Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HYMS Y1 > Block 6 W1 > Flashcards

Block 6 W1 Flashcards

1
Q

Define consciousness.

A

State of being aware of and responsive to ones surroundings (awareness, wakefulness, alertness).
A person’s awareness or perception of something - involves perception, cognition and action.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the levels of consciousness.

A
  1. Fully conscious
  2. Clouding of consciousness
  3. Confusional state
  4. Delirium
  5. Lethargy
  6. Obtundation
  7. Stupor
  8. Hypersomnia
  9. Minimally responsive state
  10. Unresponsive Wakefulness syndrome
  11. Akinetic mutism
  12. Locked-in syndrome
  13. Coma
  14. Brain death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define locked-in syndrome.

A

Patient has awareness, sleep-wake cycles and meaningful behaviour but is isolated due to facial and body paralysis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define minimally conscious state.

A

Patient has intermittent periods of awareness and wakefulness and displays some meaningful behaviour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define unresponsive wakefulness syndrome.

A

Patient has sleep-wake cycles, but lacks awareness. Only displays reflexive and non-purposeful behaviour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define chronic coma.

A

Patient lacks awareness and sleep-wake cycles. Only displays reflexive behaviour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define brain death.

A

Patient lacks awareness, sleep-wake cycles and brain-mediated reflexive behaviour.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the normal and abnormal loss of consciousness.

A

Normal - sleep
Abnormal - coma, anaesthesia, unresponsive wakefulness syndrome.
Malaria - leading cause of loss of consciousness.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How is consciousness assessed?

A

ABC
History
Screening examinations and neurological examination
Glasgow coma scale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the AVPU assessment.

A

A - patient is awake
V - patient responds to verbal stimulation
P - patient responds to painful stimuli
U - patient is unresponsive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the Glasgow coma scale.

A 
Eye opening:
- none 1
- to pain 2
- to loud voice 3
- spontaneous 4
Verbal response:
- none 1
- incomprehensible words 2
- inappropriate words 3
- confused, disoriented 4
- oriented 5
Motor response:
- none 1
- extensor posturing 2
- abnormal flexion posturing 3
- withdraws from pain 4
- localises pain 5
- obeys command 6
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the GCS results.

A 
E + V + M = 3 - 15
90% less than or equal to 8 = coma
>=9 not in coma
9-11 moderate severity
>=12 minor injury
8 - critical score
<=8 at 6 hours - 50% die
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define brainstem death.

A

Irreversible loss of capacity for consciousness + irreversible loss of capacity to breathe.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the NHS definition of death.

A

Person must be unconscious and fail to respond to outside stimulation.
Person’s heartbeat and breathing can only be maintained using ventilator.
Must be clear evidence that serious brain damage has occurred and it can’t be cured.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the criteria for classification of death?

A
  • aetiology of irreversible brain damage
  • patient is deeply comatose, unresponsive, requiring artificial ventilation
  • not caused by depressant drugs
  • not caused by primary hypothermia
  • not caused by potentially reversible circulatory, metabolism and endocrine disturbances
  • not caused by potentially reversible causes of apnoea such as muscle relaxants and cervical cord injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe the absence of brain-stem reflexes.

A
  • pupil response
  • corneal reflex -> stroke cornea with tissue or cotton wool
  • vestibular-ocular reflex -> inserts ice-cold water into each ear, usually causes eye movement
  • cranial nerve motor response -> apply supraorbital pressure to elicit motor response
  • cough/gag reflex
  • respiratory effort - ventilator disconnected 5mins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Describe the neurological basis of consciousness.

A 
Brainstem areas (reticular activating system) + cerebral cortex are essential for consciousness (memory, language, emotion, attention).
No single cortical area is crucial for maintaining consciousness.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe the reticular activating system.

A

Collection of nuclei found throughout midbrain and extends into hindbrain (pons and medulla) and spinal cord.
Diffuse area, no clear anatomical boundaries.
Consists of 4 principle sets of nuclei:
- sends output to every part of CNS
- belong to various diffuse neuromodulatory systems
NTs - Dopamine + NA - hyper vigilance, ACh (low - sleep, high - awake), Serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the locus coeruleus.

A

In pons, sends info to nearly all CNS. Active during arousal, novel stimuli, mediates sympathetic effects of stress.
Hypoactivity - depression
Disorder - anxiety, panic, PTSD
NT - NA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the raphe nuclei.

A

Collection of nuclei in midline of brain, pons and medulla.
Project to large areas of CNS.
Cells in rostral parts active during awake state.
Projections help regulate circadian rhythm, enkephalin release.
Disorder - depression, OCD
NT - serotonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the ventral segmental area.

A

Ventral region of midbrain.
Projects mainly to frontal cortex and limbic system.
Involved in reward circuitry of brain - reinforces pleasurable sensations, motivation, intense emotion.
Disorders - drug addiction, schizophrenia, PD, ADHD
NT - dopamine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the cholinergic nuclei.

A

Basal forebrain nuclei - projects to all cortical areas especially frontal.
Dorsolateral pontine nuclei - projects to basal ganglia, thalamus, hypothalamus, brainstem and cerebellum.
Active during states of arousal, induce wakefulness and REM sleep.
Contribute to synaptic plasticity and involved in learning and memory.
Disorders - Alzheimer’s, amnesia, dementia
NT - ACh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What does damage to anterior hypothalamus cause?

A

Insomnia (shorter sleep)

VLPO - ventrolateral preoptic nuclei - GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What does encephalitic damage to posterior hypothalamus cause?

A 
Sleeping sickness (longer sleep)
Tuberomammilary nucleus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the role of RAS in sleep.

A

Involved in regulating sleep-wake cycle, arousal and attention.
Damage - loss of consciousness and coma.
Ascending RAS:
- awake -> cholinergic fibres increases firing
- asleep -> cholinergic fibres decreases firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the activities during awake state.

A
  • ACh system active
  • sensory thalamus facilitated
  • reticular nucleus inhibited
  • thalamocortical neurones active
  • EEG desynchronous (fast activity, low amplitude)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the activities during asleep state.

A
  • ACh system inactive
  • sensory thalamus inhibited
  • reticular nucleus active
  • thalamocortical neurones slow
  • EEG synchronous
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Describe the oscillations in EEG.

A

Oscillations generated by interaction between 3 types of neurones:

  • thalamocortical (thalamus)
  • reticular (reticular nucleus)
  • corticothalamic (cerebral cortex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the 2 main types of sleep?

A
  1. Synchronised, non-REM sleep
    - EEG waves are slow and synchronised
    - dominated by low frequency activity (delta waves)
  2. Desynchronised, REM sleep
    - rapid eye movement
    - every 90-120 minutes
    - high frequency activity in EEG (like awake state)
    - paradoxical sleep
    - abolition of muscle tone
    - associated with dreams.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Describe the waves of sleep.

A 
Awake - high freq, beta waves
Drowsy - alpha waves
Stage 1 - theta waves
Stage 2 - sleep spindles and mixed EEG activity
Slow-wave sleep - low freq, delta waves
REM sleep - high freq, beta waves
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

List disorders of sleep.

A

Common:
- psychiatric condition including anxiety
- orthopnea (SOB)
- enuresis (bladder control)
- epilepsy (neuronal seizures)
Rare:
Narcolepsy - spontaneous transition from wakefulness to REM caused by mutation of orexin receptor gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the short-term consequences of sleep deprivation?

A
  • slower reflexes
  • memory disorders
  • muscle fatigue
  • mood swings
  • aggressive behaviour
  • disorientation
  • hallucinations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the long-term consequences of sleep deprivation?

A
  • obesity
  • diabetes
  • high BP
    Insomnia can be insidious and self-perpetuated by bad sleep habits.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Describe the circadian rhythm.

A

Body has an internal clock, which may be demonstrated by light deprivation.
24.5-25.5 hours.
Neurones in retina, project to suprachiasmatic nucleus (SCN) of the hypothalamus. SCN innervates multiple nearby structures setting up a biological clock. SCN secrete neuropeptide vasopressin - indirectly modulates pineal gland - releases melatonin -> sleep promoting neurohormone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What are the 3 main types of memory storage?

A
  1. sensory store - kept in visual neurones (<500ms)
  2. short term store - product of attention, need to keep thinking about it to remember (few seconds)
  3. long term store - maintains info, change synapses in brain (minutes to lifetime)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Define semantic encoding.

A

Thinking about the meaning of the word/how it fits in a sentence makes you remember it better than what it looks like (physical) and sounds like (acoustic).
More meaningful -> less interference.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Describe context dependency in memory.

A

The environmental conditions where you learn makes a difference:

  • match between environmental contexts of encoding and recall
  • spatial memory = powerful cue -> flooding back of memories.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Describe state dependency in memory.

A

Can recall info better when you feel the same as when you learnt it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Describe mood dependency in memory.

A

More likely to recall unhappy info encoded in sad mood when you’re sad.
Emotion = cue for retrieval - depression stabilises sad mood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 2 LTM stores.

A
  1. hippocampus (damaged in amnesia) - unique experiences of people/places/objects in events (episodic memory)
  2. anterior temporal lobe (atrophy in SD) - similarities between experiences to create concepts (semantic memory)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does sleep help memory?

A

Slow wave sleep is important for memory consolidation - period of sleep enhances memory relative to wakefulness - deep sleep consolidates memory.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe the multi-store model of memory.

A

Encoding occurs in hippocampus - forms links between elements of an episode. Neurones in the hippocampus binds together things in a memory to re-instate the full picture of the memory.
e.g. cliff top walk when my dog dug up a weird old tin:
Familiar character (dog) - anterior temporal lobes
Object (old tin) - inferior temporal cortex
Place (cliff) - parahippocampal area
Each area project to hippocampus by long term potentiation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How is memory retrieved from hippocampus?

A

One element of the story is a cue - brings back whole experience so memories are basically associations (via hippocampus).

44
Q

Why do we forget from our short term memory?

A

Things slip out over time when we are distracted - decay and displacement.

45
Q

Why do we forget from our long term memory?

A
  • failure to encode deeply
  • cues are ineffective -> can’t access memory
  • interference from similar memories -> competition between memories
46
Q

What are the common causes of amnesia?

A

LTM impairment

  • Alzheimer’s disease
  • viral infection -> attacks midline areas of brain after travelling up cranial nerves (enters brain and influences memory structures - especially herpes simplex)
  • long-term alcoholism: Korsakoff’s syndrome -> destroys memory structures
  • head injury -> poor retrieval of events just prior to injury and normal retrieval of events from childhood - hippocampus not needed to connect the different parts of memory
  • anoxia -> CO poisoning, hippocampus is earliest part affected as needs lots of O2.
47
Q

What are the structures damaged in amnesia?

A

Hippocampus and other limbic structures e.g. fornix, mammillary body and parahippocampal cortex.

48
Q

What is preserved in amnesia?

A
  1. Non-declarative memory - people with amnesia still have good motor memory, shows that hippocampus not required for some types of non-conscious long-term learning.
  2. Semantic memories from declarative memory - normal retention of factual knowledge, normal on tests such as providing definitions, naming pictures, understanding sentences. Shows that hippocampus is not final store of knowledge.
49
Q

Describe the temporal gradient in amnesia.

A

Not all episodes are lost - older memories are preserved. Because memories become more reliant on neocortex and less dependent on hippocampus over time, following consolidation. Childhood memories are preserved because they get consolidated by sleep and are transferred from hippocampus to cortex.

50
Q

What is semantic dementia?

A

Subtype of frontotemporal dementia.
Due to deterioration in temporal lobes - causes progressive loss of conceptual knowledge across modalities and can’t recognise objects.

51
Q

What are the things that remain intact in semantic dementia?

A
  • memory for recent events
  • phonology/syntax
  • visual-spatial skills
  • non-verbal reasoning
    Not intellectual deficit
52
Q

What is reverse temporal gradient in semantic dementia?

A

Impaired repository of distant events as well as facts.

53
Q

What is behavioural genetics?

A

Interdisciplinary scientific effort to establish a causal link between genes, behavioural traits and neural mechanisms.
Aims to distinguish the genetic and environmental contribution to behaviour and the interactions between the two.

54
Q

How has Francis Galton affected behavioural genetics?

A

Identified the normal distribution across a population for intelligence. Developed the statistical concepts of regression and correlation. Designed early twin studies but championed eugenics - the active promotion of selective mating to promote what are judges to be desired characteristics.

55
Q

What are behaviours?

A

Cognitive abilities and disabilities, psychopathology, personality, substance use and abuse, health and well-being behaviour.

56
Q

Define polygenic inheritance.

A

Large number of genes contribute cumulative small effects towards significant heritability of a behavioural phenotype, with a normal distribution.

57
Q

Define heritability.

A

Proportion of phenotypic variance that can be accounted for by genetic differences among individuals.

58
Q

How has discovery of DNA affected behavioural genetics?

A

Genetic testing for single gene disorders identifying those affected - for intervention and prognosis.

59
Q

What are the finding from large scale twin and adoption studies?

A

Largely polygenic inheritance for behaviour.

Genome wide association studies linking smaller units than genes and copy number variants to behavioural phenotypes.

60
Q

Differentiate between shared and non-shared environment.

A

Shared - non-genetic factors experienced by all siblings or twins (same house).
Non-shared - non-genetic factors which don’t correlate between siblings and twins, including any error of measurement in behavioural trait concerned. Accounts for all differences between identical twins brought up in same house.
For most behavioural traits, the impact of non-shared environment is greater than shared environment.

61
Q

What is considered to be environment?

A

Prenatal, nutrition, illness and social factors.

62
Q

Define gene-environment correlation.

A

Life experiences correlated with genetic propensity.

63
Q

Define gene-environment interaction.

A

Effects of environment can depend on genetics and the effects can depend on environment.

64
Q

What are the quantitative genetics research methods?

A

Adoption studies - comparing those reared together and apart.
Twin studies - comparing identical and fraternal, in long-term cohorts.
Combo - twins adopted apart.

65
Q

What are the molecular genetics research methods?

A

Candidate gene studies
Genome wide association studies - using SNPs and copy number variants in large numbers
Multivariate genetic analysis - to examine genetic mediation of behavioural associations within individual twin pairs.

66
Q

Describe adoption studies.

A

Direct comparison of behavioural phenotype in genetic relatives can evidence the genetic contribution and comparison in environmental relatives.
First adoption study of schizophrenia - Heston 1966 -> compared incidence in adopted offspring of women with schizophrenia with that of matched adoptees whose parents had no known mental illness -> 10% incidence.

67
Q

What are the limits of adoption studies?

A

Gradual decline in adoption in high-income countries. Adoptive parents and adoptees may be substantially different from normal population. Prenatal environment may make contribution before adoption. Open adoptions.

68
Q

Describe twin studies.

A

Comparison of behavioural trait concordance in monozygotic twins vs. dizygotic twins. Assumed equal environment.

69
Q

Describe the genetic and environmental influences on food preferences.

A

Food preference have moderate heritability and shared environment has no effect. All the non-genetic contribution is non-shared environment, the unique environment as experienced by that individual has substantial effect.

70
Q

What are the limits of twin studies?

A

May not be generalisable. Impact of complete follow up and lost data. Measurement errors.

71
Q

Describe genome wide association studies.

A

Large scale molecular genetic studies of unrelated individuals, including comparison of cases vs. controls.
10 mill SNPs in our DNA, most with no known effect on function but some are biomarkers for genes with known function.
Autism spectrum disorder - novel locus + significant overlap with schizophrenia.

72
Q

Describe the regulation of gene expression and its effect on behaviour.

A

DNA methylation can silence a particular gene and hence change its contribution to behavioural traits through life course or in response to environment.
Increased serotonin transporter gene DNA methylation is associated with bullying victimisation and blunted cortisol response to stress in childhood.

73
Q

What are the 10 replicated findings?

A
  1. all psychological traits show significant genetic influence e.g. intelligence, major mental disorder.
  2. no traits are 100% heritable
  3. heritability is caused by may genes of small effect (polygenic)
  4. phenotypic correlations between psychological traits show significant and substantial genetic mediation
  5. heritability of intelligence increases throughout development
  6. age to age stability is mainly down to genetics
  7. most measures of environment show significant genetic influence
  8. most associations between environmental measures and psychological traits are significantly mediated genetically
  9. most environmental effects are not shared by children growing up in same family
  10. abnormal is normal - polygenic effects influence normal variation in mental disorder symptoms, personality and cognitive abilities.
74
Q

What is the criteria for a neurotransmitter?

A

Must be synthesised or present in presynaptic neurone.
Must produce response in postsynaptic neurone.
Must be a mechanism of removal.
Specific receptors for substance must be on postsynaptic neurone.
Same response must be obtained when chemical is experimentally placed on target.

75
Q

Describe the different class of NTs.

A

Subdivided into:

  • small molecule NT
  • neuropeptides
76
Q

Describe small molecule NT.

A

Generally mediate fast transmission and released from low freq stimulation (small vesicles) and high freq (small and large vesicles).
Enzymes that make these NT are made in Golgi, then transported town MTs to synaptic terminals where they make NT from precursors.
Most NT i.e. NE/GABA released from small, clear vesicles.

77
Q

Describe neuropeptides.

A

Mediate slow synaptic signalling and released from high freq stimulation.
Molecule is directly made from AA in Golgi, then passed to terminal via MT - much faster.
e.g. somatostatin/vasopressin.

78
Q

What are the types of receptors?

A

Inotropic - ion channel, binding of NT leads to channel opening and ions can more dependent on gradient -> fast transmission.
Metabotropic - receptors coupled to transmembrane proteins i.e. GPCRs - leads to effect within cell.

79
Q

Describe acetylcholine.

A

Acts on nicotinic and muscarinic receptors.

Found mostly in ANS - PreG of sympathetic and PreG and PostG on parasympathetic.

80
Q

What is the role of acetylcholine?

A

In CNS as memory (hippocampus), learning (basal forebrain), sleep (thalamus), thermoregulation (brainstem).
Death of cholinergic neurones of forebrain, which project to cortex and hippocampus leads to Alzheimer’s - so treat by acetylcholinesterase inhibitors.

81
Q

How is acetylcholine synthesised?

A 
From choline (diet) and acetyl CoA -> choline acetyltransferase. 
Exocytosed into vesicles - once used broken down by acetylcholinesterase and reabsorbed.
82
Q

Where is nicotinic receptors found?

A

NMJs, autonomic ganglia, adrenal medulla and CNS.
Nicotinic Nn - postganglion neurones and some presynaptic.
Nicotinic Nm - skeletal motor endplate.
Blocked by curare.

83
Q

Where is muscarinic receptors found?

A 
Peripheral tissues, ANS and CNS.
5 subtypes:
M1, 3, 5 - coupled to G protein/PLC
M2, 4 - coupled to Gi/open K+ channel
Blocked by atropine.
84
Q

What are the amino acid NTs?

A

Glutamate
GABA
Glycine

85
Q

Describe glutamate.

A

Nearly all excitatory neurones in brain are glutaminergic.

86
Q

How is glutamate synthesised?

A

Glutamate broken down to glutamine post-synaptically and taken up from synaptic cleft by glutamate transporters on presynaptic terminal and glial cells - converted back to glutamate by glutaminase.

87
Q

What are the main receptors for glutamate?

A

AMPA, NMDA and kainate.

88
Q

Describe how glutamate binds to receptors.

A

APMA and NMDA co-exist.
Glutamate binds AMPA -> depolarisation and Na+ influx -> conformational change in NMDA receptor, releasing Mg2+ ion and allowing Ca2+ influx -> activates 2nd messenger pathway.

89
Q

Describe GABA.

A

Most inhibitory neurones in CNS use this or glycine.

90
Q

How is GABA synthesised?

A

Precursor is glutamate - de-carboxylated to GABA by glutamic acid decarboxylase.
Transporters found in glial cells and presynaptic neurones reabsorb GABA/glycine.

91
Q

What are the main receptors for GABA?

A

GABA-A - inotropic and allows Cl- to enter and hyper polarise cell.
GABA-B

92
Q

What is the clinical significance of GABA?

A

Epilepsy - uncontrolled excitation of the brain due to imbalance between excitatory/inhibitory NT.
Agonise GABA receptors - inhibit brain activity e.g. diazepam.
Increase GABA content within brain - sodium valproate.

93
Q

How is glycine synthesised?

A

Glucose -> serine -> glycine.

Reabsorbed by transporters on glial cells or presynaptic neurones then cleaved to break it down.

94
Q

Describe the glycine receptor.

A

Inotropic receptor - ligand gated ion channel -> inhibitory NT and linked to Cl- ions.

95
Q

What is the role of glycine?

A

Major spinal cord inhibitory NT - acts mainly in brainstem and spinal cord.
Inherited defects in receptor channel found in hyperekplexia (exaggerated response).

96
Q

List the amine NTs.

A

Noradrenaline, adrenaline, dopamine and serotonin.

97
Q

How are amines synthesised?

A

Precursor - tyrosine -> converted to L-DOPA then to dopamine by dopa decarboxylase -> converted to norepinephrine and then epinephrine.

98
Q

How are amines inactivated?

A

Reabsorbed in neuronal/extra neuronal tissues.
Broken down by MAOa (serotonin/NE) and MAOb (dopamine) enzymes.
Diffuse away from receptors.

99
Q

What are the dopamine systems in the brain?

A
  1. Mesolimbic - reinforcement
  2. Mesocortical - planning
  3. Nigrostriatal - movement
100
Q

What are the dopamine receptors?

A

D1 and D5 - coupled to Gs

D2, D3 and D4 - coupled to Gi

101
Q

Where is noradrenaline found?

A

In locus coeruleus and projects to various parts of brain.

Released from sympathetic postganglionic fibres in PNS.

102
Q

How is NA synthesised and degraded?

A

Dopamine -> NA by dopamine beta-hydroxylase.

Degradation - 2 routes using MAO and COMT

103
Q

How is adrenaline synthesised?

A

NA N-methylated by PNMT to adrenaline in cytosol then stored in vesicles.

104
Q

How is serotonin synthesised?

A 
From tryptophan (meat/dairy).
Project from raphe nuclei.
105
Q

What is the role of serotonin and receptors?

A

Mood, emotions and sleep - decreases in depression.

7 types of 5-HT Rs - most metabotropic except 5-HT3 - inotropic.

106
Q

Where is serotonin stored and broken down?

A

Stores in vesicles by same monoamine transporter, VMAT for catecholamines.
Reabsorbed mediated by serotonin transporter and then re-concentrated back into vesicles by VMAT.
Broken down by MAO - oxidised to 5-HIAA, which is further metabolised in pineal gland to melatonin.

107
Q

Describe substance P.

A

Tachykinin family - slows smooth muscle contraction.
Binds all 3 receptors neurokinin I - binds strongest to NK1.
Wide distribution dorsal horn of spinal cord, amygdala, medulla, hypothalamus, substantial nigra, cerebral cortex and striatum.
Present in C fibres and pain transmission.

HYMS Y1 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions