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psychobiology Flashcards

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1
Q

what are the three fundamental assumptions in psychobiology?

A
  1. behaviour is dependent upon body function
  2. the brain is the primary body area involved
  3. try not to completely neglect the role of other body areas
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2
Q

what is dualism?

A

cartesian duality - the belief that both physical and mental substance is fundamental

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3
Q

what is physicalism (monism)?

A

matter> mind
physical substances are more fundamental to a persons psychology

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4
Q

what is idealism (monism)?

A

mind> matter
mental substances are more fundamental to a persons psychology

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5
Q

what is neutral monism?

A

a hypothetical third substance is fundamental to a persons psychology, physical and mental substances are derivative to this.

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6
Q

what is reductionism?

A

when a phenomenon is defined in terms of the more elementary processes that underlie it (simplifies it)

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7
Q

what are the three levels of reductionism?

A

macro anatomical level (largest) - functional interaction of different brain areas
micro anatomical level - functional interaction of different brain cells
macro molecule level (smallest) - functional interaction of individual protein molecules

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8
Q

what is a cell?

A

fundamental building block of all biological organisms generated by mitosis followed by differentiation

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9
Q

what is the brain?

A

neurones, information processing and transmitting element of nervous system

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10
Q

what is glia?

A

supporting cells, has functions that neurones cannot do

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11
Q

name the characteristics of a neurone?

A
  • fully differentiated
  • cannot undergo mitosis
  • typically can’t be replaced in mature nervous systems but can be regenerated in certain parts of the brain throughout our life
  • tumours of neurones are very rare
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12
Q

what is the cell body?

A

(soma) integrates information

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13
Q

what are dendrites?

A

(dendritic tree) branch like processes on the cell body, receives information from other neurones

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14
Q

what is an axon?

A

(typically myelinated to speed up transmissions) long filament like process, branches, conveys information away from the cell body to other neurones that end in terminals

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15
Q

what is a synapse?

A

a gap between the pre and postsynaptic neurone that connects one terminal to another

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16
Q

does communication with and between neurones need to be slow or fast?

A

fast, specifically for reflexes

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17
Q

what kind of process are signals?

A

electric, this is because it is not via diffusion of chemicals as that would be too slow

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18
Q

what is resting membrane potential an example for?

A

electrical excitability

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19
Q

what is electrical excitability?

A

describes the potential movement of particles if allowed

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20
Q

what occurs when a neurone is in a passive state?

A

energy is being spent/used up in order to maintain an unstable state

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21
Q

what occurs to a neurone in an unstable state when a trigger occurs?

A

the pent up energy is released which creates the signal/action potential

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22
Q

what does the resting membrane potential depend on and why?

A

the fact that the cell membrane of a neurone is a lipid (fatty layer) which makes charged ions unable to pass through easily

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23
Q

what within the cell membrane acts as an ion transporter for sodium and potassium?

A

proteins

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24
Q

describe the transportation of sodium and potassium ions

A

more sodium ions are moved outside of the membrane where in exchange potassium ions are moved inside the membrane.

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25
Q

what charges are sodium and potassium?

A

single positive charges

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26
Q

what are cations?

A

+vely charged ions

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27
Q

what are anions?

A

-vely charged ions

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28
Q

what are chloride ions?

A

chloride ions are anions (-ve) and do not leak through the membrane

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29
Q

what is the resting membrane potential difference?

A

-70mV

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30
Q

what is the myelin sheath?

A

made from oligodendrocytes and insulates neurones and speeds up action potential as well as blocking interference from other neurotransmitters

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31
Q

what are nodes of ranvier?

A

they are spaces between myelinated sections of the axon

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32
Q

‘action potentials are the basic code for information in the brain’
what are the characteristics of this code?

A

AP’s are always the same size and shape
they either occur or do not
size of AP holds no information
frequency (rate) of AP’s codes information

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33
Q

does an action potential increase or decrease as it travels underneath the myelin sheath?

A

decreases due to the insulating properties

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34
Q

as action potential jumps between nodes what occurs?

A

full action potential is regenerated at nodes between the myelinated axons which saves energy

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35
Q

what do sensory receptors do?

A

respond to sensory stimulation directly with membrane depolarisation

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36
Q

what are the three main neurotransmitters in synaptic transmission and plasticity?

A

Glutamate
GABA
Monoamines

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37
Q

what are the three main receptors in synaptic transmission and plasticity?

A

Ionotropic
Metabotropic
Selective binding

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38
Q

what is a ligand?

A

a ligand is a chemical that interacts with the receptors, an example is a neurotransmitter

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39
Q

what do ligands interact with?

A

the binding site on receptors

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40
Q

what are the characteristics of selectivity of binding?

A
  • only specific ligands will fit in a binding site
  • due to the 3D shape of the receptor
  • but some drugs bind to more than one receptor type
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41
Q

what is affinity?

A

how well a ligand binds to a receptor

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42
Q

what does a high affinity mean?

A

that receptors are saturated (completely bound) by very dilute solutions of ligands

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43
Q

what does a synaptic transmission produce?

A

a small postsynaptic potential

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44
Q

what are the characteristics of an ionotropic receptor?

A
  • directly coupled to an ion channel
  • ligand binds -> ion channel opens
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45
Q

how does a metabotropic receptor work?

A
  • more complex
  • ligand binds and changes 3D shape of the receptor
  • this activates a G-protein that is connected to the receptor inside the neurone
  • this activates an intracellular signalling cascade
  • can either alter ionotropic receptors to make them more or less excitable or can alter protein synthesis
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46
Q

what are two amino acid derivatives?

A

glutamate and GABA

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47
Q

what are the characteristics of glutamate?

A

derived from glutamic acid
most abundant neurotransmitter
excitatory
binds to at least 8 different receptors

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48
Q

what are the characteristics of GABA?

A

Gamma-aminobutyric acid
made from glutamate
most abundant inhibitory neurotransmitter
binds to both ionotropic and metabotropic GABA receptors

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49
Q

what influences the probability of an action potential firing?

A

post synaptic neurones integrating across many inputs

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50
Q

what size are post synaptic potentials?

A

they are very small as the opening of a single channel is insufficient to produce enough hyperpolarization to alter action potential rates

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51
Q

what is LTP?

A

Long term potentiation, a process involving persistent strengthening of synapses that leads to a long lasting increase in signal transmission between neurones

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52
Q

what occurs in NMDA receptors for induction?

A

Magnesium block, depolarisation removes the block, calcium entry into postsynaptic neurone, blocking NMDA receptors impairs the induction of LTP

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53
Q

what occurs in AMPA receptors for expression?

A

more AMPA receptors, larger excitatory post synaptic potential (glutamate binding to more receptors), more glutamate release

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54
Q

what is learning?

A

acquisition of behavioural information

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55
Q

what is memory?

A

the retention of information

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56
Q

what is a principle of learning?

A

memory gets better with more learning

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57
Q

what is the law of diminishing returns?

A

states the continuous equal effort of learning results in less additional improvement or benefit

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58
Q

what is the role of surprise in learning?

A

the amount of knowledge is proportional to the amount of surprise at the outcome

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59
Q

what is the rescorla-wagner rule of learning?

A

∆V = αβ(λ − ΣV)

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60
Q

explain the rescorla-wagner rule

A

the change in the level of memory = speed we learn about the environment and predictors of the outcome X speed we learn about the outcomes (maximum that can be learnt/asymptote - what is already known before any learning)

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61
Q

explain what blocking is

A

blocking describes a situation where there is two stimuli, one of which blocks the learning of the other due to its predictive value.

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62
Q

what is pharmacokinetics?

A

routes of drug administration

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63
Q

what is pharmacodynamics?

A

examples of agonists, antagonists and allosteric modulators

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64
Q

what is quantifying drug effects?

A

efficacy and potency

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65
Q

what are psychoactive drugs?

A

(psychotopric) drugs which alter your transmission to affect a mood or behaviour, they can be found in plants or compounds that have been synthesised in a chemical laboratory

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66
Q

what are the 6 routes of adminstration?

A
  1. oral (ingestion)
  2. rectal (anus)
  3. other mucous membranes:
    sublingual, buccal and nasal
  4. transdermal
  5. inhalation
  6. injection: intravenous, intramuscular and subcutaneous
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67
Q

what is sublingual?

A

under the tongue

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68
Q

what is buccal?

A

inside the cheek

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69
Q

what is intravenous?

A

into the vein

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70
Q

what is intramuscular?

A

into the muscle

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71
Q

what is subcutaneous?

A

into the skin

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72
Q

where does absorption via oral administration often occur?

A

small intestines

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73
Q

what is the rate of oral administration?

A

slow

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74
Q

when is it best to take oral administration?

A

on an empty stomach

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75
Q

name advantages of oral adminstration

A

easy
allows for drug to be out of the system
limited infection risk

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76
Q

name disadvantages for oral administration

A

stomach is very acidic so some drugs may be broken down
foodstuffs in guts can make absorption unpredictable
some drugs irritate the stomach and induce vomiting
blood supply from gut routed to liver so first pass effect may occur and prevents the whole drug to reach circulation

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77
Q

what is the first pass effect?

A

liver metabolism breaks down active drugs to metabolites for elimination, the first pass effect is the extent to which a drug is metabolised by the liver before reaching systemic circulation. from the GI tract, drugs pass via the portal vein into the liver. the result of first pass metabolism means that only a proportion of the drug reaches the circulation.

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78
Q

name advantages of rectal administration

A

can be used if person is vomiting or unconscious

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79
Q

name disadvantages of rectal administration

A

unpredictable rate of absorption
not well accepted by some

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80
Q

name advantage of other mucous membranes

A

avoid first pass metabolism

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81
Q

name a disadvantage of other mucous membranes

A

all relatively slow compared with inhalation/injections

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82
Q

name the steps of drug administration

A

absorption
distribution
metabolism
elimination

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83
Q

briefly describe how absorption occurs

A

unless given via intravenous, a drug must cross cell membranes before it can get round the body in blood plasma

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84
Q

what are the factors that affect diffusion of drugs across lipid membranes?

A
  • lipid-soluble and small molecules drugs diffuse the best
  • un-ionised drug molecules are more lipid soluble
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85
Q

do drugs know where to go within the body?

A

they don’t, drugs circulate throughout the body in plasma then enter tissue sites, they encounter receptors for which they have affinity, bind and begin the pharmacological response

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86
Q

what occurs during distribution?

A

the target for psychoactive drugs is usually the brain but in blood plasma a drug will reach all parts of the body

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87
Q

why do side effects occur for psychoactive drugs?

A

they can be due to binding at receptors outside the brain.

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88
Q

why do some drugs get temporarily inactivated?

A

by storage in fat or attached to blood plasma proteins , the blood brain barrier acts as a selective barrier to drug distribution

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89
Q

what occurs during metabolism?

A

converts the drug chemically into another compound, this can be inert and can also be active or even more active. this mainly takes place in liver contains enzymes that help metabolism

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90
Q

what are the different routes of elimination?

A

urine
breath
sweat and hair

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91
Q

how do drugs get eliminated via urine?

A

via the kidneys but this is only possible for water-soluble compounds, fat-soluble drugs may be metabolised to make them water-soluble

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92
Q

what is drug half life?

A

half life is a measure of duration of drug action aka time taken for amount of drug in plasma to fall by 50%. this impacts how frequently a drug has to be taken

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93
Q

name the characteristics of transdermal patches

A

controlled release from a reservoir through a membrane, long duration of action, potential for allergic reactions to the patch or adhesives. drug must be potent or else patches needed are too large, sweat and moisture may lift the patch

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94
Q

name the characteristics of inhalation

A

gases, aerosols, smoke. it is very fast, gases can leave and enter lungs quickly and can cause damage to lungs

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95
Q

name the characteristics of injection (IV)

A

very fast, allows accuracy in dose, can cause clots/infection

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96
Q

name the characteristics of intramuscular

A

not as fast as IV or inhalation but faster than others

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97
Q

name characteristics of subcutaneous

A

drug diffuses into area between skin and muscle, slowest form of injection, can only inject small volumes

98
Q

what are the factors affecting choice of route of administration

A

ease of administration
desired onset and duration of action
quantity of drug to be administered
balance of risk versus benefits

99
Q

how do psychoactive drugs bring about their effects?

A

most drugs that affect behaviour alter chemical neurotransmission (agonist) , can either enhance the effects of a neurotransmitter or dampen or block the effects of a neurotransmitter (antagonist)

100
Q

what is a direct agonist?

A

mimics effects of a neurotransmitter by binding to postsynaptic receptors in a similar way and producing a similar postsynaptic response

101
Q

what is an indirect agonist?

A

enhances the action of a natural neurotransmitter

102
Q

what is a direct antagonist drug?

A

binds to a receptor but has NO physiological effect at that receptor e.g naloxone which blocks opioid receptors

103
Q

what is an indirect antagonist drug?

A

dampens neurotransmitter activity by inhibiting the release/production of neurotransmitters e.g reserpine - reduces transport of monoamines into storage vesicles in neurone terminals

104
Q

how can direct antagonists be classified as?

A

‘full’ or ‘partial’ agonists
depending on the extent to which they mimic the effects of the endogenous neurotransmitter

105
Q

what is an inverse agonist drug?

A

produces the opposite physiological changes to an agonist

106
Q

what is allosteric modulation?

A

a chemical (modulator) binds to a different part of the receptor than the neurotransmitter and by doing so alters the receptors response to the neurotransmitter

107
Q

what is the quantifying drug effect?

A

the magnitude of a drug-receptor effect depends on its concentration at the target site and the affinity of the drug for the receptor site. this can be quantified by a dose-response curve

108
Q

what is ED50?

A

a measure of potency, the amount of drug required to produce a specific effect indicates potency and Ed50 is the dose producing half the maximal effect

109
Q

describe the difference between efficacy and potency

A

a potent drug is not necessarily the most clinically effective, a drug can be potent without being efficacious. an efficacious drug might not be very potent but this is only a problem if giving it in a large dose is problematic

110
Q

what is memory consolidation?

A

when acquisition leads to the long term memory store

111
Q

what is de novo protein synthesis?

A

the formation/making of new proteins within neurones in the brain

112
Q

what are specific proteins?

A

proteins that are needed to be made in order for these memories to consolidate within the amygdala

113
Q

give an example of a specific protein

A

ARC

114
Q

are more or less proteins expected with more learning

A

more amount of specific protein

115
Q

what is a NMDA receptor?

A

a receptor of glutamate, the primary excitatory neurotransmitter in the human brain

116
Q

what happens when NMDA receptors are blocked?

A

LTM is gone and STM is impaired meaning they are required for memory acquisition

117
Q

what are the three factors contributing to differences in drug effects?

A

individual differences
experience
context

118
Q

explain how individual differences contribute to differences in drug effects

A

person related factors and environmental influences may influence the response to a drug outside of dose administration

119
Q

what are kinetic differences?

A

for same doses, a different amount of drug reaches site of action

120
Q

what are pharmacodynamic differences?

A

for same drug concentrations at site of action, different physiological responses occur

121
Q

what is an idiosyncratic response?

A

person may experience an atypical drug reaction such as hypersensitivity, hyposensitivity and allergic reaction

122
Q

what might an idiosyncratic response reflect?

A

reflect genetics, prior exposure to viruses or toxins etc

123
Q

what are the 5 factors contributing to differences in drug effects between people?

A

body size
age
health
sex
ethnicity/race

124
Q

describe how body size may cause differences in drug effects between people

A

the same dose produces a smaller response in a larger person as drug is distributed in greater blood volume so would require a larger dose

125
Q

describe how age may cause differences in drug effects between people?

A

metabolism - liver may be less able to metabolise many drugs as with age comes a decrease in liver function and liver mass is reduced

excretion - kidneys are less able to excrete drugs into the urine

drug-disease and drug drug interactions - chronic disease states and the use of multiple medications may have an effect

compliance - 40% of older people do not take drugs as directed

126
Q

describe how sex may cause differences in drug effects between people

A

compared with men, women have on average lower plasma volume, higher proportion of body fat, differences in drug response according to phase of menstrual cycle and metabolise some drugs differently

127
Q

describe what biotransformation of alcohol is?

A

alcohol is first metabolised by the enzyme alcohol dehydrogenase. this enzyme converts alcohol into the metabolite acetaldehyde, a steady amount of approx 10ml of 100% ethanol can be metabolised per hour

128
Q

describe the first stage of the metabolism of alcohol

A

Alcohol (alcohol dehydrogenase, enzyme in liver and stomach) —-> acetaldehyde (highly reactive and toxic)

129
Q

describe the second stage of the metabolism of alcohol

A

Acetaldehyde —-> acetic acid —-> oxidised to CO2 and H2O (yields energy)

130
Q

describe how presence of food in the stomach may cause differences in the metabolism of alcohol between people

A

drinking on a full stomach retains alcohol in the stomach for longer so that more is metabolised by gastric alcohol dehydrogenase

131
Q

how does sex may cause differences in the metabolism of alcohol between people

A

on average, equivalent amounts of alcohol have greater effect on women than on men as men have a greater vascular capacity, greater body mass on average, alcohol more diluted in blood of men, men have higher levels of gastric alcohol dehydrogenase so less alcohol will get into the blood of men

132
Q

how and why might responses to alcohol or nicotine vary according to a person’s racial/ethnic group?

A

genetics, some genetics differences map onto racial/ethnic groups and affect drug response i.e. how a person responds to the drug itself however race/ethnicity is not a perfect marker for these genetic differences. genetic ancestry may be more relevant than a person’s self identified race

133
Q

what are the different kinds of tolerance?

A

metabolic tolerance - typically, the drug is metabolised faster with repeated use as some drugs induce enzymes in the liver which contributes to their biotransformation

cellular tolerance - neurones adjust their functioning to compensate for the action of the drug on the cell e.g change amount of transmitter synthesised or released, or change number of receptors

sensitisation - response to drug increases over time, opposite of tolerance and common for stimulant drugs

134
Q

explain placebos effects

A

a placebo is a drug that lacks any intrinsic pharmacological activity (i.e. it is pharmacologically inert) and can produce effects that are indistinguishable from a “real” drug: both behavioural and physiological. in addition to this, expectancies of specific effects have an effect on effectiveness of drugs

135
Q

what does psychoactive mean?

A

whether it will effect the brain or not

136
Q

what is compliance?

A

how often does it have to be taken

137
Q

what does ED mean?

A

effective dose

138
Q

what does LD mean?

A

lethal dose

139
Q

how does the blood brain barrier work?

A

blood brain barrier separates the brain from the body and is really small/thin. things can only travel through either between the cells or directly through the cell.

140
Q

why is the amygdala important for the fear emotional response?

A

amygdala target areas control responses that make up the biological component of the fear emotional response and is ideally-placed to be a key node in emotional responses

141
Q

what lobe is the prefrontal lobe placed in?

A

frontal

142
Q

what do people believe the pre frontal cortex is responsible for?

A

emotional decision making

143
Q

what are the three findings of functional studies in PFC?

A
  1. decreased activity of PFC in young people with history of violent behaviour
  2. decreased activity of PFC in murderers and increased activity of amygdala
  3. vPFC is not specific to anger/aggression; inhibits other emotional states
144
Q

what is memory extinction?

A

the process that underlies the reduction of a conditioned response when the conditioned stimulus no longer predicts the unconditioned stimulus

145
Q

once memory extinction occurs can the memory resurface?

A

yes, the memory can recover and resurface

146
Q

what is the PAG?

A

periaqueductal grey

147
Q

where is the PAG located?

A

around the central aqueduct deep in the brain

148
Q

what are the steps of emotional regulation?

A

PFC inhibits amygdala (keeps it under control), the amygdala then activates PAG, through that the amygdala can coordinate the biological response

149
Q

what is the interim summary on emotion?

A

emotions are the result of complex two way interactions between physiological state and cognitive processes

150
Q

what system is involved in emotion?

A

limbic

151
Q

what is the amygdala involved with concerning emotion?

A

attributes emotional significance to events

152
Q

what is the ventral PFC involved with concerning emotion?

A

emotional decision making

153
Q

what is the PAG is involved with concerning emotion?

A

the selection of defensive emotional responses

154
Q

what are emotions driven by?

A

biologically significant stimuli

155
Q

what are the adaptive benefits of emotions?

A

find food/water/mates
avoid danger
signal

156
Q

how can emotions be maladaptive?

A

phobias
PTSD
drug addiction/non-homeostatic obesity

157
Q

what do emotional facial expressions signal?

A

internal state

158
Q

during what time are facial expression more readily observed?

A

social situations

158
Q

are facial expressions alone sufficient in determining the internal state?

A

no

159
Q

what 6 expressions are consistently identified?

A

anger
sadness
happiness
fear
disgust
surprise

160
Q

are emotional facial expressions global?

A

there are social cultural differences in terms of facial expressions

161
Q

what is the amygdalas involvement in recognition of emotional facial expressions?

A

damage to the amygdala impairs recognition of emotional facial expressions but does not affect ability to recognise identity nor recognition of emotion from tone of tone

162
Q

what can amygdala patients do to recognise emotional expressions?

A

can be trained

163
Q

which side of the brain/face is more expressive?

A

left side of the face
right side of the brain

164
Q

what is activation in dorsolateral PFC and anterior cingulate associated with?

A

associated with attempts to control unwanted prejudicial responses to black faces

165
Q

what is white matter?

A

it is composed of myelinated axons and provides connections between different cortical regions

166
Q

what are these connections essential for?

A

cognitive function

167
Q

what does the variability in white matter underlie?

A

individual differences in our cognitive abilities

168
Q

what does white matter damage result in?

A

in the breakdown of connectivity which leads to cognitive deficits such as disconnection syndrome

169
Q

what is essential to brain development and maturation?

A

white matter changes and strengthening of connections between different cortical regions

170
Q

what are some neurodevelopmental disorders a result of?

A

of abnormal connectivity

171
Q

does white matter change?

A

white matter changes as we learn or practise new skills (brain plasticity)

172
Q

what is used to non-invasively study white matter and connectivity in the human brain?

A

brain imaging techniques, DTI (diffusion tensor imaging) and tractography

173
Q

what is incentive motivation?

A

behaviour is drawn towards rewards e.g food

174
Q

what is incentive value referring to?

A

the value of rewards depends upon current drive state e.g food not as attractive when full

175
Q

what signals do insulin produce?

A

signals relating to nutritional state

176
Q

what signals do dopamine produce?

A

signals relating to food reward

177
Q

what reduces appetite in women?

A

intranasal insulin

178
Q

what is the DSM-5 definition of PTSD?

A

triggered by exposure to actual or threatened death, serious injury or sexual violation and causes clinically significant distress or impairment in the individuals social interactions, capacity to work or other important areas of functioning

179
Q

what are the 4 diagnostic clusters of PTSD?

A

re-experiencing (flashbacks)
avoidance (avoiding triggers or reminders of their trauma)
negative cognitions (low moods or depression)
arousal (more responsive or reactive to stimulation)

180
Q

what did activation of the amygdala correlate with in PTSD patients?

A

symptom severity

181
Q

what is the correlation between activity in amygdala and PFC?

A

negative

182
Q

what happens to cortisol in PTSD?

A

it is reduced

183
Q

what does enhanced noradrenaline do to traumatic memories?

A

potentiate (increase the effect)

184
Q

how does cortisol and NA compete with eachother?

A

low cortisol -> high NA

185
Q

what is NA important for?

A

emotional memories

186
Q

what may prevent PTSD?

A

attenuating (reducing the effect) of NA

187
Q

extinction is known to depend upon the ___

A

PFC

188
Q

what might impaired PFC function result in?

A

weaker extinction and so enhanced persistence of traumatic memory

189
Q

what are PTSD patients impaired at?

A

fear memory extinction

190
Q

what is consummatory behaviour?

A

stereotyped/reflexive= hypothalamus

191
Q

what is preparatory behaviour?

A

flexible/goal-directed=amygdala

192
Q

what is homeostasis?

A

the maintenance of an ideal, stable physiological environment where deviation s from the ideal result in a need state or physiological deprivation state

193
Q

what does a need or physiological deprivation
state result in?

A

a psychological state called drive state where the drive activates and directs behaviour

194
Q

what is the homeostatic theory?

A

early homeostatic drive explanations of behaviour suggest that the body detects a deviation from a physiological set point. when the set point is restored the body sends out a signal to stop acting which is an example of a negative feedback system.

195
Q

what is hedonic reward?

A

unrelated to motivational drive, rewarding properties of stimuli alter behaviour

196
Q

what is liking?

A

liking = sensory pleasure (unconscious)
can be conditioned
brainstem
hierarchal control

197
Q

what is wanting?

A

wanting = motivational incentive value
not sensory pleasure
not cognitive
can also be conditioned to stimuli
mesolimbic dopamine

198
Q

describe the formation of the nervous system

A

neural plate closes
it is pulled down to create a neural groove with neural folds
BMP releases neural crest cells

199
Q

what is proliferation?

A

rapid cell divisions regardless of cell type, neurogenesis refers to birth of neurones

200
Q

what is neurogenesis?

A

neuronal proliferation as it leads to exponential increase in the number of new neurones (adult isn’t as fast)

201
Q

what is neural migration?

A

neurones begin to migrate from where they were produced to start forming our cerebral cortex

202
Q

what is specific neuroanatomy?

A

six layered cerebral cortex
subcortical structures
connectivity

203
Q

what is axonal formation and synaptogenesis?

A

as axons begin to form, synapses start to grow which is the early stages of connectivity

204
Q

what is neuronal and circuits refinement?

A

sometimes rapid neurogenesis can lead to defective cells. only 50% neurones end up becoming part of the brain and the rest are intentionally killed as part of the development process.

205
Q

what processes refine the neural circuits?

A

apoptosis
synaptic pruning

206
Q

what is myelination?

A

regional variation in the pattern of white matter pathways maturation

207
Q

what is neuronal differentiation?

A

a process by which different subpopulations/types of neurones are generated. these subpopulations are specific to different parts of the brain, play different functions and use different neurotransmitters

208
Q

what is axonal growth?

A

formation of an axon

209
Q

what is adult neurogenesis?

A

generation of new neurones

210
Q

how are neurones functional?

A

they differentiate, migrate, form connections and myelinated

211
Q

what are the types of neurodegeneration?

A

“normal” age related decline
neuro traumatic diseases
neurodegenerative diseases
neuropsychiatric diseases

212
Q

what are the consequences/mechanisms of neuroedegeneration?

A

death of neurones
fewer neurones take up less space -> smaller brain
loss of synaptic connections
axons degenerate
less “white matter”
smaller brains

213
Q

what are the types of degeneration?

A

Fast
- stroke
- hypoxia
Slow
- neurodegenerative diseases
- normal age related decline
- repeated concussion

214
Q

what are the general causes of neurone death/synapse loss?

A

hypoxia
excessive activity
idiopathic/sporadic
neuronal dysfunction, protein aggregations
monogenetic (Huntington’s disease)

215
Q

what is hypoxia?

A

lack of oxygen
cant generate enough energy
neurons die
strokes, transient ischaemic attack etc

216
Q

describe excessive activity?

A

exciotoxic lesions in rodents
glutamate hypothesis in epilepsy

217
Q

what is neuronal dysfunction, protein aggregations?

A

causes the neurone to undergo apoptosis
this apoptosis is not beneficial
compare to essential apoptosis in development

218
Q

what is monogenetic (huntington’s disease)

A

caused by mutation in a single gene
simpler than other degenerative disorders
mutation in the huntingtin gene
initial degeneration of neurones in the basal ganglia

219
Q

what is the difference between neuronal death during development neurodegeneration?

A

apoptosis or programmed cell death enable elimination of defective or excessive cells characterised by cell shrinkage etc. necrosis enables eliminations of cells damaged by external physiochemical stress characterised by cell swelling and loss of membrane integrity

220
Q

define alzheimer’s disease

A

amyloid plaques
poor memory for recent events; other cognitive problems, emotional and personality changes, amyloid plaques and neurofibrillary tangles

221
Q

define Parkinson’s disease

A

lower dopamine in substantia nigra
motor tremors, stiffness and slow movement; disease progression is also associated with cognitive deficits, loss of dopaminergic neurones, neurodegeneration of other brain regions affecting other neurotransmitters

222
Q

define huntington’s disease

A

affected basal ganglia
uncontrolled movements associated with neurodegeneration in the basal ganglia, emotional and cognitive problems

223
Q

what are the clinical characteristics of alzheimer’s disease?

A

memory
initially, poor memory for recent events
more so than age related memory decline
other areas
- deficits in spatial navigation
- changes in ppersonality
- aggression/apathy
- depressive symptoms

224
Q

name and describe the two main types of alzheimers?

A

sporadic/late onset
- no obvious cause or heritability
- most common
- apolipoprotein E (APOE)

early onset
- <10% oof cases
- 1-2% familial (inherited)

225
Q

describe neurodegeneration in AD

A

initial areas of degeneration (temporal lobe)
general neuronal loss
neurofibrillary tangles
amyloid plaques
synaptic loss
- correlates with cognitive impairment
- particularly affects cholinergic and glutamatergic synapses

226
Q

what are the two types of treatments for alzheimers?

A

drug and targeting pathology

227
Q

how does drug treatment for alzheimers work?

A

initial aim of boosting cholinergic transmission
prolong presence of remaining ACh in the synapse
Acetylcholinesterase inhibitors
not very effective
nicotine patches

228
Q

how does targeting pathology work for treating alzheimers?

A

divert APP away from amyloid
antibodies for amyloid
not very effective

229
Q

what are the three main types of parkinsons disease?

A

idiopathic, drug induced and genetic

230
Q

what is idiopathic parkinsons disease?

A

no identifiable cause
most common

231
Q

what is drug induce parkinsons disease?

A

can be caused by antipsychotic medication
slightly different from parkinsons disesase

232
Q

how rare is genetic parkinsons disease?

A

<5%

233
Q

what are the clinical characteristics of parkinsons disease?

A

motor function and non-motor function

234
Q

what is motor function?

A

tremors
rigid muscles
slowness or absence of movement
initially unilateral
very early symptoms in facial expressions

235
Q

what is non-motor functions?

A

cognitive effects
emotional effects
not just a consequence of being aware of the movement problems
can characterise as a general slowing of brain function

236
Q

what does degeneration in parkinsons disease look like?

A

degeneration is extensive before symptoms appear
80% neuron loss
would help to detect before such loss

237
Q

what are the treatments for parkinsons disease?

A

drugs, cell transplantation, deep brain stimulation, repair and recovery, possible in peripheral nervous system

238
Q

how does drug treatment work for parkinsons disease?

A

aim of replacing/increasing dopamine
but dopamine is rapidly metabolised
also does not cross the BBB
levodopa (L-DOPA)
dopamine agonists

239
Q

how does cell transplantation work for parkinsons disease?

A

aim of enhancing the function of remaining dopamine circuitry

240
Q

how does repair and recovery work for parkinsons disease?

A

possible in peripheral nervous system
cut finger nerve
axon regrows
connects to sensory cell or muscle
only if cell body remains intact

241
Q

why is CNS recovery not normal for parkinsons disease?

A

complexity of connection, as connections mature they change compared to those in the developing brain and are different to the stable connections in the PNS. also, would need to reconnect correctly which is possible in the spinal cord but almost impossible in the brain

First year Psychology (4 decks)

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