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Brain & behaviour > Lecture 2 - Brain Evolution > Flashcards

Lecture 2 - Brain Evolution Flashcards

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1
Q

Define Vertebrate

A
  • A creature with a backbone and a spinal cord
  • Inverterbrates are animals like insects, or those with exo-skeletons
  • In vertebrates - skeleton is on inside, proteted by muscle and bone
  • Examples: fish, amphibians, reptiles, birds, mammals
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2
Q

When did Vertebrates come about?

A

530 Million Years Ago

- Cambrian Explosion Period

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3
Q

What does the brain look like in simple vertebrates

  • optic stuff
  • **√
A
  • Might just have a spinal cord with some bulbs on top
  • very large midbrain
  • this area contains optic lobe (sight and movement towards stimulus)
    •In non-mammals this is called the optic tectum, (larger in proportion to other areas)
    •in mammals this called the superior colliculus (smaller in proportion to other areas)
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4
Q

What does the spinal cord do in vertebrates?

A

Coordinates simple movements and reflexes

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5
Q

What does the cerrebellum do in vertebrates?

A

Motor learning

- coordinatio of movement, combining and organising movements

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6
Q

How does the evolution of mammals brains compare to other animals?******X

A
  • Cerebrum (neocortex) has expanded far more than other brain areas over evolution
  • Cortex size corresponds to body size and cognitive complexity
  • Midbrain is present in animals but gets smaller the more complex the animal
  • cerebrum needs space so it folds
  • Brain size depends on body size - males have heavier brains than females as they are bigger
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7
Q

What does a fishes brain look like?

******√

A
  • Cerebrum is very small
  • large olfactory bulb (eye sight is poor)
  • pituitary gland to reproduce
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8
Q

What does a frogs brain look like?

A
  • Bigger than fishes because they live on land as well, which is more complex than under water
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9
Q

What does a alligator brain look like?

******X

A
  • Massive olfactory

- optic is a bit better

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10
Q

What does a shrew brain look like?

******X

A
  • cerebellum and olfactory are important

- some lateral/ central fissures here to make more space

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11
Q

What does a Horse brain look like?

A
  • small brain but lots of fissures & gyri
  • Social animal so cortex is folded
  • Cerebellum much larger than humans - need to coordinate all 4 legs over a fast pace on tricky terrain
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12
Q

Which are the deep-brain structures that have been present since early common ancestor?
***********

A
  1. Brain stem
  2. Limbic System
    - Amygdala (emotions - especially negative ones)
    - Hippocampus (LTM - glutamate)
  3. Striatum
    - basal ganglia
    - striatal complex - movement (parkinsons, DA)
  4. Nucleus Accumbens
    - Pleasure & Reward
    - addiction
    - DA (VTA)
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13
Q

Outline the 2 systems present in common ancestors

A
  1. Meso-limbic reward system
    - amygdala, hippomcampus
    - DA - rewards
  2. Social Behavioural Network
    - pre-optic area
    - sexuality, parental care, aggression
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14
Q

How do monkey and humans brains differ?**

******√

A
  • Differences depending on demands of species
  • Monkeys have larger sensory and motor areas
  • Humans have mostly large pre-frtonal areas (planning, complex cognition)
  • Higher order chimps have much larger social structures
  • Gorillas brains are more complex - they have more wrinkles
  • Humans have smaller areas - more space is on association areas - e.g. pre-frontal area
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15
Q

Outline the grey matter of the cortex

******√

A

On the outside

  • Made up of: CELL BODIES, DENDRITES AND SYNAPSES
  • important in info processing
  • enlarged by folding
  • 6 layer structure (Brodmann)
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16
Q

Outline the white matter of the cortex

A

Deeper structures within cortex

  • made up of: AXONS
  • Myelin sheaths are high in lipids, giving them a white appearance
  • Deeper nuclei with unique neuronal populations and specific functions
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17
Q

What did Brodmann (1909) do?

**√

A

Looked at the brain under microscope and found the cells in each layer were different

  • because they had different functions
  • 6 areas in this, each have different functions
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18
Q

Outline Corticial Macrostructure

A

Grey matter on outside (info processing)

White matter on inside (Deeper nuclei)

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19
Q

Outline Coritical Microstructure (Brodmann)

******√

A

6 layers, each with specific cell types

  • stretch from grey matter to white matter
  • Cytoarchitecture of these cells corresponds to function
  • how the layers build up and by which cells give it a unique appearance
  1. Molecular
  2. External Granular
  3. External Pyramidal
  4. Internal Granular
  5. Internal Pyramidal
  6. Polymorphous
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20
Q

Outline Long-range cortical connectivity

A

For long range connections: it is mediated by glutamate

- connections from and to specific layers all mediated by glutamate (Excitatory)

21
Q

Outline Interneurones

**√

A

Small, local neurons
- lie in between the 6 layers

  • Mainly GABA/ Glycine (inhibitory)
  • They balance the activity of these long range connections down to and from these deeper layers
22
Q

Outline Spiny and Non-spiny neurons

**√

A
  1. Spiny Neurons
    - look like classic neurons
    - regulated by Glutamate (Excitatory)
  2. Non-spiny neurons
    - Lots of different shapes and sizes and types
    - Interneurons
    - Regulated by GABA (inhibitory)
23
Q

What are the 2 terms for the complexity of neurotransmission

*****√

A
  1. Divergence
    - DIFFERENT effects from SAME Neurotransmitter
    - One NT Can have different effects, depending on which receptor there is
    - e.g. Dopamine can have different effects on DA (1-5)
  2. Convergence
    - SAME effect from DIFFERENT NT’s
    - Depends on receptors
    - DA can excite a cell but so can glutamate
24
Q

What are the 2 main cortical Neurotransmitters

A
  1. Glutamate
    - Generally excitatory
    - Huge receptor diversity
    - Linked to many disorders, especially epilepsy (overexcited)
  2. GABA
    - Generally inhibitory
    - Huge receptor diversity - lots of differing effects
    - Range of drugs target receptors
25
Q

What are the two types of Ionotropic Glutamate Receptors? and outline ionotropic glutamate
******X

A
  1. AMPA (Kainate) Glutamate Receptor
  2. NMDA Glutamate Receptor

Called ionotropic because its linked to ion channels

Very fast, linked to influx of sodium into the cell and depolarisation

26
Q

Outline the AMPA (Kainate) Iontropic Glutamate Receptor

********XXXX

A
  • Majority in the cortex
  • Allows sodium to come in, even if its a very small change in charge
  • The presence of glutamate is the only thing required for ion flux
  • Linked to potassium and sodium

DEOPLARISING (Excitatory) Effect

27
Q

Outline the NMDA Ionotropic Glutamate Receptor

********XXXX

A
  • Magnesium is blocking the channel, so you need a very large depolarisation to expell the magnesium
  • This allows sodium and calcium to come in
  • Important for long term potentiation - learning and memory.
  • Via feedback to pre-synpatic neuron, it strengthens the conncetions: what wires together fires together
28
Q

What does NMDA stand for?

A

N-Methyl D-Aspartate

29
Q

What can happen in NDMA over time

******

A

Excitotoxicity

  • After a while, the massive calcium influx can destabilise the cell, meaning:
  • Cell starts swelling up because it needs more water to stabilise its gradient - can damage cell
  • Hypoxia: leads to memory or learning problems
  • In hypoxia, NMDA doesnt work as well, so calcium keeps rushing in and doesnt stop - damages the cell
30
Q

Outline Metaboropic Glutamate Receptor
********
XXXXXXX

A

Linked to G-proteins, not to ions

  • Much slower - either Slow Excitatory (Group 1), Slow Inhibitory (Group 2 & 3)
    1. Glutamate binds to receptors
    2. This causes G-protein Phosphorylation
    3. This modulates sensitivity
    4. Through pathways, this can open other ion channels
    5. Can cause changes in proteisn in gene expression
    6. This effects calcium release

This makes this receptor much slower, as the glutmate causes release in g-proteins, which then influence release
- its not a direct binding and effect

31
Q

What are the 2 issues/ CNS Disorders related to Glumate

******

A
  1. Epilepsy
    - too much excitatory transmission in a certain area
    - too much glutamate release
    - linked to mGlu1 and mGlu5
    - Can trigger wider glutamate release and hence cause seizures - whole brain going off
  2. Excitotoxicity
    - Large amounts of glutamate release landing on NMDA receptors - e.g. during Hypoxia, epielpsy or traumatic head injury
    - Too much calcium rushing into cell = death of neurons

Also linked to Sz and ADHD but other NT’s are involved here

32
Q

What are the 2 types of GABA receptors?

******

A

Has similar receptor Sub-types to glutamate

  1. Ionotropic receptors (faster)
    - GABA-A
    - GABA-C
  2. Metabotropic receptors (slower working)
    - GABA-B
33
Q

Outline Ionotropic GABA receptors

********

A

GABA-A

  • In the cell there is already lots of negative chloride
  • GABA opens up the Chloride channel, allowing more chloride to come in. This hyperpolarises the cell, and makes it much less likely to fire
  • harder to fire

GABA-C
- does a similar thing on CL- channel, but less widespread than A subtype

34
Q

Outline Metabotropic receptors

A

GABA-B

  • Acts on second messengers
  • G-Protein again used in a similar war
  • lets calcium in too
35
Q

What is GABA like in a developing brain?***

A

In a developing brain, GABA is actually excitatory!

36
Q

What is the structure of the GABA-A receptor

A

5 Subunits

  1. Alpha 1
  2. Alpha 1
  3. Beta 2
  4. Beta 2
  5. Gamma 2
37
Q

Outline GABA-A Agonists

******

A

Means they act like GABA
- increase channel opening further

Muscimol is a GABA-A Agnosits - a psychoactive musrhoom alkaloid - induces hallucinations

Some epilepsy treatments also act on GABA-B

38
Q

Outline GABA-A Antagonists

A

Occupy GABA site but dont open the channel
- hence blocking the effect of GABA on GABA-A

Biscuculline is a GABA-A Antagonists: plant alkaloid
- but can cause seizures so not really used

Poisons work in a similar way

39
Q

Outline GABA-A Allosteric Modulators

******√

A

A modulator can either: Enhance (positive AM) or decrease (negative AM) channel opening in response to GABA binding

40
Q

Outline GABA-A Positive Allosteric Modulators

******

A

Enhance Channel Opening

  • despite behing ‘positive’ they actually hyperpolarise
  • Generally have a sedative action
    1. Barbituates
    2. Benzodiazepines
    3. Alcohol (Ethanol)
    4. Neuroactive Steroids
    5. Anesthetics
41
Q

Outline GABA-A Negative Allosteric Modulators

A
  1. Flumazepine
    - treats Benzo OD - knocks BZ off and stops inhibition
    - stops influx of choride into cell
  2. Sarmazenil:
    - Similar, but just used in Vetinary medicine to reverse anaesthesia, anxiogenic and convulsant
42
Q

When was the first BZ discovered and by who?

A

Leo Sternbach in 1955 discovered them

43
Q

When was Valium invented?***

A

1963, also known as diazepam

44
Q

How do Benzos work

A

They enhance the effect of GABA on GABA-A

  • Allow the channel to be open for longer and allow more calcium in
  • Its hard for neuron to fire, calming down the brain
  • Becomes so negatively charged that its difficult for any Action Potential to overcome this
45
Q

What are the effects of Benzos?
5 things
******√

A
  • sedative (calms)
  • Anxiolytic (anti-anxiety)
  • Hypnotic (sleep-inducing) - helps you sleep
  • Anticonvulsant (anti-epilepsy)
  • Muscle relaxant
46
Q

What are Benzo’s used to treat?

******

A
  • Panic disorder
  • Anxiety
  • insomnia
  • Agitation
  • Seizures
  • Muscles Spasms
  • Alcohol withdrawal
47
Q

What are side effects of Benzos?

**xxx

A 
X - very addictive and sleep/ anxiety problems if you come off of them
X - tolerance builds need to take more
X - drowsy and dizzy
X - decreased alertnes
X - memory problmes
X - cognitive function is impacted
X - very dangerous with alcohol
X - withdrawal and rebound effects
48
Q

What are the paradoxical effects of Benzos?

**XXX

A
  • Can lead to an increase in seizures in epileptics
  • Aggression
  • Violence
  • impulsivity
  • irritability
  • suicidal behaviour

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