~ 0-4 weeks formation of the neural tube

ectoderm tissues develops a neuroectoderm which becomes the neural plate, which begins to change shape folding inwards, the folds fuse towards which creates the neural tube

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19
Q

Describe the development of the CNS during the secondary neurulation.

A

Secondary neurulation: ~4th week, neural tube differentiates into 3 interconnected chambers
Primary vesicles: Forebrain, Midbrain, Hindbrain

We go from 3 primary vesicles into five secondary brain vesicles
Forebrain -> telencephalon and Diencephalon
Midbrain -> Mesencephalon
Hindbrain -> Metencephalon and Myelencephalon

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20
Q

State all 4 stages of the neurogenesis stage of the development of the CNS.

A

~ 8 weeks structures of the CNS are formed, but amount of cells and tissue rapidly increases… through NEUROGENESIS[birth of neurons]
*neurogenesis continues during life, but here is the developmental window where we see extensive growth of the brain

Stages of Neurogenesis:
Proliferation
Migration
Differentiation
Myelination & Synaptogenesis
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21
Q

Describe the Proliferation stage of Neurogensis.

A

Proliferation Stage: Production of new cells, these new cell are produced from the ventricular zone

Ventricular zone: A layer of cells that line the inside of the neural tube

Progenitor cells(arise from the ventricular zone): undifferentiated cells that divide and give rise to the CNS

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22
Q

How are the two forms of division the progenitor cells (cells of the ventricular zone) undergo?

A

Symmetrical division: each cell division gives rise to two identical cells; increases the size of the ventricular zone and the brain that develops from it

Asymmetrical division: cell division that gives rise to another progenitor cell and a neuroblast which then differentiates into glia cell OR neuron, which migrates away from the ventricular zone towards its final resting place in the brain

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23
Q

what do Asymmetrical division give rise to?

A

Radial glia cells = glia that offer scaffolding to migrating neuroblasts (and intermediate progenitor cells)

Cajal-Retzius (CR) cells =migrate to the end of radial glia, just inside pia, important for radial migration of neurons

Migrating neuroblasts, migrate up the glial fiber and find the particular layer they are supposed to stay in and differentiate from there

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24
Q

what is the “Inside-out” development?

A

Each new cell to be produced must pass through all the cells that came before it

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25
Q

What happens once a cell has migrated to their layer?

A

Differentiation of cells begin once migrated and express their genes to make proteins

Enables the cell to acquire distinctive characteristics ( appearance and function) within their particular region

Fate of the cell depends on where it “lands”

25
Q

What are the 6 layers of the cortex?

A
Molecular (lamina I)
External granular (lamina II)
External pyramidal (lamina III)
Internal granular (lamina IV)
Internal pyramidal (lamina V)
Multiform (lamina VI)
26
Q

Explain the Lamina of the cortex.

A

Cell structure and organisation varies between different regions of the cortex
Presence and thickness of lamina depend on section of cortex
Morphological differences relate to functional differences
lamina IV) (sensory) vs. lamina V(motor)

27
Q

How are the Laminas IV and V represented in the Somatic Sensory cortex and Primary motor cortex.

A
Lamina IV (sensory) is prominate in the somatic sensory cortex
 VS. it is negligible in the primary motor cortex

vice versa for Lamina V

28
Q

Are Lamina layers uniform?

A

No, layers are dependent on the cortical surface. Layers are not uniform across the cortex

29
Q

Describe the Development of the CNS: Myelination and Synaptogenesis.

A

Migratory neurons settle, differentiate and begin to form neuronal connections via dendrites and axons, creating a vast neural network
Myelination is produced – caudal to rostral development
Both myelination and synaptogenesis continue throughout life

30
Q

How do axons find their way?

A

Axons form synapses with target cells by following a chemical gradient.

Spontaneous electrical activity during early development is critical in forming synapses.

Survival of the fittest axon prevails- neural Darwinism.

31
Q

How are synapses formed?

Roger Sperry’s experiments

A

Roger Sperry’s experiments with newts proved it is not random (1943).
Exp 1: Cut optic nerve and then observed regrowth of optic nerve, connecting fibres to tectum
Exp 2: Made same cut, rotated eye by 180degrees and observed regrowth of fibres
Conclusion: Axon migration to a target cell is programmed.

32
Q

what is Apoptosis?

A

Apoptosis (programmed cell death) begins at around 3 months if the axon does not make contact with a postsynaptic cell.

33
Q

what did Rita Levi-Montalcini wanted to see from neurons and muscles

A

she wants to see how neurons form synapses with muscles
so when a neural synapses with a muscle fiber that muscle will deliver a hormone called nerve growth factor.
Nerve growth factor (NGF) determines survival of axons (and synaptic connection) in PNS. NGF cancels the program for apoptosis.
We see the same programming within the CNS in that only axons that are able to develop healthy synapses with other neurons will survive.

34
Q

What are some experiences that can change the brain?

A

Intrauterine(within the uterus) environment and brain development
Exposure to toxins(alc.) or viral infections
Exposure to stress

From birth to the grave
Exposure to chronic stress [ experience sleeping prob. , depression, cognitive impairments]
Social Isolation [ neg. impacts on the brain in life]
Nutrient intake [determine health span of life and brain]
Physical activity

35
Q

How can isolation effect dendritic branching (ex. fish)?

A

Fish reared in isolation develops fewer branches than a fish reared with others

36
Q

How does Congenital blindness and neural network structure interact

A

CB participants display enhanced processing of tactile and auditory stimuli

In experiments feeling braille letters and other objects – CB are more accurate in differentiating touch-based stimuli

During touch tasks, blind participants displayed activity of the occipital cortex

If occipital cortex is inactivated ( using TMS) – there is interference with ability to differentiate braille symbols (does not impact sighted participants)

37
Q

How do the brains of musicians look different than brains of non-musicians?

A

Participants: 15 piano and 15 control (6 y.o)
15-month prospective[over-time] study
Baseline morphology similar between groups
Post-intervention Results: Relative to controls –piano group displayed enhance performance on behavioural tasks (finger motor, melody/rhythm) & enhanced volume of R precentral gyrus, corpus callosum, and R primary auditory regions, experience changes the brain

Behavioural measures correlated with volumetric data

38
Q

How can exercise among older adults (study) effect the Left and Right sides of the Hippocampus?

A

120 sedentary older adults
Randomized to 1-year aerobic[increasing heart rate] affects the training group or stretching [does not increase heart rate] control group
MRI at baseline, 6 month and 1 year

Results AE group showed increased volume in L (2.12%) and R (1.97%) HC over 1 year relative to a decrease in the L (1.40%) and R (1.43%) volume of the HC in controls.

39
Q

How can plasticity of the brain be observed following an injury/surgery?

A

Cameron Mott – hemispherectomy (removal of R cortical hemisphere) due to Rasmussen’s disease

She was able to regain function after time with physiotherapy

Left side of the brain was able to compensate for the many functions previously responsible by the right hemisphere

She gets tired easier than her peer and needs a little more time to assimilate knowledge, and never regained full use of her left arm

These are small challenges considering what her life was like prior to the surgery

40
Q

what is the nucleus, genes and DNA?

A

In each nucleus we have all of our genetic info.

Genes act like a set of instructions, our growth, characteristics/phenotypes

DNA stands for Deoxyribonucleic acid, biological macromolecules that holds our genes

41
Q

How is DNA packaged?

A

DNA is packaged very tightly by wrapping the DNA structure along specialized proteins that are called histones

By wrapping the structure around the histones, it is able to form nicely packed structures called chromosomes

42
Q

How many chromosomes does each cell contain? Where do we inherit the chromosomes? And where are the chromosomes located in the cell?

A

46 chromosomes in each cell.

We inherited chromosomes from our biological parents, 23 from the father and 23 from the mother

Sex chromoses will determine our sex, either XX[female] or an XY[male]

We have 23 pairs and these pairs are located in the nucleus of our cells

43
Q

Describe Deoxyribonucleic acid (DNA) and Ribonucleic acid (RNA). (Nucleic Acids)

A
Deoxyribonucleic acid (DNA): The “information molecule”
Double stranded structure
4 nitrogenous bases: adenine, guanine, cytosine, thymine

Model for synthesis of RNA molecules
Ribonucleic acid (RNA):
Single stranded structure
4 bases: adenine, guanine, cytosine, uracil
Template for synthesis of proteins: Order of bases determine sequence of amino acids of protein
Proteins can make up the structure of cells or act as enzymes to regulate chemical reactions.

both are made up of 3 parts

44
Q

What three laws of inheritance

did Johann Gregor Mendel discover?

A
  1. Law of Segregation: Each inherited trait is defined by a gene pair; offspring inherit one genetic allele from each parent when sex cells unite in fertilization.
  2. Law of Independent Assortment: Genes for different traits are sorted separately from one another so that inheritance of one trait is not dependent on inheritance of another.
  3. Law of Dominance: An organism with alternate forms of a gene will express the form that is dominant.
45
Q

What is an Allele?

A

Variety of a gene

46
Q

what is a Genotype?

A

Homozygous [inherited 2 similar alleles] vs heterozygous [different alleles] (DD, dd, or Dd)

  • upper-case means dominate, lower-case mean recessive
    (e. g. 5HTT l/s[risk for anxiety], APOE e4[risk for alzhemiers])
47
Q

How does the Phenylthiocarbamide (PTC) taste sensitivity test tell you if you are a “supertaster”?

A

Tells you if you carry the dominant allele

Off-spring of on parent have (TT) and the other (tt) will always be a “supertaster”

48
Q

Phenylthiocarbamide (PTC) taste sensitivity

- What are the four outcomes for the off-spring when both parents have (Tt)?

A

There is a 3/4 chance of being a super taster

Child 1: TT - Homozygous, “super taster”
Child 2: Tt - Heterozygous, “Supertaster”
Child 3: tT - Heterozygous, “Supertaster”
Child 4: tt - Homozygous, “non-supertaster”

49
Q

What are Autosomal genes?

A

found on autosomal, these are carried regardless of sex and codes for various characertisitcs ex. How our body works

50
Q

What are sex-linked and sex-limited genes?

A

Sex-linked: Genes on a sex-chromosome (e.g., recessive gene on X chromosome – e.g. red-green colour deficiency)

Sex-limited genes: Genes on an autosome (e.g. autosomal genes influenced by hormonal conditions – e.g., bearded males)

51
Q

Why is red-green colour blindness more prominate in males vs. females?

A

The gene that codes the particular phenotype or behaviour stems from a recessive gene on the X chromosome

If a male baby has the recessive gene for colour blindness located on the X genes, they do not have a homologous gene to counteract that recessive phenotype.

however in females to express the phenotype of colour blindness they must hold two recessive genes b/c they have two X chromosomes, therefore a homologous genes to counteract a recessive gene on one of their X chromosomes

52
Q

How can genetic mutation(Alterations in genetic code) occur? (3 ways)

A

Evolutionary mutation

  • E.g., FOXP2 evolutionary mutation from chimpanzee which modified human brain and vocal apparatus to enable language development
  • Selective advantage of certain genes – e.g., sickle cell anaemia confers resistance to malaria (note sickle cell trait is highest in West Africa)

Duplication[too many chromosomes]
- (e.g.,Down syndrome, Trisomy 21)
A single pair of chromosomes would have 3 chromosomes vs 2

Deletion[fewer amount of chromosomes]
- (e.g., William’s syndrome, deletion on chromosome 7)
Occurs at random, deletion of 23 genes along chromosomes 7

53
Q

What is Epigenetics?

A

Changes in the expression of a gene without changing the genetic code – turning a gene on or off
Turned on or off by Tags: acetyl groups and methyl groups

54
Q

What is Epigenetic inheritance?

A

Changes in the expression of a gene without changing the genetic code through generations.

The Dutch famine and risk for obesity in offspring (including grandchildren!).

Parental trauma exposure associated with increased risk for PTSD, mood and anxiety disorders in offspring (e.g., Holocaust survivors).

People with PTSD tend to be non-responsive to stressors, rather experience hypo cortisol levels

Same results in offspring of those with PTSD

55
Q

How much of genes do Identical (MZ) and Fraternal (DZ) twins share?

A

Identical (MZ) twins share 100% of their genes

Fraternal (DZ) twins share 50% of their genes

56
Q

What is it called if both twins carry a phenotype vs. if only one carried a certain phenotype? And what is it an important indicator of?

A

If both twins carry the disease/phenotype, they are concordant
If only one twin carries the disease/phenotype, they are discordant

Rate of concordance in MZ twins is an important indicator of heredity

If ex. Concordance rate of depression is 60-70% it means there is a large genetic contribution but there is still a% that can modify the genetic contribution

57
Q

What can adoptions studies do?

A

a nice method to explore heredity vs. environment

58
Q

What are the examinations of Candidate Gene approach and GWAS when testing genetics?

A

Candidate gene – examination of a single gene and its association with a behaviour based on theory

  • APOEe4 of the APOE gene as a risk factor for Alzheimer’s disease
  • ignores the complexity of our system, it ignores how this gene does not act in isolation

GWAS[genome wide association studies] – examine all genes and determine differences between two groups with a particular behaviour of interest
- Discover mutations at several loci for particular phenotype

59
Q

What is Targeted Mutations, when testing genetics? (mouse example)

A

Animal models of disease
Knockout (alt, knock in) genes
remove a part of a gene from the genetic makeup of the rodent, so this is called ‘knocked out’ or ‘knock in’
- knockout animal models are experiments, where you are removing particular genes
- ‘knock in’ where you are introducing a new genetic trait

60
Q

Give an example of Targeted Mutations study among mice.

A

“knock out/in example”
leptin is a protein hormone that regulates energy metabolism, it basically signals to us when we’ve had too much to eat
Leptin is in the hypothalamus of the brain
Without Functional leptin, you are unable to feel full
“Leptin knockout mouse model”
When you knock out leption, the mouse are never full so they become obese